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Studies explore potential, concerning connection between COVID-19 and Alzheimer’s disease – KARE11.com

Posted: February 19, 2021 at 3:52 am


According to a recent study, the number of deaths attributable to Alzheimers and dementia during the pandemic has jumped by 12% in Minnesota alone.

MINNEAPOLIS Several new studies show a possible and concerning connection between COVID-19 infections and those who already have or may develop Alzheimers and other dementia.

In fact, one study is even researching whether a COVID infection may increase a persons chance for developing dementia of which Alzheimers is the most common form down the road.

Latest studies: jump in ALZ deaths, Alzheimers patients twice as likely to contract COVID

According to data from the Centers for Disease Control and Prevention (CDC), the number of deaths attributable to Alzheimers and dementia during the pandemic has jumped by 12% in Minnesota alone. Leaders with the Alzheimers Association, Minnesota-North Dakota note the reasons for the increase among the 99,000 Minnesotans living with Alzheimers may vary but could include: reduced access to physicians and health care during the pandemic, a disruption to daily routines and care provided by family members and other caregivers, and the simple toll of social isolation.

Meantime, a recent study by Case Western University published in Alzheimers & Dementia: The Journal of the Alzheimers Association also found those with dementia have double the risk of contracting COVID-19 when compared to those without dementia. The study further noted that 20% of patients with dementia died when they contracted COVID, compared to just over 5% of people without dementia.

One big study: does getting COVID lead to dementia down the road?

But perhaps the most alarming study relates to whether a COVID infection could lead to developing dementia later in life.

It seems like large organizations, like the Alzheimers Association, have the presence of mind, no pun intended, to start looking at cognitive consequences of this disease, said Dr. Michael Rosenbloom, a behavioral neurologist and clinical director of the HealthPartners Center for Memory and Aging.

Rosenbloom noted doctors are already seeing signs of how COVID affects the brain, short-term, with patients becoming confused or having memory issues after infection. But now a new international study supported by the Alzheimers Association with technical guidance from the World Health Organization will look at the potential for COVIDs long-term effects on the brain, by following 40,000 patients from nearly 40 countries for at least two to three years.

We know that this is a virus that does have a predilection for the central nervous system. And so, for instance, it is not uncommon for patients who are infected with COVID-19, especially if theyre elderly, to present with delirium and altered mental status, Rosenbloom shared with KARE 11s Karla Hult.

Rosenbloom further noted the study builds upon an area of scientific research related to other respiratory viruses, like the 1918 influenza pandemic or severe acute respiratory syndrome (SARS). Years after those viruses attacked the global population, scientists noted an increase in other issues, including: memory problems, anxiety, and psychosis.

Doctors fear COVID-19 could leave its lasting mark by creatively attacking the brain: targeting the area of the brain responsible for both the sense of smell and short-term memory; creating blood clots that cause strokes; triggering a destructive immune response; or simply, cutting off oxygen.

If a patient has respiratory failure and the brain is deprived of oxygen, this can further impact cognition and will also have downstream consequences over time, Rosenbloom said.

The study will further compare cognitive symptoms based on the care patients received during their COVID-related illness. Scientists will also evaluate whether COVID contributes to cases of familiar dementia like Alzheimer's or if patients develop a "COVID-specific" dementia.

And while the study may not deliver initial results until early 2022, Rosenbloom and others are already braced for what the findings may mean for the current health care crisis related to Alzheimer's and other dementia.

You can imagine that we may have COVID clinics, patients post-COVID presenting with cognitive decline. And these numbers are probably going to be vast because of how infectious this disease is, and how many patients have been infected not just in the United States but throughout the world, Rosenbloom said, adding, This potentially could present a crisis for individuals or physicians in my field of work."

And on that point of concern and awareness, Rosenbloom and other neurologists have a familiar ally.

If there is a link and more people are diagnosed because they had COVID disease, it would be astronomical the cost, the financial cost. And of course, devastating, emotionally to all of us, said Sue Spalding, Chief Executive Officer of the Alzheimers Association, Minnesota-North Dakota.

Spalding noted the concern is a huge reason why the Alzheimer's Association supports the global, ongoing study and why advocates continue to encourage COVID-19 vaccinations for everyone, especially those in long-term care centers or vulnerable communities. The CDC also recommends that front-line health workers and residents and staff in long-term care settings be among the first groups to receive vaccination.

For more information on the sweeping global study, click here.

And check out alz.org for information on support or other Alzheimer's research.

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Studies explore potential, concerning connection between COVID-19 and Alzheimer's disease - KARE11.com

First-in-Human Clinical Trial to Assess Gene Therapy for Alzheimer’s Disease – UC San Diego Health

Posted: at 3:52 am


Researchers at University of California San Diego School of Medicine have launched a first-in-human Phase I clinical trial to assess the safety and efficacy of a gene therapy to deliver a key protein into the brains of persons with Alzheimers disease (AD) or Mild Cognitive Impairment (MCI), a condition that often precedes full-blown dementia.

The protein, called brain-derived neurotrophic factor or BDNF, is part of a family of growth factors found in the brain and central nervous system that support the survival of existing neurons and promote growth and differentiation of new neurons and synapses. BDNF is particularly important in brain regions susceptible to degeneration in AD.

In previous published research, principal investigator Mark Tuszynski, MD, PhD, professor of neuroscience and director of the Translational Neuroscience Institute at UC San Diego School of Medicine, and colleagues described the prevention and reversal of brain cell degeneration and death in animal models.

Mark Tuszynski, MD, PhD, professor of neuroscience and director of the Translational Neuroscience Institute at UC San Diego School of Medicine.

We found that delivering BDNF to the part of the brain that is affected earliest in Alzheimers disease the entorhinal cortex and hippocampus was able to reverse the loss of connections and to protect from ongoing cell degeneration, said Tuszynski. These benefits were observed in aged rats, aged monkeys and amyloid mice.

Amyloid mice are genetically engineered to inherit a mutation in the gene encoding the amyloid precursor protein, and as a result develop amyloid plaques aggregates of misfolded proteins in the brain that are considered a hallmark characteristic of AD.

BDNF is normally produced throughout life in the entorhinal cortex, an important memory center in the brain and one of the first places where the effects of AD typically appear in the form of short-term memory loss. Persons with AD have diminished levels of BDNF.

But BDNF is not easy to work with. It is a large molecule and cannot pass through the blood-brain barrier. As a result, researchers will use gene therapy in which a harmless adeno-associated virus (AAV2) is modified to carry the BDNF gene and injected directly into targeted regions of the brain, where researchers hope it will prompt production of therapeutic BDNF in nearby cells.

The injections are precisely controlled to contain exposure to surrounding degenerating neurons since freely circulating BDNF can cause adverse effects, such as seizures.

The three-year-long trial will recruit 12 participants with either diagnosed AD or MCI to receive AAV2-BDNF treatment, with another 12 persons serving as comparative controls over that period.

This is the first safety and efficacy assessment of AAV2-BDNF in humans. A previous gene therapy trial from 2001 to 2012 using AAV2 and a different protein called nerve growth factor (NGF) found heightened growth, axonal sprouting and activation of functional markers in the brains of participants.

The BDNF gene therapy trial in AD represents an advance over the earlier NGF trial, said Tuszynski. BDNF is a more potent growth factor than NGF for neural circuits that degenerate in AD. In addition, new methods for delivering BDNF will more effectively deliver and distribute it into the entorhinal cortex and hippocampus.

Despite billions of dollars of research investment and decades of effort, there are only two symptomatic treatments for AD. There is no cure or approved way to slow or stop progression of the neurological disorder that afflicts more than 5 million Americans and is the sixth leading cause of death in the United States.

Numerous clinical trials are ongoing to assess pharmaceutical remedies. Tuszynski said gene therapy, which debuted in 1980 and has been tested on multiple diseases and conditions, represents a different approach to a disease that requires new ways of thinking about the disease and new attempts at treatments.

We hope to build on recent successes of gene therapy in other diseases, including a breakthrough success in the treatment of congenital weakness in infants (spinal muscular atrophy) and blindness (Leber Hereditary Optic Neuropathy, a form of retinitis pigmentosa), Tuszynski said.

BDNF gene therapy has the potential, unlike other AD therapies currently under development, to rebuild brain circuits, slow cell loss and stimulate cell function. We are looking forward to observing the effects of this new effort in patients with AD and MCI.

For more information on this Phase I clinical trial, contact Michelle Mendoza at 858-249-3015 or email alphastemcellclinic@ucsd.edu

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First-in-Human Clinical Trial to Assess Gene Therapy for Alzheimer's Disease - UC San Diego Health

Alzheimers Q&A: Are massage or touch therapies beneficial for those with Alzheimer’s disease? – The Advocate

Posted: at 3:52 am


No treatment plan is perfect for those with Alzheimers disease, but massage/touch therapies can provide viable interventions and increase quality of life, curb and calm disruptive behaviors, improve blood circulation levels and generally lift an affected person's spirits.

Scientists and studies have long found that people of all ages who are regularly touched tend to be less anxious, recover from illness more quickly and feel safer and more nurtured.

Some research has found that for those with Alzheimers, human touch plays an integral role in promoting overall well-being. Just five minutes of hand massage, for instance, can induce a physical relaxation response and reduce levels of cortisol, a hormone released during times of stress.

Massage/touch therapy has also been found to raise levels of serotonin, a neurochemical that promotes feelings of calm and reduces anxiety.

Massage and touch have been suggested as nonpharmacological interventions to reduce and/or manage a range of conditions associated with Alzheimers and dementia-related disorders, such as anxiety, agitated behaviors and depression. However, because the research is so limited in scope, it is not possible to draw general conclusions about the benefits of these therapies for those with these conditions.

Some studies have found that using calming music and hand massage reduced verbal agitation, a benefit sustained for up to one hour. Another study found that hand massage/touch therapies were somewhat beneficial in agitatedindividuals. Hand massages were given for five minutes in the mornings and afternoons for 10 days, and results showed these interventions decreased the frequency and intensity of agitated behaviors during morning care routines, but not during evening care.

People with Alzheimers disease dont lose the capacity for human emotion or recognition of a caring touch. There are several benefits massage therapy offers people with Alzheimers disease, including increased body awareness and alertness, as well as a reduction in the feelings of confusion and anxiety. You also build reassurance and trust and help calm agitation, said Ann Catlin, founder of the Center for Compassionate Touch and an expert in the field of massage therapy in elder care and hospice.

Additionally, Catlin said she believes massage therapy can also help ease the effects of isolation, loneliness and boredom while encouraging feelings of worthiness and well-being.

While some people with Alzheimer's respond well to being touched or having their hands massaged, others could have a negative response. Some connect it to long-term memories of emotional or physical pain. Therefore, such therapies need to be applied on an individual basis.

Questions about Alzheimer's disease or related disorders can be sent to Dana Territo, the Memory Whisperer, owner of Dana Territo Consulting, LLC, at thememorywhisperer@gmail.com.

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Alzheimers Q&A: Are massage or touch therapies beneficial for those with Alzheimer's disease? - The Advocate

SciSparc to Conduct a Phase IIa Clinical Trial in Alzheimer’s Patients Using the Company’s Proprietary Cannabinoid-Based Treatment – PRNewswire

Posted: at 3:52 am


TEL AVIV, Israel, Feb. 17, 2021 /PRNewswire/ --SciSparc Ltd. (formerly known as Therapix Biosciences Ltd.) (OTCQB: SPRCY) a specialty, clinical-stage pharmaceutical company focusing on the development of cannabinoid-based treatments, today announced it has signed an agreement with The Israeli Medical Center for Alzheimer's, to conduct a phase IIa clinical trial to evaluate the safety, tolerability and efficacy of SCI-110 (formerly THX-110) in patients with Alzheimer's disease and agitation using the Company's proprietary cannabinoid-based technology.

The study's primary objective is the safety of SCI-110 and the secondary objective is the ability of the compound to ameliorate agitation and other behavioral disturbances in patients with Alzheimer's disease.

The study will be initiated immediately after receipt of all the required approvals from the Institutional Review Boards(IRB) and the Israeli Ministry of Health (MoH).

The study, titled "Clinical Study Protocol Phase II-a open label trial to evaluate the safety, tolerability and efficacy trend of SCI-110 in patients with Alzheimer's Disease and agitation," will be conducted under the leadership of Dr. Alona Raveh, MD, Principal Investigator and board-certified geriatrician.

The drug product, SCI-110, is a unique proprietary combination of Dronabinol (synthetic delta-9-tetrahydrocannabinol (-THC), and Palmitoylethanolamide (PEA).

Alzheimer's disease is the most common type of dementia, accounting for over two-thirds of cases of dementia. Alzheimer's disease is a neurodegenerative disease that causes progressive and disabling impairment of cognitive functions including memory, comprehension, language, attention, reasoning and judgment. Symptoms of Alzheimer's disease depend on the stage of the disease. Neuropsychiatric symptoms like apathy, social withdrawal, disinhibition, agitation, psychosis, insomnia, poor appetite and wandering are also common in the mid to late stages.

The current pharmacological treatment of agitation in Alzheimer's disease has an unsatisfactory benefit/risk ratio and often involves using off-label drugs. Antipsychotic drugs, which are the most frequently used drugs for this purpose, are only marginally better than placebo.

"As the population of the world continues to age, Alzheimer's disease is one of the most common diseases affecting the elderly. Alzheimer's disease is frequently associated with neuropsychiatric symptoms such as agitation and aggression, especially in the severe stages of the illness. However, the limited efficacy and high-risk profiles of current pharmacotherapies for the management of agitation and aggression in Alzheimer's disease left us, the caregivers, with no good treatment alternatives. We are always in the search for new, innovative treatment solutions, and I hope SCI-110 may represent such a solution," said Nitai Eliash, the Chief Executive Officer of the Israeli Medical Center for Alzheimer's, where the trial will take place.

"We believe there is strong scientific rationale for exploring SCI-110 in patients with Alzheimer's disease and agitation and we appreciate very much the collaboration and opportunity to study our innovative proprietary drug candidate, SCI-110, at the leading center in Israel for the treatment of Alzheimer's disease patients," stated Dr. Adi Zuloff-Shani, PhD, Chief Technology Officer of SciSparc.

About SciSparc (OTCQB:SPRCY):

SciSparc Ltd. is a specialty clinical-stage pharmaceutical company led by an experienced team of senior executives and scientists. Our focus is on creating and enhancing a portfolio of technologies and assets based on cannabinoid pharmaceuticals. With this focus, the Company is currently engaged in the following drug development programs based on THC and/or non-psychoactive cannabidiol (CBD): SCI-110 (formerly THX-110) for the treatment of Tourette syndrome and for the treatment of obstructive sleep apnea; SCI-160 (formerly THX-160) for the treatment of pain; and SCI-210 (formerly THX-210) for the treatment of autism spectrum disorder and epilepsy.

About The Israeli Medical Center for Alzheimer's:

The Israeli Medical Center for Alzheimer's (IMCA) is the only medical center in Israel exclusively devoted to the treatment of Alzheimer's disease patients. IMCA was founded in 1994 as a public, not for profit foundation, and in July 2001 it opened as an active medical center. The Alzheimer's center treats hundreds of patients a year, as inpatients, outpatients and as part of its diagnosis and counseling services. Numerous studies are conducted at the center in collaboration with researchers at universities.

Forward-Looking Statements:

This press release contains forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995 and other Federal securities laws. For example, SciSparc is using forward-looking statements when it discusses expectations regarding the potential for approvals needed for the initiation of the Phase IIa study, the safety of SCI-110 and the ability of SCI-110 to treat Alzheimer's disease. The transaction described here may never be consummated and definitive agreement(s) may not be executed, and, if executed, such agreement(s) may be subject to conditions before it can be completed. In addition, the market for products contemplated by the letter of intent is in a period of regulatory and business uncertainty and financial and business results from such businesses are uncertain. Historic results of scientific research and clinical and preclinical trials do not guarantee that the conclusions of future research or trials will suggest identical or even similar conclusions. Because such statements deal with future events and are based on SciSparc's current expectations, they are subject to various risks and uncertainties and actual results, performance or achievements of SciSparc could differ materially from those described in or implied by the statements in this press release. The forward-looking statements contained or implied in this press release are subject to other risks and uncertainties, including those discussed under the heading "Risk Factors" in SciSparc's Annual Report on Form 20-F filed with the SEC on June 15, 2020, and in subsequent filings with the U.S. Securities and Exchange Commission. Except as otherwise required by law, SciSparc disclaims any intention or obligation to update or revise any forward-looking statements, which speak only as of the date they were made, whether as a result of new information, future events or circumstances or otherwise.

Investor Contact:[emailprotected] Tel: +972-3-6167055

SOURCE SciSparc Ltd.

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SciSparc to Conduct a Phase IIa Clinical Trial in Alzheimer's Patients Using the Company's Proprietary Cannabinoid-Based Treatment - PRNewswire

Study finds apples reduce risk of Alzheimer’s disease – Know 5 other health benefits of the nutritious fruit – Times Now

Posted: at 3:52 am


Study finds apples reduce risk of Alzheimer's disease - Know 5 other health benefits of the nutritious fruit  |  Photo Credit: iStock Images

New Delhi: If someone has not heard the saying An apple a day, keeps the doctor away in their whole life, they have probably been living under a rock, or may be on another planet. Apples have been touted as one of the best fruits to add to your diet, and for all the right reasons. While apples have many health benefits, researchers have recently found that the nutritious fruit may be extremely healthy for the brain, and even reduce the risk of brain disorders such as Alzheimer's disease.

According to the study, natural compounds found in apples can reduce the risk of developing Alzheimer's disease, and even other forms of dementia. High concentrations of phytonutrients found in the fruit help in the creation of neurons, a process that is called neurogenesis. Neurons are a highly excitable cell that transmits information to parts of the body via electrical signals and they boost our learning and memory abilities. Two compounds quercetin in apple peel and dihydroxy benzoic acid (DHBA) in apple flesh generated neurons. The experiment was found to have a positive result in the brains of mice.

However, it was found that apple juice did not significantly contribute to neurogenesis, suggesting the benefits apply to eating the whole apple and not just a glass of juice.

Disclaimer: Tips and suggestions mentioned in the article are for general information purpose only and should not be construed as professional medical advice. Always consult your doctor or a dietician before starting any fitness programme or making any changes to your diet.

Get the Latest health news, healthy diet, weight loss, Yoga, and fitness tips, more updates on Times Now

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Study finds apples reduce risk of Alzheimer's disease - Know 5 other health benefits of the nutritious fruit - Times Now

Online Seminar To Examine Health Disparities and Alzheimer’s – WHMI

Posted: at 3:52 am


By Jon King / jking@whmi.com

A virtual seminar next month will feature some of the nations top experts in the field of health equity and Alzheimers disease.

The Alzheimers Association is hosting the virtual Dr. James S. Jackson Seminar on Health Equity and Alzheimer's Disease on Wednesday, March 3rd from 5 - 6:30pm. Named in honor of the late-Dr. James Jacksons research at the University of Michigan, it will feature the latest research involving underserved communities, bringing together some of the nations top experts in the field of health equity and Alzheimers disease.

According to the Alzheimers Association, COVID-19 has laid bare some undesirable truths: underserved communities are disproportionately impacted by the pandemic adding that In the field of Alzheimers and dementia, statistics point to a similar troubling trend. The Association says the event is particularly timely with new research from Case Western Reserve University showing African Americans with dementia have close to three times the risk of being infected with COVID-19 as white individuals with dementia.

Jennifer Lepard, Alzheimers Association Michigan Chapter president and CEO said that while their goal is to work toward a world without Alzheimers and all other dementia, they cant do that without listening to and understanding the needs of diverse communities locally. Registration details for the March 3rd seminar are available online at alz.org/jackson-seminar.

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Online Seminar To Examine Health Disparities and Alzheimer's - WHMI

The Problem of Alzheimer’s: A Podcast with Jason Karlawish – GeriPal – A Geriatrics and Palliative Care Blog

Posted: at 3:52 am


Where are we with Alzheimers? Are we about to see a revolution in how we diagnose and treat it with Amyloid PET scans and the amyloid antibody aducanumab (which is currently on FDAs desk for approval)? Or are we still in the same place where there is no meaningfully effective treatment? Or is it somewhere in between, given the data that we have on comprehensive dementia care?

We talk today with Jason Karlawish, a professor of medicine, medical ethics and health policy, and neurology at the University of Pennsylvania Perelman School of Medicine. In addition to being a geriatrician extraordinaire, he is the author of the new book The Problem of Alzheimers: How Science, Culture, and Politics Turned a Rare Disease into a Crisis and What We Can Do About It.

In addition to talking about PET scans and new drugs like aducanumab, we discuss with Jason about the history of Alzheimers, the history of how we care for and fund caregivers, and where we go from here.

So take a listen and check out Jasons book!

You can also find us onYoutube!

Listen to GeriPal Podcasts on:

TRANSCRIPT

Alex: This is Alex Smith.

Eric: And, Alex, who is our guest today?

Alex: We are delighted to welcome to the GeriPal Podcast Jason Karlawish, who is a geriatrician and is Co-Director of the Penn Memory Center and a Professor of Medicine at the University of Pennsylvania, Perelman School of Medicine. Welcome to the GeriPal Podcast, Jason.

Jason: Thank you. Great to be here, Alex and Eric.

Eric: It's great to have you. Alex and I just finished reading your book, The Problem of Alzheimer's, and we're really excited to talk to you about it. It is really a truly wonderful book. So very researched with stories that I've never heard about before, about the history of Alzheimer's, the history of geriatrics. It is quite amazing. But before we get on that topic, we always start off with a song request. Do you have a song for Alex?

Jason: I do. Robert Johnson, Sweet Home Chicago.

Alex: And why this song?

Jason: Two reasons: one personal and the other ties to the book, believe it or not. Personal, I came of age in Chicago. It's where I went to college and then I went to medical school and then came back for fellowship, and critical points in my personal and my academic intellectual development were in Chicago. So it's really just my sweet home.

Jason: But also Robert Johnson, an interesting story, kind of forgotten, kind of disappeared from the scene, but then rediscovered. Kind of like Alzheimer's disease, nearly forgotten, but then rediscovered. So I just thought it had a nice symmetry.

Alex: That's great. Here's a little bit. (singing)

Jason: All right.

Eric: That was awesome. I can't believe Ken Kovinsky hasn't yet made us do that song.

Alex: No, he did. We did that on our first podcast.

Alex: That was better than the first podcast, but I still am not good at the blues. That's good. I hope. People, if you're listening and you're a future guest, please request the blues because I will get better over time, I promise.

Eric: Jason, again, thank you. First of all, where can people find this book?

Jason: So The Problem of Alzheimer's: How Science, Culture, and Politics Turned a Rare Disease into a Crisis and What We Can Do About It is available in hardback, in Kindle/e-book, and in audio book, wherever fine hardback, Kindle/e-book, audio books are sold.

Jason: Bound, please, if you can, but also your local bookstore, Amazon, yada, yada, St. Martin's Press, a division of Macmillan. If you get the audio book, you get to listen to me read the opening chapter and the closing chapter. In between is an actor.

Eric: Nice. I've got to start off by asking, because we had a fair amount of authors come on our show. We talked about their books. This was incredibly detailed. The amount of references and the stories and going into the history, we're going to go through all of that. It must have been ... This is your second book. How did you decide, "I'm going to write a book on the problem with Alzheimer's"?

Jason: The idea had been gestating, germinating, pick your odd biological metaphor, for probably a decade, and I'm so glad I didn't write it when I first thought of it, because I really had to arrive at this book the way it was done. A lot of attention in creating it was how much is this book about me as a doctor of Alzheimer's care versus about the disease, and I finally think I arrived at that reconciliation.

Jason: It's interesting, the working titles for the book originally was My Profession: Confessions of an Alzheimer's Doctor, a wonderful play on profession and confession. That helped move it along. Then I'm like, "No, no, no." Then it was called The House of Alzheimer's to capture this construction of the disease, if you will, dare I say social construction, and that didn't work, actually. That hung on for a while.

Jason: Then it was called The Disease of the Century. Then I was at a party during the pandemic, a small party, socially gathered. Very socially gathered. I told something about the book and they said, "Oh, it's about COVID, the disease of the century."

Eric: COVID screws up everything, man.

Jason: I know. But then this is the title, The Problem of ... Anyway, so it was a journey to get to that ... Those titles, I think, showed the journey of getting to the book as it is now. I agree, the observation with the prior book and this book are both heavy with using history as a means to tell a story. I dare would never call myself a historian, just like a historian doesn't call themselves a neurosurgeon. But many neurosurgeons like to become historians, but that's another story.

Eric: Then taking another step back, even before the book, why Alzheimer's? Why is this such an important issue? I mean there are a lot of problems in geriatrics, caring for older adults, in medicine. Is there something that drew you to Alzheimer's?

Jason: Yeah. I lay that out in the book. In part three, I bring things up to present time and put myself into it and a bit of the story how I moved from critical care to geriatrics, and then within geriatrics made Alzheimer's the focus. Some of that's personal, events around the destructive care that my grandfather received, and some of it's academic, namely long-standing interest in issues of ethics and human values.

Jason: If you had to pick the one specialty, I would argue, that most brings those things together, it's geriatrics. It's certainly in the top, I think. Then if you had to pick the one disease within geriatric syndrome, it's dementia.

Jason: And so, for me, it was, has been, and I think, for a while, at least it's going to remain the focus that allows me to do what I like to do across all those areas.

Eric: Yeah. Alex, before we're talking on the four sections, any other questions that you have?

Alex: I just want to say that I also agree this is a tremendous book. Really enjoyed reading it. So delighted to see familiar characters in it, including yourself, of course. But also Mike Weiner, who's at the VA in San Francisco, where Eric and I practice, and Rita Redberg, who is a professor of cardiology at UCSF and played an integral role in steering this committee about should we be screening for Alzheimer's with amyloid PET scans, and Steve Pearson, who was my residency director and is now head of ICER, Institute for Clinical Effectiveness Research, of which I'm a part and have a meeting on Thursday, as well as just learning all of this tremendous history about the formation of Alzheimer's Association, policy changes. We're going to get into some of this now.

Alex: But also very different from your prior book, Open Wound: The Tragic Obsession of Dr. William Beaumont, which I read and we reviewed on GeriPal previously ... I think Dan Matlock wrote that review ... which was much more of a historical, fictional account, whereas this is nonfiction.

Jason: This is definitely nonfiction.

Alex: This is much more similar to being mortal, with more history, but still including the personal stories which bring it home and make it very particular and specific for the readers. So kudos to you on writing this, and we should launch into it.

Jason: All right.

Eric: All right. We're going to break it down by section. The first section, and correct me if I'm wrong on any of this, is really the changing meaning and definition of Alzheimer's disease. Again, really encourage, if people want more in depth, really do read this book if you're interested in Alzheimer's disease or the history of dementia, history of geriatrics. It's like it's all in there.

Eric: But I'm going to start off with one quote, where you actually ... You tell one of your patients' wives that, "Mr. Harrison pushed back when I labeled his wife as mild stage. 'Her anger was so disruptive, this had to be severe,' he continued. The counter severity of the emotional behavioral problems are not factored into staging."

Eric: I'm just going to stop there. It was really lovely written. It was the first time I thought, "Oh, yeah." When I say mild disease, I'm thinking it from my medical lens, but there are so many other lenses including like from a personal perspective for this husband. "It's not mild. It's taking all of my resources."

Jason: Exactly, yeah. So it must be severe, yeah. Yeah, I know. Part One: Alzheimer's Unbound is all about the changing meanings, emphasis on meanings, plural. The particular quote that you pulled there was this husband who ... I'm staging the disease by the way we're supposed to, which is the severity of impairments and IADLs and then BADLs. We don't put behavior into that because it waxes and wanes, as we know.

Jason: And yet for him, it was all about the severity of her anger, which made the disease, at least we would say, so I think subjectively, ethically, if you will, severe. That theme runs through that part, which is how do you see what is this disease and, therefore, what do you talk about when you talk about Alzheimer's? Much of it, of course, Alzheimer's Unbound, about how the professional community has had its changing meanings.

Jason: I started out with the view ... I was trained in the dementia and then is it Alzheimer's. I realized as I wrote the book that I occupied personally, this transformative period where we want from you must go through the door of dementia to enter the house of Alzheimer's to now this unbound sense of what Alzheimer's is where you don't have to have any clinical problems, if you will, to be labeled with it.

Jason: And so, that's what that part's about. We truly, I mean you guys too, have lived through that revolution and redefinition and recasting of the disease and all the messiness that follows from that.

Eric: Well, let's talk about that. So what does it take to get a label of Alzheimer's disease now?

Jason: I think now it depends on where you go, and I don't mean that flippantly. But if you think of the disease the way that the field is transformed, and I talk about that in the Republic of Alzheimer's Disease, the chapter about this coalescing of the biomarker revolution into a recasting of the disease as a biomarker, biological diagnosis akin to cancer, et cetera. There's a lot of logic to that for many reasons that are commendable.

Jason: But what that does is it unlimbers the disease from many clinical correlation, any clinical reality. If you had to pick one disease that was so hard bound to clinical care, it was Alzheimer's. You had to have dementia.

Jason: Of course, there's that interregnum period of mild cognitive impairment where you don't have dementia, but you're not normal anymore. You're in the middle. That's one other way to define what Alzheimer's is. That is to say the clinical state of MCI or dementia caused by Alzheimer's. Or maybe never mind that, that's just the syndromic staging and it's all about the biology.

Jason: My point is that I wanted to put the origins of all those streams of thought out there. How did we get to them and what have been the controversies that surround them now and going forward?

Eric: Yeah. One big controversy right now is when we think about ... I'd love to talk about this thinking about Alzheimer's disease before it gets clinical, but how and whether or not new imaging, like amyloid PET scans, are really changing the way we're thinking about it or should think about it, or is it still very much in the it needs to be in certain centers is, it's very much a research-

Jason: Alex mentioned Dr. Redberg, who's at your institution. I think one of the high-low moments in the modern history of Alzheimer's was the committee that she chaired, the MEDCAC committee, the Medicare Advisory Committee on Coverage or whatever it is. It's this committee that's charged with advising CMS, the Centers for Medicare & Medicaid Services about the evidence to support covering something.

Jason: And so, Eli Lilly brings the first commercially available amyloid radio tracer for their review, and hopefully their agreement, that the evidence is sufficient to support its use in clinical practice. I got the transcript to that hearing. It's publicly available. You have to have the patience to read it.

Jason: And it was a disaster. That is to say from the perspective of Lilly. I mean it is a fascinating ... Someone ought to make a play out of it, because you witness this coming together of the biomarker Alzheimer's field with the wider field of medicine ... And these were smart people, I mean Redberg and others. These were not off-the-street, I-don't ... I mean they knew the science, and they could not convince the one and the other ... In particular the Alzheimer's field, could not convince the wider smart field of medicine that this is a test you should use in clinical practice.

Jason: It's this interesting moment where ... I don't want to say two cultures, but two ways of thinking about the disease cannot come together. It ends with the committee voting that the evidence is not sufficient to support its use in clinical practice.

Jason: What's interesting, of course, is that that was a day in January where it was preternaturally warm in Baltimore and there was a thunderstorm at the end of the day, which there used to be an expression "thunder in the winter" or something. It's impossible until global warming, of course. Just to me, that just captured how unusual that day ... The sort of oddities of that day.

Jason: But, simply, it shows how difficult it has been and remains to translate this biomarker-based definition into wide clinical practice, and that hearing laid it all out.

Eric: Yeah, I can imagine the challenges. A, you'd have to show it actually significantly changes management or what happens. B, it also links the biomarker, let's say amyloid, to the disease. Later on, I think in section three, you also talk about, maybe it was before, the heterogeneity. There is a lot of differences. How sure are we ... Like everything that we're seeing is related to this biomarker, which is amyloid. How do you put the-

Jason: Well, the funny thing about that hearing was that they went in with the argument that for people with mild cognitive impairment, this test is really good. They were right and they were wrong. They were right because if you come to my Penn Memory Center and I spend the effort and time to figure out that you truly have mild cognitive impairment, and I walk you through imaging, I can see the value of an amyloid scan in your case to figure you out.

Jason: But that's at a Penn Memory Center where we have the ability to do that kind of work up. MCI is this fragile little bird in the spring, that out in the wide world, it just can't survive, namely you put MCI out in the ... And this is what I think Redberg and rest were on to, which is they're not going to figure out MCI ...

Eric: Yeah. You have your 50-year-old who's going to come to your clinic. You're just going to order your PET amyloid for everybody.

Jason: Exactly.

Eric: Oh, PET amyloid's positive. Oh, my goodness.

Jason: That's what they figured out and that's what the field ... And that still remains today that we have this idea of MCI which works well if you come to a place like Penn or the Mayo Clinic, where it was discovered. But in wide clinical practice remains this mysterious protean, "I guess you've got MCI if you've got a memory complaint," or, "I don't want to have to stay you have Alzheimer's disease."

Jason: And so, that's one problem. Then, of course, the other problem is the more we understand the biology of the disease, the more complex we see it as, that is to say the discoveries of things like TDP-43, vascular disease, ubiquitin. This is not one disease. It's many disease. It's best thought as Alzheimer's diseases. And that's what the science has arrived at now.

Eric: Yeah. I love that analogy you also make with cancer. You can't think of cancer as one disease. I also think it's interesting when we think about it, because it links to ... Medicine really loves defining people with pre-diseases, like prediabetes.

Eric: That great paper that just came out in JAMA Internal Medicine on prediabetes with editorial on that, basically showing that a lot of people with prediabetes ... More people convert to normal than convert to diabetes-

Alex: Among older adults.

Eric: Among older adults. Sorry. Thank you, Alex. What's the title of that editorial, Alex, again? I love that title.

Eric: Yeah. It was like Two Risk Factors Removed or something. I think a lot of the worry is when we're doing around PET MRIs, what are we actually measuring here? I'd just love, Jason, for my own knowledge, like let's say you have somebody in your memory clinic. So you've got the expertise now. Somebody comes in with an MCI, you do this PET scan. How many people will actually ... Like not everybody with a positive PET will develop dementia over three years, most. Where are we with the knowledge around ...

Jason: So in locally classified amnestic MCI, where you also see neurogeneration, meaning evidence of atrophy on MRI, and then add to that not just amyloid, but a tau marker, you've got pretty good prognostic ability that, over five years, they're going to experience cognitive decline.

Jason: Having said that, though, and to get to the label of MCI, as I point out in the book, is tremendously challenging. The folks at the Mayo Clinic had the luxury of the Mayo medical record, the Mayo system to really figure that out, and wide clinical practice that's so fungible.

Jason: But where the field will go is much like in cancer and cardiovascular disease. Where there is a drug, a treatment, it will help define the disease. So there will be some sort of druggable and, therefore, that'll be a definition of the druggable form of Alzheimer's.

Jason: You see that in the history of MS as well. As MS treatments were developed for multiple sclerosis, it carved out different kinds of MS that responded more or less differently to the various treatments that were developed since beta interferon in the early '90s.

Jason: So I mean I think the future for this disease is more or less druggable targets based on various different biological measures. Where? I think the bottom line will be the bottom line, which is what's the return on this expense in terms of delaying disability, et cetera?

Eric: Don't we have a druggable target, Aricept, memantine, Namenda?

Jason: No, those drugs were developed to develop a research infrastructure. I had a lot of fun on the part of the book called The Birth of Alzheimer's. It ends with hope in a pill. Hope in a pill is the story of the cholinesterase inhibitors.

Eric: I love that chapter, by the way.

Jason: Yeah. Ken Covinsky gets quoted in that.

Eric: It was so great just to learn the history of tacrine and all of these things as a geriatrician. I've never prescribed tacrine. I've heard about it, and it was great just to see like how it actually developed over time.

Jason: Yeah, the story on the cholinesterase inhibitors is one that I think ought not to be forgotten. I'm afraid it's being a little bit repeated now with the story about aducanumab that's under FDA review as we speak.

Jason: But essentially there was great hope, promise, and desire for something that worked. Unfortunately, there's nothing like those kind of emotions in people who can't admit their emotions to compel those people to do things. So the scientific community really went over the top on the benefits of the cholinesterase inhibitors, publishing in New England Journal in an editorial that said it was a triumph for the scientific method, et cetera.

Jason: Ultimately, the study that got tacrine going was found essentially to be fraudulent. They didn't know that at the time they published the story, the research report, but the NEJM editors would subsequently admit that they had concerns about the design of the study.

Jason: The point I try to bring out in that section was you've got an awful disease, no treatments, a desire to show progress. That's a dangerous brew to make bad decisions, especially if your culture is we can't admit the emotional aspects that drive us. [crosstalk 00:22:48].

Alex: Right.

Eric: I feel like you linked later to ... What's the antibody called again? Ada-something.

Jason: Oh, aducanumab.

Eric: There you go. I could never remember those names. Basically, that story of that drug seem to perfectly mimic the story of what was happening-

Jason: There are strange parallels between current events and past events. No surprise.

Eric: Yeah. Maybe we can figure out, tease out some statistical significant differences if you ... Maybe tease around the numbers a little bit. But what's the clinical benefit of it? It seemed like that was a potential question that's happening right now. Is that right?

Jason: It is. That is a very pithy summary. One of the things I talk about in the hope in a pill and that chapter is the difficulty that began in the cholinergic hypothesis era, and still persist today, of having a coherent, understandable language to talk about how have we successfully treated this disease. It's very different than cancer or cardiovascular disease, where in the end, it's are you alive or dead, because death in this disease is something that is not an end point we want to delay. We have a very weird relationship with death with this disease.

Alex: Yeah. Is there anything more that we want to talk about with imaging? Because I want to ask a little bit more about treatment, which we've moved into. Eric, did you want to mention the oculo-prescriptive reflex, or should we skip over that?

Eric: No, I'm going to skip over that. I've got some backlash over that.

Alex: Let's skip that one.

Eric: I think the main thing is-

Alex: Listeners, you can figure out what that might mean [laughter]. You see something on amyloid and that leads to a prescription.

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The Problem of Alzheimer's: A Podcast with Jason Karlawish - GeriPal - A Geriatrics and Palliative Care Blog

Cassava Sciences Announces Significant Program Progress and Expected Key Milestones in 2021 for Its Clinical Program in Alzheimer’s Disease -…

Posted: February 9, 2021 at 6:55 pm


AUSTIN, Texas, Feb. 08, 2021 (GLOBE NEWSWIRE) -- Cassava Sciences, Inc. (Nasdaq: SAVA), a clinical-stage biotechnology company developing product candidates for Alzheimers disease, today announced significant program progress and expected milestones for 2021.

We started 2021 with tremendous momentum, led by results of a 6-month interim analysis from an open-label study of simufilam, our drug candidate for Alzheimers disease, said Remi Barbier, President & CEO. I believe the rest of the year may be equally exciting.

Cassava Sciences strategic focus for 2021 is to advance simufilam in a Phase 3 clinical program in Alzheimers disease, to expand drug manufacturing capabilities in support of the clinical program, and to continue to lead the Company to deliver the full potential of its product portfolio.

Cassava Sciences 2021 Scientific and Clinical OutlookCassava Sciences product portfolio includes a small molecule drug for the treatment of Alzheimers disease, called simufilam, and an investigational blood-based diagnostic to detect and monitor the progression of Alzheimers disease, called SavaDx.

Expected progress and key milestones in 2021 across Cassava Sciences product portfolio are summarized below.

Other Expected Milestones and Announcements for 2021

Slide DeckA copy of Cassava Sciences latest corporate presentation is available on its website https://www.CassavaSciences.com, under the Investors/Presentations page.

About Alzheimer's Disease Alzheimers disease is a progressive brain disorder that destroys memory and thinking skills. Currently, there are no drug therapies to halt Alzheimers disease, much less reverse its course. In the U.S. alone, approximately 5.8 million people are currently living with Alzheimers disease, and approximately 487,000 people age 65 or older developed Alzheimers in 2019.1 The number of people living with Alzheimers disease is expected to grow dramatically in the years ahead, resulting in a growing social and economic burden.2

About SimufilamSimufilam is a proprietary, small molecule (oral) drug that restores the normal shape and function of altered filamin A (FLNA), a scaffolding protein, in the brain. Altered FLNA in the brain disrupts the normal function of neurons, leading to Alzheimers pathology, neurodegeneration and neuroinflammation. The underlying science for simufilam is published in peer-reviewed journals, including Journal of Neuroscience, Neurobiology of Aging, Journal of Biological Chemistry, Neuroimmunology and Neuroinflammation and Journal of Prevention of Alzheimers Disease.

Cassava Sciences is also developing an investigational diagnostic, called SavaDx, to detect Alzheimers disease with a simple blood test.Simufilam and SavaDx were both developed in-house. Both product candidates are substantially funded by peer-review research grant awards from the National Institutes of Health (NIH). Cassava Sciences owns worldwide development and commercial rights to its research programs in Alzheimers disease, and related technologies, without royalty obligations to any third party.

About Cassava Sciences, Inc.Cassava Sciences mission is to discover and develop innovations for chronic, neurodegenerative conditions. Over the past 10 years, Cassava Sciences has combined state-of-the-art technology with new insights in neurobiology to develop novel solutions for Alzheimers disease. For more information, please visit: https://www.CassavaSciences.com

For More Information Contact:Eric Schoen, Chief Financial Officereschoen@CassavaSciences.com(512) 501-2450

Cassava Sciences open-label study of simufilam in Alzheimers disease is funded by clinical research grant #AG065152 from the National Institutes of Health (NIH/NIA).

The content of this press release is solely the responsibility of Cassava Sciences and does not necessarily represent the official views of the NIH/NIA.

Cassava Sciences Safe HarborThis news release contains forward-looking statements, including statements made pursuant to the safe harbor provisions of the Private Securities Litigation Reform Act of 1995, relating to: our strategy and plans; the treatment of Alzheimers disease; the status of current and future clinical studies with simufilam, including the interpretation of an interim analysis of open-label study results; planned enrollment and other changes to the open-label program; our intention to initiate a Phase 3 clinical program with simufilam in 2nd half 2021; results of our EOP2 meeting with FDA and the timing of further announcements; our ability to manufacture drug supply for a Phase 3 program and to enter into a long-term commercial drug supply agreement; the timing of validation studies with SavaDx; our ability to expand therapeutic indications for simufilam outside of Alzheimers disease; expected cash use in future periods; plans to publish results of a Phase 2b study in a peer-reviewed journal; verbal commentaries made by our employees; and potential benefits, if any, of the our product candidates. These statements may be identified by words such as may, anticipate, believe, could, expect, forecast, intend, plan, possible, potential, and other words and terms of similar meaning. Drug development and commercialization involve a high degree of risk, and only a small number of research and development programs result in commercialization of a product. Our clinical results from earlier-stage clinical trials may not be indicative of full results or results from later-stage or larger scale clinical trials and do not ensure regulatory approval. You should not place undue reliance on these statements or any scientific data we present or publish.

Such statements are based largely on our current expectations and projections about future events. Such statements speak only as of the date of this news release and are subject to a number of risks, uncertainties and assumptions, including, but not limited to, those risks relating to the ability to conduct or complete clinical studies on expected timelines, to demonstrate the specificity, safety, efficacy or potential health benefits of our product candidates, the severity and duration of health care precautions given the COVID-19 pandemic, any unanticipated impacts of the pandemic on our business operations, and including those described in the section entitled Risk Factors in our Annual Report on Form 10-K for the year ended December 31, 2019 and future reports to be filed with the SEC. The foregoing sets forth many, but not all, of the factors that could cause actual results to differ from expectations in any forward-looking statement. In light of these risks, uncertainties and assumptions, the forward-looking statements and events discussed in this news release are inherently uncertain and may not occur, and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Accordingly, you should not rely upon forward-looking statements as predictions of future events. Except as required by law, we disclaim any intention or responsibility for updating or revising any forward-looking statements contained in this news release.For further information regarding these and other risks related to our business, investors should consult our filings with the SEC, which are available on the SEC's website at http://www.sec.gov.

4, 5 Source: Alzheimers Association. Disease Facts and Figures. https://www.alz.org/media/documents/alzheimers-facts-and-figures-2019-r.pdf

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Cassava Sciences Announces Significant Program Progress and Expected Key Milestones in 2021 for Its Clinical Program in Alzheimer's Disease -...

Roche refreshingly cautious on Alzheimer’s hopeful gantenerumab amid growing hype from rivals – FierceBiotech

Posted: at 6:55 pm


As Eli Lilly and Biogen stir up hope in the Alzheimers disease drug space, Roches pharma CEO is not getting dragged into hype over its effort gantenerumab.

Roche is certainly committed to gantenerumab, an antibody that binds to and clears aggregated beta amyloid fibers, despite it failing a phase 3 trial back in 2014. The Swiss pharma resurrected gantenerumab in 2017 and is now running two more phase 3 trials, although it was hit by another setback last year.

That came from a phase 2/3 study, sponsored by Washington University School of Medicine, with support from groups including Lilly and Roche. Investigators randomized 194 people with an early-onset, inherited form of Alzheimers to take either Lillys solanezumab, Roches gantenerumab or placebo and tracked them for up to seven years.

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Both of these anti-amyloid beta antibodies failed to improve outcomes, with the findings showing neither drug was effective in dominantly inherited Alzheimer's disease (DIAD). The primary endpoint tracked cognition annually for four years using four tests of early-stage disease, the results of which were combined to give a composite score.

Lilly has already seen enough data to say it has no plans to seek approval in the subpopulation of DIAD patients enrolled in the phase 2/3. Solanezumab has already failed in the broader Alzheimers population, leading Lilly to give up on the asset in 2016, but its still working through a study, A4, in people with amyloid buildup but no signs of cognitive impairment.

RELATED: Lilly hails Alzheimer's win with donanemab, boasting 'significant slowing of decline'

The Big Pharma did chalk up a small win last month, however, with a different asset: donanemab (once known as LY3002813), which works an active immunotherapy designed to stimulate a patients immune system to attack and destroy beta amyloid plaques that are believed to form in the brain and spur the memory-wasting disease.

Its antibody goes after a modified form of beta amyloid called N3pG, and targeting this produced in its midstage results a significant slowing of decline in a composite measure of cognition and daily function in patients with early symptomatic Alzheimer's disease compared to placebo.

It did not hit all of its secondaries and details were sparse, but shares still jumped on the news last month.

The drug that has come closest to backing up this amyloid idea is Biogens aducanumab, which binds to aggregated beta amyloid and causes it to be cleared from the body.

It had, in fact, been on the edge of being scrapped, but Biogen drilled down into the data and thought it saw a glimmer of hope, so it's gone to the FDA for approval. Its PDUFA was originally set for March, but an expert outside panel said it shouldn't be approved late last year.

Last month, the FDA said it was in fact delaying a decision on the med by as much as three months, until June 7. Usually, this is bad news, but Biogens shares jumped, presumably as a sign that it might be approved, as it wasnt an outright rejection.

Despite the roller coaster ride in Alzheimer's over the years, and Roches own failure in DIAD patients, the Swiss major last year talked up the differences between the phase 2/3 flop and its ongoing late-phase studies to explain its continued confidence that gantenerumab may succeed.

Outside observers took a different position. Analysts at Jefferies expected the phase 2/3 trial to fail and accepted that the small size of the study and initial use of potentially suboptimal doses may have contributed to the lackluster data. Even so, the analysts said the failure again suggests the ongoing gantenerumab phase 3 studies are high risk.

Roche is set to find out whether that risk has paid off when it posts data from the phase 3 program in 2022. The program is assessing whether increasing the gantenerumab dose above the level used in earlier, failed trials will lead to better outcomes.

Given the talking up of Alzheimers prospects once again in the face of the glimmers from Biogen and Lilly, analysts on Roches financial call Thursday were quick to ask about how the C-suite viewed the future of gantenerumab, and that ongoing test.

RELATED: Biogen bullish on Alzheimer's drug approval, sees Lilly data as positive despite AdComm rejection

For once, the answer was measured (and very different from highly bullish Biogen at the J.P. Morgan healthcare conference last month, which also pointed to Lillys data as more hope for its once-failed candidate).

Well, believe me, it's on all of our minds, said Roches pharma chief Bill Anderson of the drug. We have lots of reasons to believe, and we have reasons to be concerned. Until there's a definitive, unassailable, pivotal result or pair of pivotal results, I think we have to handicap all these studies. And that's just how it is when you're pioneering in a new area. So, I can give you the five reasons we're excited. And then I would still say, I don't know.

He said, on reflection, success is likely a tossup. This is a difficult, difficult disease, he said. We don't understand the pathophysiology of Alzheimer's disease, and we're targeting something that is in a huge evidence that it's linked to Alzheimer's, but the causative role that it plays, we don't know. And the data that came out from another company (Eli Lilly), they did last quarter, people got really excited about, and I want to be excited to. But again, that's a little bit of a slight tweak on the MoA. It's a novel endpoint. It's a small data set. And we haven't seen the data yet. So I'm not going to take that and run off to celebrate.

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Roche refreshingly cautious on Alzheimer's hopeful gantenerumab amid growing hype from rivals - FierceBiotech

Ben-Gurion University Researchers Introduce New Method for Diagnosing Neurological and Psychiatric Conditions – PRNewswire

Posted: at 6:55 pm


BEER-SHEVA, Israel, Feb. 9, 2021 /PRNewswire/ -- Researchers at Ben-Gurion Universityof the Negev (BGU) have developed a new method for rapidly diagnosing brain blood vessel pathology that may lead to neurodegenerative diseases, such as Alzheimer's disease, as well as other neurological and psychiatric conditions, including epilepsy, traumatic brain injury and stroke. The novel method is based on analysis of EEG patterns using proprietary algorithms and was invented by Dr. Dan Milikovsky and Prof. Alon Friedman, MD-PhD, Departments of Physiology and Cell Biology, Cognitive and Brain Sciences, Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev.

The novel diagnostic method is based on findings from the lab of Prof. Friedman that patients with Alzheimer's disease and other brain conditions display nonconvulsive epileptic seizure-like activity that can be detected by EEG recordings. The study was published in the highly ranked Science Translational Medicine Journal [i]. This abnormal activity reflects pathological changes in dysfunction of the brain blood vessels, which contribute, according to recent studies, to the pathogenesis of various neurodegenerative and other neuro-psychiatric disorders.

"Research from our lab and others, shows that the pathological changes in the brain blood vessels, which are usually referred to as the blood-brain barrier (BBB), contribute to the formation of Alzheimer's disease and other brain disorders. Since dysfunction of the BBB is also a key component in the pathogenesis of epilepsy, we hypothesized that BBB dysfunction in Alzheimer's patients would also trigger abnormal brain activity that could be detected by EEG, an accessible and affordable tool used in the clinic, and serve as a diagnostic method for these conditions," explained Prof. Friedman. "Indeed, we find abnormal, epileptic-like EEG recordings in many patients with Alzheimer's disease as well as epilepsy, which reflect brain blood vessel pathology and can serve both for diagnosis as well as a therapeutic target."

The technology was successfully tested on animal models and dozens of patients and is now been validated on large databases of EEG records of thousands of patients.

"This new approach for diagnosing neurological conditions based on analysis of changes of blood vessels in the brain can be valuable for the early detection of Alzheimer's disease and other neurological conditions, at the stage when treatment can still slow down disease progression. The technology offers a biomarker for immediate results and allows for the continuous monitoring of the progression of the neurological condition and response to treatment," said Josh Peleg, CEO of BGN Technologies. "We are now seeking a potential industry partner for the further development of this promising method for a variety of applications, from monitoring of ICU patients, to patients after stroke and head injuries and for the diagnosis of vascular pathology in early Alzheimer's disease."

About BGN Technologies

BGN Technologiesis the technology transfer companyof Ben-Gurion University, the third largest university in Israel. BGN Technologies brings technological innovations from the lab to the market and fosters research collaborations and entrepreneurship among researchersand students. To date, BGNTechnologieshas established over 100 startup companiesin the fields of biotech, hi-tech, and cleantech, and has initiated leading technology hubs,incubators, and accelerators.Over the past decade, BGN Technologies has focused on creating long-term partnerships with multinational corporations such as Deutsche Telekom, Dell-EMC, PayPal, and Lockheed Martin, securing value and growth for Ben-Gurion University as well as the Negev region.For more information, visit the BGN Technologies website.

[i] Milikovsky1 et al. (Dec. 2019), Paroxysmal slow cortical activity in Alzheimer's disease and epilepsy is associated with blood-brain barrier dysfunction. Science Translational Medicine: Vol. 11, Issue 521, eaaw8954.

Media Contact:Tsipi HaitovskyGlobal Media LiaisonBGN TechnologiesTel: +972-52-598-9892E-mail: [emailprotected]

SOURCE BGN Technologies

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Ben-Gurion University Researchers Introduce New Method for Diagnosing Neurological and Psychiatric Conditions - PRNewswire

Global Alzheimer’s Disease Treatment Market Report 2020: Market is Expected to Recover in 2023 – Forecast to 2030 – ResearchAndMarkets.com – Yahoo…

Posted: at 6:55 pm


The "Alzheimer's Disease Treatment Global Market Report 2020-30: COVID-19 Growth and Change" report has been added to ResearchAndMarkets.com's offering.

Major players in the Alzheimer's disease treatment market are Allergan, Eisai Co. Ltd., Novartis AG, Pfizer Inc., Merz Pharma, H. Lundbeck A/S Biogen, AstraZeneca, and F. Hoffmann-La Roche Ltd.

The global Alzheimer's disease treatment market is expected to decline from $3.46 billion in 2019 to $3.42 billion in 2020 at a compound annual growth rate (CAGR) of -1.26%.

The decline is mainly due to the COVID-19 outbreak that has led to restrictive containment measures involving social distancing, remote working, and the closure of industries and other commercial activities resulting in operational challenges. The entire supply chain has been disrupted, impacting the market negatively. The market is then expected to recover and reach $4.96 billion in 2023 at a CAGR of 13.21%.

The global Alzheimer's disease treatment market consists of sales of drugs used to treat Alzheimer's disease. Alzheimer's disease is a progressive neurological disorder causing degeneration of brain cells, resulting in dementia (a condition that causes a decline in thinking, behavioral and social skills). The progression of this disease causes severe memory impairment and the person may lose the ability to carry out everyday tasks.

North America was the largest region in Alzheimer's disease treatment market in 2019. Asia-Pacific is expected to be the fastest-growing region in the forecast period.

In January 2020, Biogen Inc., an American multinational biotechnology company, acquired Pfizer Inc. for an upfront payment of $75 million with up to $635 million in potential additional development and commercialization milestone payments. Through this acquisition, Biogen plans to develop the Phase 1 asset for the treatment of Sundowning in Alzheimer's disease (AD) and Irregular Sleep Wake Rhythm Disorder (ISWRD) in Parkinson's disease (PD). Pfizer Inc. is an American multinational pharmaceutical corporation engaged in the discovery, development and manufacture of healthcare products including medicines and vaccines.

Story continues

The Alzheimer's disease treatment market covered in this report is segmented by drug class into cholinergic; memantine; combined drug; AChE inhibitors; immunoglobulins and by drug type into cholinesterase inhibitors; NMDA receptor antagonists.

Lack of techniques for diagnosing Alzheimer's disease (AD) is expected to limit the growth of the global Alzheimer's disease treatment market. There is no definitive blood test, brain scan, or physical exam to diagnose AD, and so many conditions can produce symptoms like dementia, which is the primary clinical symptom of AD, making the diagnosis complicated. The lack of a single test for diagnosis, specialists such as neurologists, neuropsychologists, geriatricians and geriatric psychiatrists use a variety of approaches for diagnosis to confirm dementia, but it is still difficult to find the cause resulting in late diagnosis. Lack of proper and quick diagnosis for AD hampers the market growth as it leads to a reduced number of diagnosed cases and thereby reduces the consumption of AD drugs.

Increasing R&D investments and collaborations due to the emerging technologies for the treatment is a key trend in Alzheimer's disease (AD) treatment market. The Alzheimer's Association is assisting with funds to researchers in search of innovative therapeutic approaches and seeks more government funding for Alzheimer's studies. Technologies such as ?-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors and anti-amyloid inhibitors are emerging in the AD market. For instance, Comentis and Astellas collaborated and entered the BACE inhibitor field on their peptidomimetic series. Manufacturing companies such as AC Immune, Adamas Pharmaceuticals, INmune Bio, Intra-Cellular Therapies, vTv Therapeutics are more focused on R&D investments with their research molecules in the clinical trials to achieve a breakthrough for the treatment of AD.

The increasing cases of Alzheimer's is a major factor contributing to the growth of the Alzheimer's treatment market. Alzheimer's is the most common type of dementia. The USA Alzheimer's Association expects that all the states in the US are projected to face a rise of at least 14% in the number of Alzheimer's people between 2017 and 2025 due to the increase in the geriatric population.

At the global level, the estimated new cases of Alzheimer's were 454,000 in 2010 and the number is expected to grow by 35% to 615,000 by 2030, and by 110% to 959,000 by 2050. Therefore, the increasing prevalence of Alzheimer's disease is expected to drive the growth of the global Alzheimer's disease treatment market.

Key Topics Covered:

1. Executive Summary

2. Alzheimer's Disease Treatment Market Characteristics

3. Alzheimer's Disease Treatment Market Size And Growth

3.1. Global Alzheimer's Disease Treatment Historic Market, 2015 - 2019, $ Billion

3.1.1. Drivers Of The Market

3.1.2. Restraints On The Market

3.2. Global Alzheimer's Disease Treatment Forecast Market, 2019 - 2023F, 2025F, 2030F, $ Billion

3.2.1. Drivers Of The Market

3.2.2. Restraints On the Market

4. Alzheimer's Disease Treatment Market Segmentation

4.1. Global Alzheimer's Disease Treatment Market, Segmentation By Drug Class, Historic and Forecast, 2015-2019, 2023F, 2025F, 2030F, $ Billion

Cholinergic

Memantine

Combined Drug

AChE inhibitors

Immunoglobulins

4.2. Global Alzheimer's Disease Treatment Market, Segmentation By Drug Type, Historic and Forecast, 2015-2019, 2023F, 2025F, 2030F, $ Billion

5. Alzheimer's Disease Treatment Market Regional And Country Analysis

5.1. Global Alzheimer's Disease Treatment Market, Split By Region, Historic and Forecast, 2015-2019, 2023F, 2025F, 2030F, $ Billion

5.2. Global Alzheimer's Disease Treatment Market, Split By Country, Historic and Forecast, 2015-2019, 2023F, 2025F, 2030F, $ Billion

For more information about this report visit https://www.researchandmarkets.com/r/k5oi9

View source version on businesswire.com: https://www.businesswire.com/news/home/20210204005550/en/

Contacts

ResearchAndMarkets.comLaura Wood, Senior Press Managerpress@researchandmarkets.com For E.S.T Office Hours Call 1-917-300-0470For U.S./CAN Toll Free Call 1-800-526-8630For GMT Office Hours Call +353-1-416-8900

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Global Alzheimer's Disease Treatment Market Report 2020: Market is Expected to Recover in 2023 - Forecast to 2030 - ResearchAndMarkets.com - Yahoo...

Alzheimer’s Disease Drug Market Economic Conditions, Acquisitions, Mergers, Developments and Forecast By 2029: Allergan, Eisai, Novartis, Daiichi…

Posted: at 6:55 pm


Alzheimers Disease Drug Market

Alzheimers Disease Drug Market Projections (2020-2029): The Global market Alzheimers Disease Drug theologizes is the most recent of the world business market curves. The report prospects the current and frequent collectors, technological innovations, product supplementation, and their representation of performance broadly across the foreign market.

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Prominent players in the industry covered in the report:

Allergan, Eisai, Novartis, Daiichi Sankyo, Merz Pharma, Pfizer, Johnson & Johnson, Lundbeck

Market split by Type, can be divided into:DonepezilMemantineRivastigmine

Market split by Application, can be divided into:Early to Moderate StagesModerate to Severe Stages

Market split by Sales Channel, can be divided into:Direct ChannelDistribution Channel

Ourstudypasses through ahaven ofprofound qualitative and quantitativeresearch by industryexperts andprofessionals.Within the reportcontributes a broadperceptionof thepast as well ascurrent marketvista,which implies future statistics and prospects in position with the technical developments over time. Furthermore, the report includes and provides analyses of demand and supply, microeconomic and macroeconomic elements, administrative components and growth indices through the Alzheimers Disease Drug marketplace. The report outlines keytacticsutilized bykey market participants.

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This report provides an accurate understanding and discovery of key geographic areas underway with market Alzheimers Disease Drug, including critical segments and additional segments.The report sets out aspects of territorial growth and the size and scope of the market. Additionally, the report also deals with trading information such as business range, cost and revenue margin as well as gross value. However, this understanding assists readers in the conduct of consumer experts as well as major tactic to reach market share.

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Alzheimer's Disease Drug Market Economic Conditions, Acquisitions, Mergers, Developments and Forecast By 2029: Allergan, Eisai, Novartis, Daiichi...

Lilly Announces Webcast to Provide Alzheimer’s Disease Update at AD/PD Conference – PharmiWeb.com

Posted: February 5, 2021 at 11:52 pm


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Lilly Announces Webcast to Provide Alzheimer's Disease Update at AD/PD Conference - PharmiWeb.com

Gene Linked Between Alzheimer’s Disease and COVID-19 – Contagionlive.com

Posted: at 11:52 pm


A study conducted by City of Hope, an independent biomedical research and treatment center, has discovered the gene ApoE4, which increases the risk for Alzheimers disease, can also increase the susceptibility to and severity of an infection with the coronavirus disease 2019 (COVID-19). Results from the research were published in the journal Cell Stem Cell.

The study was initially started due to an interest in assessing how a COVID-19 infection impacts the brain. Because the disease presents symptoms like a loss of smell and taste, it was believed that the virus had underlying neurological effects.

The investigators employed pluripotent stem cells (iPSCs), a type that easily becomes any kind of cell, to create neurons and helper cells called astrocytes. They infected both cells with the SARS-CoV-2 virus and found that they were susceptible to the disease. They then created 3D brain tissue models called organoids, one with and one without the astrocytes, also infecting them with COVID-19 and discovered that the astrocytes actually amplified the infection.

Additionally, the team used reprogrammed iPSCs to generate neurons from the cells of an Alzheimers patient containing ApoE4. Modifying the iPSCs with a gene editing tool so that they contained ApoE3, a neutral gene type, they created more astrocytes and neurons.

Findings showed that in comparison to the ApoE3 cells, the ApoE4 cells showed a significantly higher susceptibility to COVID-19 and had more damage inflicted on their neurons and astrocytes.

"Our study provides a causal link between the Alzheimer's disease risk factor ApoE4 and COVID-19 and explains why some (e.g., ApoE4 carriers) but not all COVID-19 patients exhibit neurological manifestations," Yanhong Shi, director of the Division of Stem Cell Biology at City of Hope and co-corresponding author said. "Understanding how risk factors for neurodegenerative diseases impact COVID-19 susceptibility and severity will help us to better cope with COVID-19 and its potential long-term effects in different patient populations."

The next step in the process will be to continue studying the impact that COVID-19 has on the brain to further understand the potential long-term neurological impacts like severe headaches experienced by some months after the initial infection.

"COVID-19 is a complex disease, and we are beginning to understand the risk factors involved in the manifestation of the severe form of the disease" said Vaithilingaraja Arumugaswami, a co-corresponding author said. "Our cell-based study provides a possible explanation as to why individuals with Alzheimer's' disease are at increased risk of developing more severe COVID-19 symptoms."

Continued here:
Gene Linked Between Alzheimer's Disease and COVID-19 - Contagionlive.com

Opinion: We still know frustratingly little about Alzheimer’s disease, but there are ways to minimize your risk – MarketWatch

Posted: February 4, 2021 at 9:55 am


This cruel and horrible disease has no cure. Let us at least be grateful Bennett has lived a long and fruitful life. He is 94, and says he was diagnosed four years ago. Comparatively few people make it to their 90s. Ive seen people destroyed by this illness in their 60s, and even in their 50s.

We are blessed that we saw Bennett working with the likes of Amy Winehouse, Thalia and Lady Gaga well into his 70s and then 80s.

Its over 25 years since I first encountered Alzheimers in my personal life, and Im horrified by how little our understanding seems to have advanced since then.

What causes Alzheimers? What can we do about it?

We dont know, says the U.S. government.

We dont know, says the British government.

We dont know, says the Mayo Clinic.

Turns out even the basic hypotheses everyone held that its caused by things called tau tangles and amyloid plaques in the brain may not even be correct.

We can produce multiple vaccines inside of a year for COVID-19, but when it comes to fighting a disease destroying tens of millions of lives a annually everyone is still sucking their pencils and saying, Hmm, yes, its very complicated.

Yes, yes, I know its not a straight comparison. On the other hand, its not completely facile, either. If we can make an illness an overwhelming priority, throw gigantic sums of money at it, cut red tape, remove roadblocks to development, and fast track approvals, well why not?

Thirty-five million people around the world have Alzheimers, including nearly 6 million in the U.S. The global number is expected to hit 135 million by 2050. Compare those numbers to the current global crisis.

And the fatality rate for Alzheimers isnt 0.5% or 1% or 2% but 100%. It is always progressive and always fatal. It effectively kills you long before it actually kills you. It also sucks gigantic amounts of money from the rest of the health system, because sufferers often need a lot of care for a long, long time.

Federal funding for Alzheimers research is $3.1 billion a year or less than 0.1% of the total U.S. cost, so far, of the COVID lockdowns.

Eli Lilly LLY, +0.28% and Biogen BIIB, -0.19% have potentially promising treatments in their pipelines. But overall the failure rate of drug discovery for Alzheimers treatments is 99%.

So what can you and I do to minimize our risks of getting this awful disease or even just delay it?

The research is often ambiguous or even contradictory. For example, some say you should follow a Mediterranean diet and go easy on things like alcohol and cheese. Or, you could follow this research, and, er, drink more alcohol and eat more cheese.

And even where scientists think theyve found a lifestyle change that could help, the research is still preliminary. Its often based on small samples, or observational real-world studies that come with heavy caveats.

But Im in middle age, and I can hardly wait around forever to take sensible steps to try to minimize my risks. Especially as it now seems cognitive decline and dementia can start decades before we show symptoms. So am I supposed to eat cheese or not?

Well, according to the scientific literature there are a handful of things that seem like they might help, which come with low downsides or costs, and which (yes, I know this is unscientific) seem intuitively to make sense.

Get more and better sleep. There are multiple studies suggesting that those who have a history of getting better sleep regularly are at lower risk of developing dementia which surely only makes sense, given the role of sleep in brain and other cell repair. For example, a recent study at the University of California, Berkeley, found that those who were getting lots of good, restorative sleep especially the so-called deep or rapid-eye-movement sleep developed fewer of the amyloid brain plaques that are probably associated with dementia. Another study finds possible links between dementia and sleep apnea.

Eat a healthy Mediterranean diet.OK, so apparently we cant yet take a position on cheese. But we already know olive oil is good for our health, and studies say those who consume it may be at lower risk of dementia, too. Research also says the same may be true of fresh fruit and vegetables. Particularly (yum) strawberries. A natural compound, fisetin, in these foods is showing sufficiently promising results that scientists at the Salk Institute are trying to use it as the basis of synthetic drugs for fighting Alzheimers. While theyre working on it, heres a reminder to pick up some strawberries.

Drink coffee.Honestly, does this even sound like medicine? Researchers say that drinking plenty of strong coffee seems to be associated with a lower risk of dementia and Parkinsons. They dont know why, because well, see above. But the effect seems to be unconnected with caffeine and lies in the roasting. So dark roasted coffee, even decaf, works much more so than light-roasted coffee. Espresso doppio, per favore. Doctors orders.

Avoid pollution. Lucky thing so many are moving out of the city, and that everyone has learned to wear a mask. We may yet end up like those cities on the Pacific Rim, where masks are standard pretty much all the time. There are now multiple studies finding links between pollution, traffic and dementia risk. Its not just traffic, either. Forest fires, power plants and other polluters pose risk. Lake Tahoe, here we come.

Get some exercise.Well, yes, we all know regular exercise is good for us. But it also seems to significantly reduce our risk of developing Alzheimers and dementia generally, according to multiple studies (including this one and this one and this one). One 44-year study suggests that women who are physically fit in middle age may be 90% less likely to develop dementia.

Work your brain.This one is surprisingly controversial. Scientists still cant conclusively say whether things like doing crossword puzzles or playing Sudoku is going to delay or prevent dementia. On the other hand, there are studies that point that way (such as here and here and here). Beneficial brain workouts may include mindfulness and meditation. And even if science hasnt or hasnt yet proved a benefit, there are no real costs, downsides or risks.

Floss.Of course! No list of healthy activities can be complete without a reminder that were supposed to floss daily. Yet it turns out there might be a link between gum disease and Alzheimers. Strange but true. So heres another reason to brush twice a day and floss daily.

Continue reading here:
Opinion: We still know frustratingly little about Alzheimer's disease, but there are ways to minimize your risk - MarketWatch

Can scientists find the holy grail of Alzheimers research? – Big Think

Posted: at 9:55 am


It can be hard to conceptualize the total damage caused by Alzheimer's. The neurodegenerative disease is a leading cause of death in the U.S., killing more than 100,000 people each year. And as Alzheimer's progresses in the brain it not only erodes memory but also causes troubling symptoms like agitation, paranoia, and aggression.

These burdens fall not only on patients but also on their loved ones, doctors, and caregivers. Economically, the cost of caring for Alzheimer's patients hit an estimated $305 billion in 2020, according to a report from the Alzheimer's Association. And that figure doesn't include an estimated $244 billion in unpaid caregiving provided by family and friends.

The number of Alzheimer's patients in the U.S. is expected to double by 2050, affecting about 14 million people. That's one reason why hospitals and health professionals are already working to bolster how they care for the elderly and Alzheimer's patients. It takes 15 years to develop new treatments, so today's research needs adequate funding.

"Caring for our older adults is a big responsibility, one that we take great pride in," said Michael Dowling, president and CEO of Northwell Health. "Our aging population will face health issues, including and especially Alzheimer's, that will require the right care at the right time. That's why we have increased our services, including at Glen Cove Hospital, and research at the Feinstein Institutes for Medical Research."

While the costs of Alzheimer's are clear, its exact causes remain frustratingly mysterious. Currently, there's no cure for the disease, nor treatments that stop its progression.

"Alzheimer's is this brain problem, and everyone sort of knows what's probably causing the problem, but nobody's been able to do anything about it," said Dr. Jeremy Koppel, a geriatric psychiatrist and co-director of the Litwin-Zucker Alzheimer Research Center.

But in recent decades, researchers have zeroed in on likely contributors to the disease. The brains of Alzheimer's patients reliably show two abnormalities: build-ups of proteins called abnormal tau and beta-amyloid. As these proteins accumulate in the brain, they disrupt healthy communication between neurons. Over time, neurons get injured and die, and brain tissue shrinks.

Still, it's unclear exactly how these proteins, or other factors such as inflammation, may drive Alzheimer's.

"We are dealing with very complicated components," said Dr. Philippe Marambaud, a professor at the Feinstein Institutes and co-director of the Litwin-Zucker Alzheimer Research Center. "The actual culprit is not clearly defined. We know there are three possible culprits [tau, beta-amyloid, inflammation]. They're working in concert, or maybe in isolation. We don't know precisely."

Many Alzheimer's researchers have spent years developing therapies that target beta-amyloid, which can accumulate to form plaques in the brain. The Alzheimer's Association writes:

"According to the amyloid hypothesis, these stages of beta-amyloid aggregation disrupt cell-to-cell communication and activate immune cells. These immune cells trigger inflammation. Ultimately, the brain cells are destroyed."

Unfortunately, clinical trials of therapies that target beta-amyloid haven't been effective in treating Alzheimer's.

In brains with Alzheimer's disease, tau proteins lose their structure and form neurofibrillary tangles that block communication between synapses.

Credit: Adobe Stock

At the Feinstein Institutes, Dr. Marambaud and his colleagues have been focusing on the lesser-explored Alzheimer's component: abnormal tau.

In healthy brains, tau plays several important functions, including stabilizing internal microtubules in neurons. But in the brains of Alzheimer's patients, a process called phosphorylation changes the structure of tau proteins. This blocks synaptic communication.

Dr. Marambaud said there are good reasons to think anti-tau therapies may effectively treat Alzheimer's.

"The main argument around why [anti-tau therapies] could be more beneficial is that we've known for a very long time that tau pathology in the brain of the Alzheimer's patient correlates much better with the disease progression, and the loss of neuronal material in the brain," compared to beta-amyloid, Dr. Marambaud said.

"The second strong argument is that there are inherited dementias, called tauopathies, which are caused by mutations in the gene coding for the tau protein. So, there is a direct genetic link between dementia and tau pathology."

To better understand how this protein interacts with Alzheimer's, Dr. Marambaud and his colleagues have been developing immunotherapies that target abnormal tau.

Immunotherapies, such as vaccines, typically target infectious diseases. But it's also possible to use the body's immune system to prevent or treat some non-infectious diseases. Scientists have recently succeeded in treating certain forms of cancer with immunotherapies, for example.

"We have developed a series of monoclonal antibodies, which are basically the therapeutics that are required when you want to do immunotherapy," Dr. Marambaud said.

Currently, Feinstein Institutes researchers are conducting promising ongoing clinical trials with anti-tau antibodies, some of which are in phase III trials under the Food and Drug Administration. Patients receive these therapies intravenously over several hours and would undergo multiple rounds of treatment. It's similar to chemotherapy.

In the short term, it's more likely that anti-tau therapies would help to stabilize Alzheimer's, not cure it.

"Just stabilization of the disease's progression will save a huge societal, but also financial, burden," Dr. Marambaud said. "As research progresses, we would improve upon these stabilization approaches to make them more and more efficacious."

Even if anti-tau therapies don't prove to be the holy grail of Alzheimer's treatments, they could potentially alleviate severe behavioral symptoms of the disease, and potentially illuminate some of the mechanisms behind psychosis.

Credit: Getty Images

When most people think of Alzheimer's, they tend to focus on the erosion of memory. But the darkest effects of the disease are often psychotic symptoms like agitation, aggression and paranoia, according to Dr. Koppel, who, in addition to researching Alzheimer's, spent decades treating Alzheimer's patients as a clinician.

"My research focus comes out of 20 years of sitting with Alzheimer's families and listening to what the primary issue is," said Dr. Koppel. "It's never memory. It starts out with memory as a diagnostic issue. But the real suffering comes from the changes that happen in the personality and the belief system that make Alzheimer's patients" ostracized or even become violent toward their loved ones.

At the Feinstein Institutes, Dr. Koppel's research focuses on alleviating Alzheimer's-related psychotic symptoms through anti-tau immunotherapies.

"It's our hypothesis that abnormal tau proteins in the brain somehow, downstream, impact the way that people think," Dr. Koppel said. "And the impact that it has is this paranoid, agitated, psychotic phenotype."

Supporting this hypothesis is research on chronic traumatic encephalopathy (CTE), a degenerative disease that involves the accumulation of abnormal tau. CTE, common among professional football players, also causes psychotic symptoms like agitation, aggression and paranoia.

What's more, research shows that as Alzheimer's patients accumulate more abnormal tau in their brains, as measured through cerebrospinal fluid, they exhibit more psychotic symptoms, and are more likely to die sooner than patients with less abnormal tau.

Given these strong connections between psychosis and abnormal tau, Dr. Koppel and his colleagues hope that anti-tau immunotherapies will alleviate psychosis in Alzheimer's patients, who currently lack safe and effective treatment options and are often given medication that is meant to alleviate psychosis in people with schizophrenia.

"We are giving medications to Alzheimer's patients that hasten their cognitive decline and lead to bad outcomes, like stroke and sudden death," Dr. Koppel said. "Nonetheless, the schizophrenia medications do treat some of the psychotic symptoms and aggressive behavior related to Alzheimer's disease, and for many families this is crucial. We just don't have many options, and we desperately need more."

Beyond treating Alzheimer's patients, anti-tau immunotherapies may shed light on other mental illnesses.

"Alzheimer's may give us a window into what happens in the brain that makes people psychotic," Dr. Koppel said. "Once you have a biologic treatment for psychosis that gets at an underlying pathophysiology, believe me, you could look at schizophrenia in new ways. Maybe it's not going to be tau, but it may be a paradigm for treating mental illness."

Dr. Marambaud said the long-term goal of anti-tau immunotherapies is to prevent Alzheimer's. But that's currently impossible because scientists lack the biomarkers and diagnostic tools needed to detect the disease before cognitive symptoms appear. It could take decades before prevention becomes possible, if it ever does.

In the short term, stabilizing Alzheimer's is a more realistic goal.

"Our hope is that the treatments will be aggressive enough so that we can at least stabilize the disease in patients identified to be already affected by dementia, with cognitive tests that can be done by the clinicians," Dr. Marambaud said. "And even better, maybe reduce the cognitive impairments."

Dr. Marambaud said he encourages the public not to lose faith.

"Be patient. It's a very complicated disease," he said. "A lot of labs are really committed to making a difference. Congress has also realized that this is a huge priority. In the past five years, [National Institutes of Health] funding has increased tremendously. So the scientific field is working very hard. The politicians are behind us in funding this research. And it's a complicated disease. But we will make a difference in the years to come."

In the meantime, the Alzheimer's Association notes that physical activity and a healthy diet can reduce the chances of developing Alzheimer's, though more large-scale studies are needed to better understand how these factors interact with the disease.

"Many of these lifestyle changes have been shown to lower the risk of other diseases, like heart disease and diabetes, which have been linked to Alzheimer's," the association wrote. "With few drawbacks and plenty of known benefits, healthy lifestyle choices can improve your health and possibly protect your brain."

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Can scientists find the holy grail of Alzheimers research? - Big Think

Alzheimer’s Treatments Showing Early Promise – AARP

Posted: January 27, 2021 at 1:49 am


Treatment for Alzheimer's disease, the devastating condition that affects more than 5 million Americans, has remained notoriously elusive for decades. Now, a small study released by drug company Eli Lilly offers at least a flicker of hope: It shows that the experimental drug donanemab may significantly slow patients cognitive decline.

The two-year study which followed 272 people whose brain scans showed Alzheimer's found that patients who took the drug had a 32 percent slower rate of decline than those who received a placebo. It's very encouraging because this is the first time a drug of its kind has had positive results in early-stage trials, says Lon Schneider, M.D., Della Martin chair in psychiatry and neuroscience at the Keck School of Medicine of the University of Southern California. The drug, known as a monoclonal antibody, works by binding to the hard plaque in the brain made from amyloid (a protein associated with Alzheimer's).

Though these initial findings are promising, Schneider says more data is needed. It may have been everyone just had a small cognitive decline, in which case the results aren't as significant, he says. (The drugmaker has said it will release this information shortly in a peer-reviewed clinical journal.)

But this isn't the only news Alzheimer's researchers are excited about. There are several new drugs either close to getting FDA approval, or in development, that promise to really change the playing field when it comes to treatment of Alzheimer's disease, says Marwan Sabbagh, M.D., director of the Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas. Here are some of the most promising contenders.

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Alzheimer's Treatments Showing Early Promise - AARP

How not to lose money because of Alzheimer’s disease – Harvard Health Blog – Harvard Health

Posted: at 1:49 am


Researchers from Maryland and Michigan recently published an article showing that six years prior to their diagnosis, individuals developing Alzheimers disease or a related disorder were more likely to miss paying a bill compared to older adults without such a diagnosis (7.7% versus 7.3%), and they were also more likely to develop subprime credit scores (7.9% versus 6.9%). As the authors concede, there were a number of problems with the study, including unequal matching of the average age of the groups (79.4 versus 74.0 years), which could mean that the results were actually due to age, rather than Alzheimers disease. The authors did attempt to adjust for this difference with their statistical analyses, but sometimes that doesnt fully correct for this type of inequality.

The biggest problem with the study, however, is that it grossly underestimates the true financial difficulties that those developing Alzheimers disease face. After reading this article, you might think, Well, these differences are only 1% or less, thats not a big deal. But the article does not address the major financial issues facing people developing Alzheimers disease: poor decision-making and the related issue of falling victim to financial scams.

How many times a week or a day does your phone ring with someone offering you a new credit card, car loan, or investment deal? How often do you get a call from someone saying they are from your credit card company or the social security office?

Scams are a huge problem, with one of every 18 cognitively intact older adults in the United States falling victim to one. But individuals with Alzheimers dementia and those in the pre-dementia stage of mild cognitive impairment are even more susceptible. In fact, research in healthy older adults suggests that susceptibility to scams may be related to shrinkage in memory-related structures in the brain some of the same structures that shrink in Alzheimers.

Individuals with Alzheimers disease fall victim to scams because they have impaired judgment and decision-making. Making financial decisions requires the coordinated function of many brain systems in order to retrieve prior information from memory, incorporate new information into memory, keep that information in mind, and analyze it. Individuals with Alzheimers disease have trouble with the brain systems involved in all of these functions.

It is this difficulty with decision-making and judgment that leads to the next two biggest financial problems in Alzheimers disease. The first is donating too much money to legitimate causes, and the second is making poor financial investments.

You may have been called recently by your local police or firefighters pension fund, in addition to calls from organizations like Save the Children. Perhaps you do want to donate to some of these causes. But did you already donate to that organization last month? How much money should you give? How frequently should you give?

It can be difficult for anyone to keep track of all of these legitimate causes, and to donate an appropriate amount within your budget. Individuals with impaired memory and judgment have much more trouble knowing which charities they have already given to recently and when they need to stop donating money so that theyll have enough for this months food, rent, and heat!

Even the most intelligent individuals with excellent memory will sometimes make poor investment decisions leading to significant financial losses. Given their complexity, it is not surprising that many individuals who eventually develop a memory disorder made poor investment decisions in the years prior to their diagnosis. Unfortunately, I have seen many families life savings wiped out in this way.

Luckily, there are some simple things that you can do to protect yourself and your loved ones from these types of financial problems.

These measures will allow one to continue day-to-day living without purchasing expensive items or giving away large sums of money.

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How not to lose money because of Alzheimer's disease - Harvard Health Blog - Harvard Health

Alector Announces First Participant Dosed in Phase 2 Study Evaluating AL002 in Individuals with Early Alzheimer’s Disease – GlobeNewswire

Posted: at 1:49 am


SOUTH SAN FRANCISCO, Calif., Jan. 25, 2021 (GLOBE NEWSWIRE) -- Alector, Inc. (Nasdaq: ALEC), a clinical-stage biotechnology company pioneering immuno-neurology, today announced that the first participant has been dosed in INVOKE-2, a Phase 2 clinical study evaluating the efficacy and safety of AL002 in slowing disease progression in individuals with early Alzheimers disease. AL002 is an investigational, humanized monoclonal antibody that targets triggering receptor expressed on myeloid cells 2 (TREM2), a transmembrane receptor protein that is expressed on a subset of innate immune cells and selectively on microglia, which serve as the immune cells in the brain. The AL002 clinical program is being developed in collaboration with AbbVie.

The role of TREM2 in Alzheimers disease was first discovered through large scale genome-wide association studies where it has been shown to have one of the most important genetic links to sporadic Alzheimers disease. Research suggests that reduction of TREM2 functionality may lead to Alzheimer's disease and other forms of dementia. Increasing TREM2 activity in the brain may prove to be an effective therapeutic approach by activating the brains immune system to target multiple pathologies that are present in Alzheimers disease, rather than focusing on a single pathology.

Loss of TREM2 activity has been shown through human genetics to be one of the notable risk factors for developing Alzheimers disease, saidRobert Paul, M.D., Ph.D., chief medical officer ofAlector. AL002 is a first-in-class TREM2 targeting antibody in Phase 2 clinical development for Alzheimers disease. By targeting this receptor, we believe it may be possible to slow the progression of this disease. Our ability to move quickly into a Phase 2 study is based on compelling preclinical and Phase 1 data showing that AL002 engages TREM2 on microglia cells in the brain, resulting in increased microglial activity. We look forward to efficiently enrolling the Phase 2 study to better understand the potential clinical benefits of AL002.

Alzheimers is a devastating disease that robs a person of their identity, and a family of their loved one. We are hopeful that AL002 may one day be a treatment option for the millions of people diagnosed with this disease, said Michael Gold, M.D., vice president, Development Neurosciences, AbbVie. We are pleased that the study was initiated rapidly and look forward to data from the Phase 2 study that will inform a potential pivotal clinical development program for AL002.

INVOKE-2 is a randomized, double-blind, placebo-controlled, dose-ranging, multi-center Phase 2 study that will enroll approximately 265 participants with early Alzheimers disease at up to 90 sites globally. The primary endpoint of the Phase 2 study is to measure disease progression utilizing the Clinical Dementia Rating Sum Boxes (CDR-SB). The CDR-SB is a validated instrument that assess both cognitive and functional domains and is used to assess (score) the severity of Alzheimers disease. The study will also employ multiple fluid and imaging biomarkers, and will assess several secondary clinical, pharmacokinetic and pharmacodynamic endpoints, as well as the safety of treatment with AL002.

To learn more about the Phase 2 study, please visit https://clinicaltrials.gov/.

About AL002AL002 is an investigational humanized monoclonal antibody that targets triggering receptor expressed on myeloid cells 2 (TREM2) with the most important genetic links to sporadic Alzheimers disease. TREM2 is a transmembrane receptor expressed on a subset of innate immune cells and selectively on microglia, which constitute the brains immune system. Reduction of TREM2 functionality may lead to Alzheimer's disease and other forms of dementia. AL002 counteracts this decreased functionality by optimizing TREM2 signaling to improve cell survival and proliferation, and activity of microglia.

Collaboration with AbbVieIn October 2017, Alector entered into a global strategic collaboration with AbbVie (NYSE: ABBV), to co-develop and commercialize therapeutics to treat Alzheimers disease and other neurodegenerative diseases. Under the terms of the agreement, Alector granted AbbVie an exclusive option to global development and commercialization for two programs, including TREM2. Following AbbVies exercise of its option for either program (or both), Alector is eligible for additional option exercise and milestone payments totaling up to $986M. Both companies will share the development costs and will split global profits equally after marketing approval.

About Alzheimers DiseaseAlzheimers disease is a degenerative brain disease and the most common form of dementia. It is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability of patients to care for themselves. In most people with Alzheimers disease, symptoms first appear in their mid-60s. The Alzheimers Association estimates that as of 2020, there are 5.8 million Americans aged 65 and older living with Alzheimers disease, and projects that number will rise to nearly 14 million by 2050.

AboutAlectorAlectoris a clinical stage biotechnology company pioneering immuno-neurology, a novel therapeutic approach for the treatment of neurodegenerative diseases. The Companyis developing a broad portfolio of innate immune system programs, designed to functionally repair genetic mutations that cause dysfunction of the brains immune system and enable the rejuvenated immune cells to counteract emerging brain pathologies. Immuno-neurology targets immune dysfunction as a root cause of multiple pathologies that are drivers of degenerative brain disorders.The Companys immuno-neurology product candidates are supported by biomarkers and target genetically defined patient populations in frontotemporal dementia and Alzheimers disease. This scientific approach is also the basis for the Companys immuno-oncology programs.Alectoris headquartered inSouthSan Francisco, California. For additional information, please visitwww.alector.com.

Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Such statements are subject to numerous important factors, risks and uncertainties that may cause actual events or results to differ materially from current expectations and beliefs, including but not limited to risks and uncertainties related to the Companys plans for and anticipated benefits and mechanism of the Companys product candidates, the timing and objectives of the Companys clinical studies and anticipated regulatory and development milestones, and Alector and its business as set forth in Alectors Quarterly Report on Form 10-Q filed with the Securities and Exchange Commission (the SEC) on November 10, 2020, as well as the other documents Alector files from time to time with the SEC. These documents contain and identify important factors that could cause the actual results for Alector to differ materially from those contained in Alectors forward-looking statements. Any forward-looking statements contained in this press release speak only as of the date hereof, and Alector specifically disclaims any obligation to update any forward-looking statement, except as required by law.

Contacts:

Media Erica JeffersonVice President, Communications and Public AffairsAlector, Inc.301-928-4650erica.jefferson@alector.com

1AB Dan Budwick973-271-6085 dan@1abmedia.comor

Investors: Alector, Inc. ir@alector.com

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Alector Announces First Participant Dosed in Phase 2 Study Evaluating AL002 in Individuals with Early Alzheimer's Disease - GlobeNewswire

Alzheimer’s Disease Treatment Market Expected to Witness High Growth over the Forecast to 2027 KSU | The Sentinel Newspaper – KSU | The Sentinel…

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TheAlzheimers Disease Treatment Marketresearch report thoroughly explains each and every aspect related to the Global Alzheimers Disease Treatment Market, which facilitates the reports reader to study and evaluate the upcoming market trend and execute the analytical data to promote the business.

Alzheimers Disease Treatment Market Insight:

Alzheimers disease treatment market is expected to gain market growth in the forecast period of 2020 to 2027. Data Bridge Market Research analyses the market to account to USD 6.65 billion by 2027 growing with the CAGR of 8.29% in the above-mentioned forecast period demand for the disease itself and not just its symptoms will help in driving the growth of the alzheimers disease treatment market.

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The report also inspects the financial standing of the leading companies, which includes gross profit, revenue generation, sales volume, sales revenue, manufacturing cost, individual growth rate, and other financial ratios.

Prominent Key Players Covered in the report:

Allergan, Eisai Co. Ltd., Novartis AG, Daiichi Sankyo Company Limited, Merz Pharma, Pfizer Inc., Johnson & Johnson Services, H. Lundbeck A/S, ONO Pharmaceutical Co. Ltd., Teva Pharmaceutical Industries Ltd., Eli Lilly and Company, TauRx, VTV Therapeutics, F. Hoffmann-La Roche Ltd., AstraZeneca, Biogen, AC Immune, AB Science, AbbVie Inc., Bristol-Myers Squibb Company, Takeda Pharmaceutical Company Limited, QR Pharma Inc., General Electric Company, and Bayer AG are few of the major competitors currently working on the Alzheimers disease Treatment Market.

Key Pointers Covered in the Alzheimers Disease Treatment Market Industry Trends and Forecast

The Alzheimers Disease Treatment market report provides successfully marked contemplated policy changes, favorable circumstances, industry news, developments, and trends. This information can help readers fortify their market position. It packs various parts of information gathered from secondary sources, including press releases, web, magazines, and journals as numbers, tables, pie-charts, and graphs. The information is verified and validated through primary interviews and questionnaires. The data on growth and trends focuses on new technologies, market capacities, raw materials, CAPEX cycle, and the dynamic structure of the Alzheimers Disease Treatment market.

Major Regions as Follows:

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The report includes accurately drawn facts and figures, along with graphical representations of vital market data. The research report sheds light on the emerging market segments and significant factors influencing the growth of the industry to help investors capitalize on the existing growth opportunities.

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Table Of Contents: Alzheimers Disease Treatment Market

Part 01: Executive Summary

Part 02: Scope of the Report

Part 03: Research Methodology

Part 04: Market Landscape

Part 05: Pipeline Analysis

Part 06: Market Sizing

Part 07: Five Forces Analysis

Part 08: Market Segmentation

Part 09: Customer Landscape

Part 10: Regional Landscape

Part 11: Decision Framework

Part 12: Drivers and Challenges

Part 13: Market Trends

Part 14: Vendor Landscape

Part 15: Vendor Analysis

Part 16: Appendix

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In the end, the Alzheimers Disease Treatment market is analyzed for revenue, sales, price, and gross margin. These points are examined for companies, types, applications, and regions.

To summarize, the global Alzheimers Disease Treatment market report studies the contemporary market to forecast the growth prospects, challenges, opportunities, risks, threats, and the trends observed in the market that can either propel or curtail the growth rate of the industry. The market factors impacting the global sector also include provincial trade policies, international trade disputes, entry barriers, and other regulatory restrictions.

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