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Eating This One Type of Food Could Slash Your Alzheimer’s Risk, New Study Finds | Eat This Not That – Eat This, Not That

Posted: October 14, 2021 at 1:58 am

Over six million people in the U.S. have Alzheimer's disease, a progressive form of dementia that can lead to severe memory loss and, in many cases, the inability to care for oneself as the disease progresses. According to the Alzheimer's Association's "Alzheimer's Disease Facts and Figures" report, one in nine adults 65 and older has Alzheimer's disease, with cases predicted to double by 2050. While there is currently no cure for Alzheimer's, new research suggests that eating a particular type of food may be able to help reduce your risk of developing the condition in the first place.

Read on to discover which dietary alterations could keep you healthier as you age. And for more great additions to your healthy living arsenal, check out The One Vitamin Doctors Are Urging Everyone to Take Right Now.

A new study published in Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring reveals that antioxidant imbalances in the human bloodstream may be a predictor of a future Alzheimer's disease diagnosis rather than a side effect of the condition.

The study's researchers found that elevated biological markers of oxidative stress can show up in the blood of individuals with Alzheimer's up to five years prior to the onset of the disease.

RELATED: This Is the #1 Diet to Follow to Prevent Alzheimer's, Says New Study

While research suggests that limiting exposure to environmental pollutants and getting enough exercise are both effective at reducing oxidative stress, they're not the only ways to lower your risk of an oxidant-antioxidant imbalance that may increase your Alzheimer's risk.

The study's authors also suggest that dietary interventionspecifically, adding additional sources of antioxidants to your dietmay help offset these imbalances, thus lowering your risk of developing Alzheimer's.

"Given that there is an increase in oxidative stress in people who develop the disease, we may regulate the antioxidant systems. For example, we could modulate the antioxidant systems, such as apolipoproteins J and D, which transport lipids and cholesterol in the blood and play an important role in brain function and Alzheimer's disease. Another avenue would be to increase the intake of antioxidants through nutrition," says Charles Ramassamy, PhD, a professor at the Institut National de la Recherche Scientifique, who supervised the study, in a statement.

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If you think that adding more antioxidants to your meal plan requires a full dietary overhaul, think again.Foods like black raspberries, blackberries, blueberries, pomegranates, strawberries, apples, plums, cherries, dates, artichokes, red cabbage, and broccoli are all packed with healthy antioxidants that may help reduce oxidative stress in your body.

RELATED: 15 Most Antioxidant-Packed Fruits & VeggiesRanked!

Antioxidant-rich fruits and vegetables aren't the only way to stave off cognitive decline, however.A 2015 review of research published in BioMed Research International found that omega-3 fatty acids, commonly found in seafood, flaxseed, and chia seeds, among other sources, also show promise when it comes to reducing the risk of cognitive impairment. "The strongest evidence in support of nutrition preventing cognitive decline in AD is for long-chain omega-3 fatty acids. Primarily, this is because long-chain omega-3 has shown promising potential to ameliorate low-grade inflammation in the early stages of this neurodegenerative disease," the review's authors explain.

For more ways to improve your cognitive function, check out The Best Foods for Your Brain After 50, Say Dietitians.

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The #1 Cause of Dementia, According to Science

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Eating This One Type of Food Could Slash Your Alzheimer's Risk, New Study Finds | Eat This Not That - Eat This, Not That

Missing link between severe COVID-19 and Alzheimer’s disease discovered – New Atlas

Posted: at 1:58 am

Early in the pandemic researchers saw disproportionately high rates of dementia patients suffering from severe COVID-19. A common hypothesis was that memory impairments associated with neurodegeneration affect a persons ability to consistently follow infection control measures such as social distancing and mask wearing. But a new study led by scientists from University College London is proposing a key gene variant, known to heighten ones risk for Alzheimers, stimulates the bodys inflammatory responses and can lead to greater susceptibility to severe COVID-19.

In 2019 a team of researchers discovered a handful of genes that could be associated with heightened risk of Alzheimers disease. A separate study last year found variants in one of these Alzheimers risk genes, OAS1, correlated with severe COVID-19 outcomes.

This new study, published in the journal Brain, proposes OAS1 regulates the inflammatory responses of certain cells. And some OAS1 variants dampen that regulatory response leading to pro-inflammatory activity, which can explain how it both heightens Alzheimers risk and severe COVID-19.

While Alzheimers is primarily characterized by harmful build-up of amyloid protein and tangles in the brain, there is also extensive inflammation in the brain that highlights the importance of the immune system in Alzheimers, says lead author Dervis Salih. We have found that some of the same immune system changes can occur in both Alzheimers disease and Covid-19. In patients with severe Covid-19 infection there can also be inflammatory changes in the brain.

Homing in on one particular OAS1 variant, dubbed rs1131454, the research first confirmed the variant can increase a persons baseline risk of developing Alzheimers disease by up to 22 percent. This variant is thought to be extremely common, carried by over 50 percent of Europeans.

Studying the molecular mechanisms of this OAS1 variant the researchers discovered it can lead to overactive inflammatory responses, and it is this action that plays a role in the progression of severe COVID-19. David Strain, a researcher from the University of Exeter, calls the new study robust and suggests the findings fit with what we know of the "cytokine storms" that are part of the severe stages of COVID-19.

We do know that one of the key pathways in development of Alzheimers disease is inflammation within the brain tissue, and, as our understanding of the pandemic has grown, we have seen many other inflammatory conditions be highlighted as risk factors for poor outcomes, therefore the results are not overly surprising, says Strain, who did not work on the this new research.

Of course, these new findings do raise a whole heap of new questions. Salih indicates the UCL research team are now looking at what role this gene variant could be playing in long COVID, or how it could be influencing some of the more acute neurological symptoms that can be associated with the disease.

We are also continuing to research what happens once this immune network has been activated in response to an infection like Covid-19, says Salih, to see whether it leads to any lasting effects or vulnerabilities, or if understanding the brains immune response to Covid-19, involving the OAS1gene, may help to explain some of the neurological effects of Covid-19.

Perhaps a more immediate outcome from these new findings could be a way to easily detect those patients most at risk of severe COVID-19. Salih even speculates a simple blood test identifying this particular genetic variant could serve as a way to identify early Alzheimers patients.

If we could develop a simple way of testing for these genetic variants when someone tests positive for Covid-19, then it might be possible to identify who is at greater risk of needing critical care, but there is plenty more work to be done to get us there, says Salih. Similarly, we hope that our research could feed into the development of a blood test to identify whether someone is at risk of developing Alzheimers before they show memory problems.

The new study was published in the journal Brain.

Source: University College London

Missing link between severe COVID-19 and Alzheimer's disease discovered - New Atlas

Virtual Alzheimer’s conference to help NY, NJ residents navigate the illness – Burlington County Times

Posted: at 1:58 am

As part of its 2021 Educating America Tour, the Alzheimer's Foundation of America will host a virtual conference Tuesday for New York and New Jersey residents.

The conference will be free to everyone, and will feature several conference aimed at helping people manage life with the illness.

"Knowledge is a useful and powerful tool that can help make any situation easier to navigate, especially something as challenging as caring for a loved one with Alzheimer's disease," AFA President and CEO Charles J. Fuschillo said. "Connecting families with useful, practical information and support that can help them now and be better prepared for the future is what this conference is all about. Whether Alzheimer's is affecting your family, you are a caregiver or just want to learn more, you can participate in this free virtual conference from the comfort of your home or office."

The programs will teach people about lifestyle changes that come with Alzheimer's, putting a healthcare team together, improving independence and more.

To register for the conference, which will be held 10 a.m.-noon Tuesday, visit http://www.alzfdn.org/tour. Those who can't make the conference or have immediate questionsare welcome to contactlicensed social workers through the AFA's toll-free helpline at 866-232-8484.

Ahmad Austin Jr. is a lifelong South Jersey resident telling stories within the healthcare and cannabis industries for Burlington County Times, Courier-Post and The Daily Journal. For story tips, reach out at aaustin@gannett.com.

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Virtual Alzheimer's conference to help NY, NJ residents navigate the illness - Burlington County Times

Support those affected by Alzheimer’s disease | Opinion – News- Graphic

Posted: at 1:58 am

To the Editor,

There are many unique challenges and needs when caring for a loved one with dementia. With a progressive disease, the caregiving journey often feels like youre putting out fires and reacting rather than being able to plan for the best way to care for a loved one. As a former caregiver for my father who had frontotemporal dementia, I understand how complicated it is to navigate the maze of health care and support services.

Over the course of three years, our family was shuffled from one specialist to the next just trying to receive a diagnosis. Living in a rural community, we were unaware of services available for my father and for myself as a caregiver. My fathers quality of life would have been so much better if we had not spent so much time trying to find support for the unique needs of a dementia patient. We felt very much alone and unsupported by the healthcare system.

Thankfully, the Alzheimers Association has introduced two pieces of legislation that can better support caregivers and families affected by the disease. First, the Comprehensive Care for Alzheimers Act would streamline health care options for those living with dementia and their caregivers, reducing costs and improving the quality and delivery of care. Second, the Alzheimers Caregiver Support Act would provide grants to expand training and support services to offer much-needed relief to the more than 11 million dementia caregivers across the nation.

Knowing that other families would have access to vital support services through these bills if they pass is the reason Im calling on my Congressperson to support. Please join me in asking Senator Mitch McConnell to cosponsor and pass the Comprehensive Care for Alzheimers Act and Alzheimers Caregiver Support Act. Together, we can build a dementia capable Kentucky and nation.

Caitlin Dunworth


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Support those affected by Alzheimer's disease | Opinion - News- Graphic

Personality traits linked with hallmarks of Alzheimer’s disease: Study – Times Now

Posted: at 1:58 am

Personality traits linked with hallmarks of Alzheimer's disease: Study  |  Photo Credit: iStock Images

Washington: New research from the Florida State University College of Medicine found that changes in the brain associated with Alzheimer's disease are often visible early on in individuals with personality traits associated with the condition. The study published in the journal Biological Psychiatry focused on two traits previously linked to the risk of dementia: neuroticism, which measures a predisposition for negative emotions, and conscientiousness, which measures the tendency to be careful, organized, goal-directed, and responsible.

"We have done studies showing who's at risk of developing dementia, but those other studies were looking at the clinical diagnosis," said Antonio Terracciano, professor of geriatrics at the College of Medicine. "Here, we are looking at the neuropathology; that is, the lesions in the brain that tell us about the underlying pathological change. This study shows that even before clinical dementia, personality predicts the accumulation of pathology associated with dementia."

The study combines data from the Baltimore Longitudinal Study of Aging (BLSA) and previously published work in a meta-analysis that summarized 12 studies on personality and Alzheimer's neuropathology. The studies combined included more than 3,000 participants. Combining results across studies provides more robust estimates of the associations between personality and neuropathology than a single individual study can typically provide.

In both the BLSA and meta-analysis, the researchers found more amyloid and tau deposits (the proteins responsible for the plaques and tangles that characterize Alzheimer's disease) in participants who scored higher in neuroticism and lower in conscientiousness. The team also found associations to be stronger in studies of cognitively normal people compared to studies that included people with cognitive problems. The findings suggest that personality can help protect against Alzheimer's and other neurological diseases by delaying or preventing the emergence of neuropathology for those strong in conscientiousness and low in neuroticism.

"Such protection against neuropathology may derive from a lifetime difference in people's emotions and behaviours," Terracciano said.

He added, "For example, past research has shown that low neuroticism helps with managing stress and reduces the risk of common mental health disorders. Similarly, high conscientiousness is consistently related to healthy lifestyles, like physical activity. Over time, more adaptive personality traits can better support metabolic and immunological functions, and ultimately prevent or delay the neurodegeneration process."

The BLSA is a scientific study of human ageing conducted by the National Institute on Aging (NIA), part of the National Institutes of Health (NIH), that began in 1958. Personality was measured using a five-factor personality test, the most common personality assessment tool. At the time of their enrollment in the BLSA neuroimaging sub-study, all participants were free of dementia or other severe medical conditions. Advances in brain scan technology used to assess in vivo amyloid and tau neuropathology made it possible for researchers to complete this work.

"Until recently, researchers measured amyloid and tau in the brain through autopsy -- after people died," Terracciano said.

He added, "In recent years, advances in medical imaging have made it possible to assess neuropathology when people are still alive, even before they show any symptoms."

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Personality traits linked with hallmarks of Alzheimer's disease: Study - Times Now

Levetiracetam improves learning and memory in people with Alzheimer’s disease and epilepsy – Epilepsy Action

Posted: at 1:58 am

Levetiracetam has been found to improve cognitive functions, like learning and memory, in people diagnosed with Alzheimers disease who also have epileptic brain activity, a study in Journal of the American Medical Association (JAMA) Neurology has found.

There are around 850,000 people with dementia in the UK. Alzheimers disease is a particular type of dementia. It affects between half and three-quarters (50-75%) of people with dementia, according to the Alzheimers Society.

According to the study, among people with Alzheimers disease, up to around three in five (60%) have seizures or silent epileptic activity in the brain. This means that epileptic activity shows up in tests, but there are no visible signs of a seizure in the person.

Lead study author Dr Keith Vossel called Alzheimers disease with epileptic activity an epileptic variant of the disease.

The study analysed 34 people with Alzheimers disease, of whom two-fifths (40%) had epileptic activity. People were split up into two groups, and received treatment with a dummy medicine or a low dose of levetiracetam for four weeks. This was alongside their current Alzheimers disease treatment. Then, the groups had a four-week break and swapped over to receive the opposite treatment.

The researchers assessed peoples abilities to problem solve, reason, remember words and navigate during treatment. People treated with levetiracetam showed a tendency towards improvement in these kinds of skills. People with silent epileptic activity were seen to have a clear benefit of this medicine to their cognitive functions.

The researchers concluded that these findings showed the importance of extended neurology assessments in Alzheimers disease patients, to identify people with epileptic activity who may benefit from levetiracetam.

The full study is available on the JAMA Neurology website.

A group of epilepsy charities, clinicians, researchers and people with epilepsy have joined forces to identifywhich areas of epilepsy need to be prioritised for research.

Levetiracetam improves learning and memory in people with Alzheimer's disease and epilepsy - Epilepsy Action

Synaps Dx Closes $10M Series A Round to Speed Commercialization of Alzheimer’s Disease Test – 360Dx

Posted: at 1:58 am

NEW YORK Synaps Dx, a company developing diagnostic tests for neurodegenerative disorders, said on Tuesday that it has closed a $10 million Series A financing round that included participation from private equity, individual and family investors, and corporate investor funds.

The Rockville, Maryland-based firm, which operates a CLIA-certified laboratory, said it will use the proceeds to scale up production and meet market demand for Discern, its minimally invasive test for the diagnosis of Alzheimer's diseaseand differentiation from other forms of dementia.

According to the firm's website, Discern is an easy-to-administer test that detects AD at the earliest stages of onset by testing for the presence of three undisclosed biomarkers that are unique to the disease. The test requires a small skin sample taken by a certified healthcare provider. In 2018, the company received US Food and Drug Administration breakthrough device designation for the test.

Autopsy-validated clinical data, which takes many years to collect, confirmed that the test has 95 percent sensitivity and specificity for diagnosing AD, Synaps Dx said. The test "reflects 30 years of research at the [National Institutes of Health National Neurologic Institute] to map the molecular pathways that create memory with mechanisms that are conserved across evolution," Daniel Alkon, chief scientific adviser at Synaps Dx, said in a statement. The research demonstrated "that the protein PKC-Epsilon is a synaptic growth master switch for memory formation," he added.

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Synaps Dx Closes $10M Series A Round to Speed Commercialization of Alzheimer's Disease Test - 360Dx

Sisters Katharine, Susan Yenke of Sudbury pay tribute to father who has Alzheimer’s disease – MetroWest Daily News

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WATCH: Sudbury's Yenke sisters honor father who has Alzheimer's disease

By hosting a fundraising volleyball match and running in the Boston Marathon, the Yenke sisters of Sudbury honored their father, who has Alzheimer's.

Tommy Cassell, MetroWest Daily News

SUDBURY There were purple balloons, purplestreamers, stickers and T-shirts, purple noise makers, necklaces and table cloths.

Anywhere you looked during the Lincoln-Sudbury girls volleyball match on Friday, purple was the color du jour.

The entire gym was an electric sea of purple, said Kathy Yenke, a Sudbury resident.

The reason for all the purple: Ernie Yenke. The longtime Sudbury Youth Football coach was diagnosed with early onset Alzheimers in 2019.

His youngest daughter, Susan, and her volleyball team hosted their inaugural Alzheimers Awareness match on Friday to raise money for research for Alzheimers. Purple is the signature color for the disease.

This is what I could do to honor him and show him how much I appreciate and love him because I do, said the 17-year-oldSusan. It was a really special night. Im glad I got to do it.

Ernie Yenke coached youth football inSudbury for 20 years. Susan was the water girl for his gridiron squads.

Hes like famous in Sudbury, she said.

When Ernie was diagnosed with Alzheimers disease which is the most common form of dementia that affects memory, thinking and behavior, according to The Alzheimers Association it rocked the Yenke family.

We kind of had to flip roles, said Susan, who has two older siblings. Weve weathered the storm pretty well but our lives have basically been flipped upside down.

Initially, the Yenke family didnt disclose Ernies diagnosis. They didnt want anyone around town to think of him differently.

That all changed, however, when Ernies oldest daughter, Katharine, decided to run in the Boston Marathon this fall for The Alzheimers Association.

Susan Yenke started a new club at her school this yearcalled The Alzheimers Awareness and Advocacy Club.

We have 58 members, she said, which includes a few players from the Lincoln-Sudbury girls volleyball team.

After finding out that Susans father had Alzheimers, L-S girls volleyball coach Greg Falcone sprung the idea of hosting an Alzheimers Awareness match on his senior captain.

When I gave the suggestion to her you could see her eyes light up and she was in, Falcone said.

On Friday, Susans parents watched the fundraising match from the stands while Katharine collected donations and handed out bracelets at the entrance of the L-S gym.

On the court, Susan led her team to a 3-0 win over Westford Academy. The senior libero compiled eightdigs and a team-high sixaces, one of which came on set point in the third frame to stage a come-from-behind victory.

That was a really cool moment in the gym, Falcone said. I was kind of holding back tears when she went back to that line.

The whole arena was doing all kinds of good things that night, the 60-year-old Erniewrote in an email.

The event raised $1,300 for The Alzheimers Association and set the stage for Mondays Boston Marathon.

Katharine Yenke was listening to the radio in April when she heard a story about a woman running in the Boston Marathon to honor her own mother, who died from breast cancer.

The tale served as motivation for Katharine to run in her first ever marathon and pay tribute to her father.

Im really happy I turned on the radio that day, Katharine, 23, said.

Katharine was one of 40 people chosen to represent Team ALZ in the Boston Marathon on Monday.

She finished the race in 5 hours, 20 minutes and 4 seconds. Along the way, she was cheered on by more than 20 family members and friends who were dressed in purple shirts that had TEAM YENKE on the back. Her younger sister even joined in on the race and ran miles 15 through 17 with Katharine.

She was in pain but (she) finished, Susan said.

Afterward, at the reception for the Alzheimers Association, Katharine learned she was the top donor for Team ALZ and No. 8 overall for all charity runners. She raised $46,000.

Donate: Help Katharine Yenke and her family raise money for The Alzheimer's Association

My dad and I cried when they announced it, Katharine said. Very surreal.

What a weekend, Ernie wrote.

All weekend, Ernie was the most engaged, talkative and joyful from all the love and support, wrote his wife, Kathy. His daughters were making a difference for him and his disease. … He was the proudest dad ever. A lasting memory to cherish forever.

Thats what this weekend was all about for the Yenke family. More time with Ernie.

The volleyball match and Boston Marathon served as two different ways for Katharine and Susan Yenke to honor their father. The Yenke family now has a sea of purple behind them to support their fight against Alzheimers disease.

It was just amazing to be able to share this experience with my dad at a time where hes going to be able to remember it and understand that the $46,000 that I raised is going to help get more time with him, Katharine said.

Anything is possible. Im just so full of love and gratitude, I could burst, Susan said. Im just so proud of my sister. Our family has faced so much adversity and challenges these past few years and this weekend almost made up for it.

Tommy Cassell is a senior multimedia journalist for the Daily News. He can be reached at tcassell@wickedlocal.com. Follow him on Twitter @tommycassell44.

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Sisters Katharine, Susan Yenke of Sudbury pay tribute to father who has Alzheimer's disease - MetroWest Daily News

Pitt Researchers Awarded Over $40 Million to Study Alzheimer’s Disease – UPMC & Pitt Health Sciences News Blog – UPMC

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For decades, the field of Alzheimers disease research wasplaguedby a dilemma:Scientists and clinicians knew that accumulation of tau protein tangles of jumbled protein fibers clogging the brains nerve cells is an important marker of disease severity. But the researchers still hadto wrestle withthetechnical limitations of detecting small amounts of tau proteins; some tools that help identify tau tangles are more sensitive than others and canflagearly Alzheimers disease whileanother tool might erroneously show that the patient is Alzheimers-free.

Theselimitations create problems for researchers who want to compare their results.If the two groups didnt use the sametau detection tools, its hard to accurately compare the findings between the studies.

Tharick Pascoal

Toput an end tothis discrepancy, researchers from the University of Pittsburgh wererecentlyawardedover$40 milliondistributedoverfive years. The National Institutes of Health grantwasgiventoDepartment of Psychiatry AssistantProfessor Tharick Pascoal,M.D.,Ph.D.

The problem of comparing tau tracers is very acute, said Pascoal. Itsoftendifficult to compare dataabout Alzheimers severityand to make conclusions that are benefitting patients the most. Im excited to help unify the standards of Alzheimers diseasediagnostics and move the field forward.

To directly measure theamount of tau protein and detect its location in the brain, researchers useslightly radioactive compounds calledtautracers,whichbind totauinthe brainand makeitvisible on a PET scanner.But the tracers arent perfect.

One frequently usedtracer called [18F]Flortaucipir can detect miniscule amounts of tauin the brain, but can also sometimes erroneously indicate the presence of tau where thereisntany.Another tautracer, [18F]MK-6240, is even more sensitive to tau but can also erroneously indicate the presence of tau in brain regions different from areas that light up with[18F]Flortaucipir which creates additional difficulties when comparingbrain scans acquiredusing different tools.

Same brain studied with different tau PET tracers

By comparingthese tracershead-to-head, the researchers are hoping to get a clear picture of the differences and similarities between thetwo, anddescribe once and for all which tracer is more appropriate to use in patients with sub-clinical Alzheimers diseaseand which for patients with symptomatic Alzheimers. Theirultimate goalis tobuilda scalethatcould be usedto harmonize scansobtained with the different tracers and help researchers and clinicians makemore informed treatment decisions.

The scientistsaimto enroll620people those with and without cognitive impairments, and patients with Alzheimers-associated dementia andfollow them for 18 months, looking at brain scans acquired with both tracers and testingpatientsfor other visual and biological markers of Alzheimers disease.

The study isexpectedto involveeightmedical centers across the United States and Canada, including Pitt, Lawrence Berkeley National Laboratory and the University of California, Washington University in St. Louis, Mayo Clinic in Rochester, Houston Methodist Neurological Institute and Brown UniversityinProvidence, as well as McGill University in Canada.

The biggest heroes of this work are the patients themselves, said Pascoal. This study wouldnt be possible without sacrifice and commitment of so many people who are contributing their time to research.

Suzanne Baker, ofLawrence Berkeley National Laboratoryin California, is a co-principal investigator on this project.

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Pitt Researchers Awarded Over $40 Million to Study Alzheimer's Disease - UPMC & Pitt Health Sciences News Blog - UPMC

Twin Cities mentor to families facing Alzheimer’s disease reminds them to ‘Look for the joy’ – Minneapolis Star Tribune

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Karla Hult calls the decade ending in 2019 the hardest of her life. That was the year Hult's beloved father died after 10 years of suffering deepening dementia caused by Alzheimer's disease. The experience inspired Hult, a KARE-11 reporter, to help other families whose loved ones have Alzheimer's. On Father's Day this year, she launched So Many Goodbyes (somanygoodbyes.com), a company through which she offers public speaking, free mentoring for families and workshops at long-term care centers. Hult is a strong supporter of the Alzheimer's Association she emceed the local organization's Walk to End Alzheimer's in September. With So Many Goodbyes, she considers herself a "captain or lieutenant" in the battle against the disease. But the association "remains the general."

Q: It's a rare family, it seems, that isn't touched by some form of dementia today. What do statistics tell us?

A: That the battle is increasingly urgent. The greatest risk factor for Alzheimer's dementia is age, and the number of Americans who are 65 and older is projected to balloon as the baby boomer generation grows older. The Alzheimer's Association estimates that the number of people 65 and older with Alzheimer's dementia will more than double by 2050, from the current 6.2 million people to 12.7 million.

Q: You say the last decade was the hardest of your life. What were some particular challenges?

A: I was grieving, I was exhausted, we were fielding questions of monumental concern. I had two children during this time, so I was bookended by babies and the disease. That was especially hard because you want to be present for your children and you want to be present for your parents.

Q: What was your relationship like with your dad?

A: My dad was the foundation of my life. He was the person I would call with questions and for advice. The sun rose and set on him and I adored him completely. To lose that moral and practical compass was really challenging.

Q: What was it like caring for him?

A: Caring for him was such an honor, but of course it was also exhausting and even heartbreaking. I was fortunate and I don't take this lightly that I had a flexible enough job that I could often see my dad. I remained his devoted and adoring daughter through every stage. Even after he no longer recognized me as his daughter, I hoped he saw me as someone who was kind, someone who respected him and loved him always. He cared for me my entire life, and he was there for me at my worst moments, my most difficult moments. But that's the perspective of a daughter who, after my visits, returned to my home, children and husband. Caregiving is uniquely hard on people like my mom, the partners who are caregiving for their loved ones every moment of every day. Those caregivers along with the caregivers working in our long-term care centers need our support and respect.

Q: What kind of help can So Many Goodbyes offer to others?

A: When I think back to the beginning of our journey, I was overwhelmed, constantly grieving, constantly trying to make important decisions. It was so challenging, trying to be an advocate for him and be present for my children. I really wanted a guide or a mentor, somebody with whom I could touch base once in a while. I want to be there for families in a very direct and profound way. I want to be available virtually, by e-mail or phone, to just connect and listen to what they're going through.

Q: What has your journey taught you about what families need most?

A: I think a lot of families feel a real need to share, vent their frustrations. I had one gentleman literally just cry with me. I was really touched later when he said, "I didn't know I needed to do that, that I needed someone to listen." As a reporter and as someone who extensively researches on a regular basis, I can look up information and give people a practical lay of the land. A lot of families don't realize what resources are available to them at the county, state or even national level. And, of course, there's the invaluable information and support from the Alzheimer's Association and the World Health Organization and National Institutes of Health. So I'm doing that legwork for them, especially if a person is overwhelmed.

Q: Your reporting skills are definitely beneficial. But your personal connection to this challenge must also resonate deeply with families.

A: Honestly, my most important service is still based on my experience as a daughter. A woman recently shared with me how her sisters were divided about whether to move their mom into long-term care. I know how that feels. I was the daughter who resisted moving my dad until we no longer could keep him safe at home. So I was able to share with this family what I realized for myself: that they would be able to return to just one role: family. When [they] visit [their] mom, [they] can hold her hand and just be with her.

Q: Are there ways to make the journey a more positive experience for families whose loved one has been diagnosed with Alzheimer's?

A: I think it's really incumbent upon the person to very consciously look for the joy. I know it's so hard, amid the grief and the exhaustion. But for your own heart, you need to savor what you still have. You still have the loved one, someone who you can hold hands with, look in their eyes. Cherish those moments.

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Twin Cities mentor to families facing Alzheimer's disease reminds them to 'Look for the joy' - Minneapolis Star Tribune

BioVie Hosting Key Opinion Leader Webinar on Neuroinflammation and Insulin Resistance and New Treatment Approaches for Alzheimers Disease – Yahoo…

Posted: at 1:57 am

SANTA MONICA, Calif., Oct. 13, 2021 (GLOBE NEWSWIRE) -- BioVie Inc. (NASDAQ: BIVI) (BioVie or the Company), a clinical-stage company developing innovative drug therapies for the treatment of neurological and neurodegenerative disorders and advanced liver disease, today announced that it will host a key opinion leader (KOL) webinar on neuroinflammation and insulin resistance and new treatment approaches for Alzheimers Disease on Tuesday, October 26, 2021 at 1:30 pm Eastern Time.

The webinar will feature presentations by KOLs Jefferson Kinney, Ph.D., University of Nevada, Las Vegas, who will discuss the basis of inflammation as a central mechanism in Alzheimers disease, and Karl Herrup, Ph.D., University of Pittsburgh School of Medicine, who will discuss the importance of age-related hyperinsulinemia and brain insulin resistance in neurodegeneration.

BioVie's management team will also discuss NE3107 for the treatment of Alzheimer's disease. NE3107s mechanism acts on both the fundamental inflammatory signaling pathways and the consequent insulin resistance that are the root causes of Alzheimers and other neurodegenerative diseases. BioVie recently announced that the Company has enrolled the first patient into the NM101 Phase III clinical study testing NE3107 for the treatment of Alzheimers Disease (AD). The NM101 study is a potentially pivotal Phase 3, randomized, double-blind, placebo-controlled, US multicenter study of NE3107 in 316 subjects with mild to moderate AD.

A live Q&A session will follow the formal presentations. To register for the webinar, please click here.

Jefferson Kinney, Ph.D., is the Founding Chair of the Department of Brain Health and holds the Reg Grundy and Joy Chambers-Grundy Chair for Brain Health in the Department of Brain Health, School of Integrated Health Sciences, University of Nevada Las Vegas (UNLV). He is the Director of the Cellular and Molecular Brain Research Laboratory and the Translational Biomarker Discovery Laboratory. Dr. Kinney earned his Ph.D. at Colorado State University and was awarded an Intramural Research Training Fellowship at the National Institute of Mental Health investigating the biology and behavior of transgenic mouse models of Alzheimers disease. He was then selected as the Helen Dorris Fellow in the Department of Neuropharmacology at The Scripps Research Institute where he conducted research on molecular mechanisms in neurological disorders. He joined the UNLV faculty in 2007. Dr. Kinneys primary research focus is on investigating cellular and molecular mechanisms underlying Alzheimers decease with particular emphasis on neuronal-glial interactions. Dr. Kinneys work is directed at understanding how specific immune signaling pathways are altered in pre-clinical Alzheimer laboratory models, as well as understanding the mechanisms underlying how Diabetes confers increased risk for developing Alzheimers disease. More recently, Dr. Kinney has expanded these investigations into biomarker discovery research projects in clinical populations. Dr. Kinneys translational research approach is aimed at identifying disease mechanisms that may serve as new therapeutic targets as well as discovering novel biomarkers that can be used in detection, diagnosis, and evaluation of treatment efficacy of Alzheimers disease. Dr. Kinneys research provides a foundation for understanding the risk of developing AD and the utility of personalized treatment approaches to preserve brain health. Dr. Kinney received the Top Tier Scientist Award, among the most prestigious honors bestowed by UNLV.

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Karl Herrup, Ph.D., received his Bachelors degree from Brandeis University in Waltham, MA and his Ph.D. in Neuroscience from Stanford University. After two postdoctoral fellowships in Neurogenetics at Childrens Hospital/Harvard Medical School, and in Neuropharmacology at the Biozentrum in Basel Switzerland he joined the faculty of the Human Genetics Department of Yale Medical School as an Assistant, then Associate, Professor. He became Director of the Division of Developmental Neurobiology at the E. K. Shriver Center in Waltham, MA before moving to the Departments of Neurosciences and Neurology at Case Western Reserve University Medical School and University Hospitals of Cleveland. While in Cleveland, he directed the University Alzheimers Center for six years. In 2006 he moved to the Piscataway/New Brunswick campus of Rutgers University to become Professor and Chair of the Department of Cell Biology and Neuroscience. In July 2012, he moved to Hong Kong to become the Head of Life Science at The Hong Kong University of Science and Technology. He returned to the United States in March 2019 to become a Professor of Neurobiology at the University of Pittsburgh. His laboratory research is focused on the biology of nerve cell death and the paradoxical role that failed cell cycle regulation plays in the process. His work includes a strong translational interest that directs his studies towards a few select human neurodegenerative diseases including Alzheimers, a very common late-life dementia, and ataxia-telangiectasia, a very rare multisystem disorder of childhood.

About BioVie BioVie Inc. (NASDAQ: BIVI) is a clinical-stage company developing transformative therapies to overcome unmet medical needs in chronic debilitating conditions. In liver disease, the Companys Orphan drug candidate BIV201 (continuous infusion terlipressin), with FDA Fast Track status, is being evaluated in a US Phase 2 study for the treatment of refractory ascites with top-line results expected in early 2022. The Company is also planning a pivotal Phase 3 study of BIV201 in the treatment of hepatorenal syndrome-acute kidney injury (HRS-AKI) in 2022. BIV201 is administered as a patent-pending liquid formulation. The active agent is approved in about 40 countries for related complications of advanced liver cirrhosis but is not available in the US or Japan. In neurodegenerative disease, BioVie acquired the assets of NeurMedix Inc., including NE3107 that inhibits inflammatory activation of ERK and NFB (e.g. TNF transcription) that leads to neuroinflammation and insulin resistance, but not their homeostatic functions (e.g. insulin signaling and neuron growth and survival). Both are drivers of Alzheimers and Parkinsons diseases. The Company is conducting a potentially pivotal Phase 3 randomized, double blind, placebo controlled, parallel group, multicenter study to evaluate NE3107 in subjects who have mild to moderate Alzheimer's disease (NCT04669028). An estimated six million Americans suffer from Alzheimers. BioVie has initiated this study and is targeting primary completion in late 2022. A Phase 2 study of NE3107 in Parkinsons disease is planned to start later this year, and related compounds have additional potential to treat certain cancers. NE3107 is patented in the United States, Australia, Canada, Europe and South Korea. For more information, visit http://www.biovieinc.com/.

Forward-Looking StatementsThis press release contains forward-looking statements, which may be identified by words such as "expect," "look forward to," "anticipate," "intend," "plan," "believe," "seek," "estimate," "will," "project" or words of similar meaning. Although BioVie Inc. believes such forward-looking statements are based on reasonable assumptions, it can give no assurance that its expectations will be attained. Actual results may vary materially from those expressed or implied by the statements herein due to the Company's ability to successfully raise sufficient capital on reasonable terms or at all, available cash on hand and contractual and statutory limitations that could impair our ability to pay future dividends, our ability to complete our clinical studies and to obtain approval for our product candidates, to successfully defend potential future litigation, changes in local or national economic conditions as well as various additional risks, many of which are now unknown and generally out of the Company's control, and which are detailed from time to time in reports filed by the Company with the SEC, including quarterly reports on Form 10-Q, reports on Form 8-K and annual reports on Form 10-K. BioVie Inc. does not undertake any duty to update any statements contained herein (including any forward-looking statements), except as required by law.

For Investor Relations Inquiries:Contact:Bruce MackleManaging DirectorLifeSci Advisors, LLCbmackle@lifesciadvisors.com

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BioVie Hosting Key Opinion Leader Webinar on Neuroinflammation and Insulin Resistance and New Treatment Approaches for Alzheimers Disease - Yahoo...

The #1 Vitamin to Take to Reduce Your Alzheimer’s Risk, New Study Says | Eat This Not That – Eat This, Not That

Posted: at 1:57 am

There are more ways to preserve your cognitive functioning than just doing the daily crossword puzzle. In fact, the foods you eat can play a role in how your mind ages in ways that scientists are just beginning to understand. Now, new research suggests that, for some, a diet rich in vitamin B12 can play a key role in fighting off Alzheimer's disease.

For the study, researchers looked at how small worms called C. elegans reacted to amyloid beta, a protein that's associated with the neurologic disorder. Typically, when these worms have Alzheimer's disease, they become paralyzed. The researchers found that, for worms who had a vitamin B12 deficiency, feeding them the vitamin changed the way they reacted to the dangerous protein. When they were fed the vitamin, it took significantly longer for the paralysis to set in.

RELATED:Surprising Effects of Taking Vitamin B Supplements, Says Science

The study indicates that vitamin B12 might play an important role in helping to fend off Alzheimer's disease. Granted, its findings should be taken with a grain of salt.

"I'm worried that people will think that eating a B12 rich diet will delay cognitive decline in all individuals," the study's lead author Jessica Tanis, PhD, told Eat This, Not That! in an interview. "Subclinical B12 deficiency affects 10-15% of individuals over the age of 60 and these are the individuals who could potentially benefit from an increase in dietary B12 intake."

To that end, Malaz A. Boustani, MD, a geriatrician, neuroscientist, and Richard M. Fairbanks Professor of Aging Research at the Indiana University School of Medicine, suggests that, if you're experiencing memory symptoms, you should ask your doctor for "a full work-up" or a complete medical examination. This includes a test for B12 deficiency.

While you're waiting for your test results to come back, there are some other dietary changes you can start making right now to fight off Alzheimer's disease. To start, try and reduce your intake of added sugars.

"There is an ever-growing body of high-quality research that demonstrates how fundamental dietary choices are in terms of charting the brain's destiny, even as it relates to Alzheimer's disease," says David Perlmutter, MD, FACN, a board-certified neurologist, and five-time New York Times bestselling author.

"Diets that are high in refined carbohydrates and sugars threaten metabolism, especially as it relates to developing elevation of blood sugar [levels]. This represents a powerful threat to brain health and has been directly associated with increased Alzheimer's risk."

Bottom line: More research is needed on whether vitamin B12 could help delay the onset of the neurologic disorder. However, if you have a vitamin B12 deficiency, increasing your consumption of foods that are rich in the vitamin could improve your overall health. As of right now, your best bet at preventing Alzheimer's disease may be eating a diet that's rich in anti-inflammatory foods including fruits and vegetables, and low in processed foods and sugar.

For more, be sure to check out the #1 Diet to Follow to Prevent Alzheimer's, Says New Study. Then, don't forget to sign up for our newsletter.

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The #1 Vitamin to Take to Reduce Your Alzheimer's Risk, New Study Says | Eat This Not That - Eat This, Not That

UK Study Suggests Personalized Medicine May be the Future of Alzheimer’s Disease Treatment – UKNow

Posted: at 1:57 am

LEXINGTON, Ky. (Oct. 8, 2021) A recently released paper from the Department of Physiology and Sanders-Brown Center on Aging (SBCoA) at the University of Kentucky College of Medicine suggests that your genetics can influence your response to Alzheimers disease pathology.

The laboratory of Donna Wilcock, Ph.D., professor in the Department of Physiology and SBCoA associate director, investigated inflammation in human brain tissue from UKs Alzheimers Disease Research Center. Brain tissue was analyzed from individuals with different forms of the genetic risk factor, apolipoprotein E (ApoE).

ApoE comes in various forms including ApoE2, ApoE3 and ApoE4. ApoE2 is typically thought of as protective and reduces the risk of developing Alzheimers disease. ApoE3 is the most common form of the gene, while ApoE4 increases the risk and severity of Alzheimers disease.

This work, led by graduate student Courtney Kloske, found that individuals with ApoE4 had a reduced inflammatory response to Alzheimers disease pathology compared to individuals with ApoE3.

This finding contradicts data found from mouse work, highlighting the need to always confirm studies in both mouse and then human tissue, Wilcock said.

Because of the differing response depending on genotype, targeting inflammation in ApoE4 patients may not be the best approach according to our research, said Kloske. This work shows that your genetic makeup may influence your response to certain types of treatment for Alzheimers disease.

The Wilcock lab hopes this work will help contribute to moving treatments closer toward precision medicine.

This work was supported by the 1F31AG069372-01, 1RF1AG057754-01, and P30-AG028383 from the National Institute of Aging. None of this work would have been possible without the research volunteers and clinical investigators at the University of Kentucky Alzheimers Disease Research Center. This work is only the responsibility of the authors and does not reflect the official views of the National Institute of Aging.

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Resting-state functional reorganisation in Alzheimer’s disease and amnestic mild cognitive impairment: protocol for a systematic review and…

Posted: at 1:57 am

This article was originally published here

BMJ Open. 2021 Oct 12;11(10):e049798. doi: 10.1136/bmjopen-2021-049798.


INTRODUCTION: The incidence of Alzheimers disease (AD) is increasing rapidly, causing a growing burden to health and economic worldwide. Several clinical trials in the past decade failed to find solutions, and there remains a lack of an effective treatment. The evidence suggests that early intervention for neurodegeneration would likely be effective in preventing cognitive decline. Cognitive decline in AD occurs continuously over a long period; however, there remains a lack of simple, rapid and accurate approach for diagnosis of amnestic mild cognitive impairment or subjective cognitive decline due to underlying Alzheimers pathology. Resting-state functional MRI (rs-fMRI) determines the functional activities of the human brain non-invasively. The amplitude of low-frequency fluctuation (ALFF), fractional ALFF (fALFF) and regional homogeneity (ReHo) are rs-fMRI indicators with high repeatability. They have been studied as early diagnostic imaging markers for other diseases and may be promising markers also for AD.

METHODS AND ANALYSIS: The following electronic literature databases will be searched from inception to December 2021: Medline-Ovid, Medline-PubMed, EMBase-Ovid, Cochrane Central and ClinicalTrials.gov. Two independent reviewers will select studies with eligible criteria, extract data and assess the quality of the original studies with our quality assessment tool individually. Missing data will be requested by sending emails to the corresponding authors. Brain regions will be presented for ALFF/fALFF and ReHo by performing activation likelihood estimation with the Seed-based d Mapping-Permutation of subject images V.6.21 software. Meta-regression will be performed to determine the potential brain regions that may strongly correlate with cognitive decline progression. Subgroup analysis, funnel plot, Eggers test and sensitivity analysis will be conducted to detect and explain potential heterogeneity.

ETHICS AND DISSEMINATION: This study does not require formal ethical approval. The findings will be submitted to a peer-review journal.


PMID:34642194 | DOI:10.1136/bmjopen-2021-049798

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Study tests two drug treatments for early-onset Alzheimer’s disease – National Institute on Aging

Posted: August 29, 2021 at 1:48 am

Treatment with either gantenerumab or solanezumab, two monoclonal antibodies, did not slow down cognitive decline in people who have a type of early-onset dementia called dominantly inherited Alzheimers disease (DIAD), according to a recent study. However, gantenerumab did reduce some biomarkers of the disease. The study, which was funded in part by NIA, was published in Nature Medicine on June 21.

DIAD is a rare form of Alzheimers disease. It is an inherited condition caused by mutations in certain genes. People who have DIAD often start having symptoms of dementia, such as confusion and problems with memory, reasoning, and judgment, between the ages of 30 and 50. Currently, there is no treatment to prevent or slow down the disease. In the study, researchers led by a team at Washington University School of Medicine in St. Louis tested whether gantenerumab or solanezumab can effectively treat this condition. This study was conducted as part of the Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU).

The researchers enrolled participants who had gene mutations that cause DIAD. Some participants had mild symptoms of dementia, while others had no symptoms. Of the 144 participants enrolled in the clinical trial, 52 received gantenerumab, 52 received solanezumab, and 40 received a placebo. Participants were followed for up to seven years. Gantenerumab and solanezumab are monoclonal antibodies that target two different forms of a protein called beta-amyloid. In people with Alzheimers disease, beta-amyloid clumps together to form plaques in the brain. This prevents brain cells from working properly.

The researchers found that in participants who had symptoms of dementia at the beginning of the trial, treatment with gantenerumab or solanezumab did not slow down or stop the worsening of these symptoms. Some participants taking solanezumab had a faster cognitive decline. Participants who had no symptoms at the start of the study did not develop symptoms during the study.

The researchers also tested whether either of the two drugs had an effect on known biomarkers of Alzheimers. Both drugs effectively hit their amyloid-beta targets. Gantenerumab reduced beta-amyloid plaques in the brain and lowered the levels of tau, a protein that forms tangles in the brain cells of people who have Alzheimers. Additionally, gantenerumab slowed down the accumulation of a protein called neurofilament light chain (NfL). High NfL levels are a sign of increased brain cell damage. Solanezumab showed effects on cerebral spinal fluid amyloid-beta but had no effect on beta-amyloid plaques. Tau levels were also not affected and NfL levels increased.

The researchers note that although this study was limited by a small sample size and a relatively short monitoring period, it presents an effective model for studying potential treatments for DIAD. In future DIAN-TU studies, the researchers plan to classify participants into smaller groups based on their disease stages for more accurate comparisons between participants who received treatments and the control group. They also plan to test higher doses of study drugs for longer periods to fully examine their efficacy in treating DIAD.

This research was supported in part by NIA grants AG042791, AG042791-S1, AG046179, AG053267-S1, and AG032438.

These activities relate to NIHs AD+ADRD Research Implementation Milestone 5.C, Initiate phase III drug trials for agents against at least 3 currently known therapeutic targets. Of these, at least one trial will be asymptomatic, at risk populations; and 10.C, Initiate 3-4 clinical research studies using common standard outcome measures.

Reference: Salloway S, et al. A trial of gantenerumab or solanezumab in dominantly inherited Alzheimers disease. Nature Medicine. 2021. Epub Jun 21. doi: 10.1038/s41591-021-01369-8.

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Study tests two drug treatments for early-onset Alzheimer's disease - National Institute on Aging

Berries might be able to slow the onset of Alzheimer’s disease – hortidaily.com

Posted: at 1:48 am

Americans are growing old and, sadly, the aging process for many means more than simply turning gray or thinning hair.

According to theUnited States Census, in about a dozen years the number of Americans over 65 will outnumber children. Further, the Centers for Disease Control and Prevention project the number of Americans living with Alzheimers disease (AD) to nearlytriple by 2060.

Berries might help slow the processFortunately, USDA-funded research may have found a tasty way to slow disease onset.Astudypublished in theAmerican Journal of Clinical Nutritionsuggests that diets high in flavonoids may protect cognitive health. Flavonoids are plant nutrients known for their antioxidant, antiviral, and anticancer properties and are found in berries, tea, dark chocolate, and other foods.

Alzheimers disease is a significant public health challenge, saidPaul Jacques,nutritional epidemiologistat theJean Mayer USDA Human Nutrition Research Center on Agingat Tufts University in Boston. Given the absence of drug treatments, preventing Alzheimers disease through a healthy diet is an important consideration.

Photo credits: Scott Bauer, K7229-19

According to Jacques, who co-authored the study, about one in nine adults over age 65 are living with AD. While memory loss is the hallmark of AD, Jacques said it has many other cognitive and behavioral changes, including difficulty carrying out simple multistep activities, such as dressing or cooking; loss of judgement and attention; and changes in behavior such as depression and agitation.

Promising flavonoidsJacquess study, one of the first truly large, long-term studies to examine the effects of flavonoids on AD, showed that diets high in certain types of flavonoids present significant promise toward preventing the onset of Alzheimers.

Our study examined the association between long-term flavonoid intakes and AD over an average follow-up of 19.6 years among 2,809 participants, he said. Results show that those who consumed the most flavonoids were more than 50 percent less likely to develop AD risks compared with those who ate the least. Plant foods, such as vegetables, fruits, berries, nuts, and seeds are good sources of flavonoids, as is a cup of green tea each day.

Age 50 is not too late to make positive dietary changes. While the risk of dementia increases over age 70, it is now believed that its preclinical stage may predate clinical diagnosis by decades he said. A healthy diet during this preclinical period may provide the best opportunity for slowing the development of AD. When you approach 50, you should start thinking about a healthier diet if you havent already.

According to Jacques, flavonoid-rich diets help more than just Alzheimers disease and related dementia.

The bottom line is that there are many reasons to consume a healthy diet, including lower risks of cardiovascular disease and some cancers. We can now add protection of cognitive health and prevention of Alzheimers disease to that list," said Scott Elliott, ARS Office of Communications

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Berries might be able to slow the onset of Alzheimer's disease - hortidaily.com

Cyclerion Therapeutics to Present at Annual Biomarkers for Alzheimers Disease Summit – Yahoo Finance

Posted: at 1:48 am

Presentation to highlight the potential of early clinical assessment of biomarkers to drive development of Alzheimers disease therapies

CAMBRIDGE, Mass., Aug. 23, 2021 (GLOBE NEWSWIRE) -- Cyclerion Therapeutics, Inc. (Nasdaq: CYCN), a clinical-stage biopharmaceutical company on a mission to develop treatments that restore cognitive function, today announced participation in the Annual Biomarkers for Alzheimers Disease Summit taking place virtually August 25-26, 2021. Chris Winrow, Ph.D., Head of Translational Medicine, will present on biomarker translation and the potential that early clinical assessment of biomarkers has to drive development of Alzheimers disease therapies, and Juli Jones, Ph.D., Head of Disease Biology, will be leading a session exploring the utilization of omics platforms in drug discovery.

Presentation Details:

Title: Exploring the Utilization of Omics Platforms in Drug DiscoveryModerator: Juli Jones Ph.D., Head of Disease Biology, Cyclerion Therapeutics, Inc.Date: Wednesday, August 25, 2021Time: 4:20 p.m. ET

Title: Leading the Vanguard Early Clinical Assessment of Biomarkers to Drive Development of Alzheimers Disease TherapiesPresenter: Chris Winrow, Ph.D., Head of Translational Medicine, Cyclerion Therapeutics, Inc.Date: Thursday, August 26, 2021Time: 2:30 p.m. ET followed by a live Q&A at 3:00 p.m. ET

About Cyclerion Therapeutics

Cyclerion Therapeutics is a clinical-stage biopharmaceutical company on a mission to develop treatments that restore cognitive function. Cyclerion is advancing novel, first-in-class, CNS-penetrant, sGC stimulators that modulate a key node in a fundamental CNS signaling pathway. The multidimensional pharmacology elicited by the stimulation of sGC has the potential to impact a broad range of CNS diseases. The most advanced compound, CY6463, has shown rapid improvement in biomarkers associated with cognitive function and is currently in clinical development for Alzheimer's Disease with Vascular pathology (ADv), Mitochondrial Encephalomyopathy, Lactic Acidosis and Stroke-like episodes (MELAS), and Cognitive Impairment Associated with Schizophrenia (CIAS). Cyclerion is also advancing CY3018, a next-generation sGC stimulator.

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For more information about Cyclerion, please visit https://www.cyclerion.com/ and follow us on Twitter (@Cyclerion) and LinkedIn (www.linkedin.com/company/cyclerion).

InvestorsCarlo Tanzi, Ph.D.Kendall Investor Relationsctanzi@kendallir.com

MediaAmanda SellersVerge Scientific Communicationsasellers@vergescientific.com

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Cyclerion Therapeutics to Present at Annual Biomarkers for Alzheimers Disease Summit - Yahoo Finance

Aluminum and Alzheimer’s disease: after a century of …

Posted: August 2, 2021 at 1:54 am

The brain is a highly compartmentalized organ exceptionally susceptible to accumulation of metabolic errors. Alzheimer's disease (AD) is the most prevalent neurodegenerative disease of the elderly and is characterized by regional specificity of neural aberrations associated with higher cognitive functions. Aluminum (Al) is the most abundant neurotoxic metal on earth, widely bioavailable to humans and repeatedly shown to accumulate in AD-susceptible neuronal foci. In spite of this, the role of Al in AD has been heavily disputed based on the following claims: 1) bioavailable Al cannot enter the brain in sufficient amounts to cause damage, 2) excess Al is efficiently excreted from the body, and 3) Al accumulation in neurons is a consequence rather than a cause of neuronal loss. Research, however, reveals that: 1) very small amounts of Al are needed to produce neurotoxicity and this criterion is satisfied through dietary Al intake, 2) Al sequesters different transport mechanisms to actively traverse brain barriers, 3) incremental acquisition of small amounts of Al over a lifetime favors its selective accumulation in brain tissues, and 4) since 1911, experimental evidence has repeatedly demonstrated that chronic Al intoxication reproduces neuropathological hallmarks of AD. Misconceptions about Al bioavailability may have misled scientists regarding the significance of Al in the pathogenesis of AD. The hypothesis that Al significantly contributes to AD is built upon very solid experimental evidence and should not be dismissed. Immediate steps should be taken to lessen human exposure to Al, which may be the single most aggravating and avoidable factor related to AD.

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New research links COVID-19 and signs of Alzheimer’s disease – Medical News Today

Posted: at 1:54 am

Scientists presenting research at the AAIC 2021, held online and in Denver, CO, have found links between COVID-19 and longer-term cognitive issues, including biological signs of Alzheimers disease.

The findings lay the ground for larger longitudinal studies to explore in more detail the neurological effects of COVID-19.

COVID-19 is primarily a respiratory condition. The Centers for Disease Control and Prevention (CDC) note that COVID-19 symptoms can include mild respiratory problems, more severe low oxygen levels and shortness of breath, and life threatening issues affecting multiple organs across a persons body.

Much research has been done to understand these acute symptoms, and there are now many different treatment options open to clinicians.

However, the effects of COVID-19 do not always end after the acute phase of the condition.

As the pandemic progressed, anecdotal evidence suggested many people who had recovered from COVID-19 were still experiencing a variety of symptoms. This became known as long COVID.

According to Dr. A. V. Raveendran, of the Government Medical College in Manjeri, India, and his colleagues, symptoms of long COVID can include profound fatigue, breathlessness, cough, chest pain, palpitations, headache, joint pain, myalgia and weakness, insomnia, pins and needles, diarrhea, rash or hair loss, impaired balance and gait, neurocognitive issues, including memory and concentration problems, and worsened quality of life.

At the AAIC 2021, researchers presented a number of studies that focus on the neurological issues associated with the longer-term effects of COVID-19.

According to Dr. Heather M. Snyder, Alzheimers Association vice president of medical and scientific relations, [t]hese new data point to disturbing trends showing COVID-19 infections leading to lasting cognitive impairment and even Alzheimers symptoms.

With more than 190 million cases and nearly 4 million deaths worldwide, COVID-19 has devastated the entire world. It is imperative that we continue to study what this virus is doing to our bodies and brains. The Alzheimers Association and its partners are leading, but more research is needed, she said.

In one study, Dr. Gabriel De Erausquin, of the University of Texas Health Science Center at San Antonio Long School of Medicine, as well as colleagues from the Alzheimers Association leading a consortium on links between COVID-19 and the nervous system, looked at neurological issues in Amerindians from Argentina who had recovered from acute COVID-19.

The 300 participants were assessed 36 months after having COVID-19. The researchers found that more than 50% of the participants had issues with forgetfulness and that around 25% also experienced executive dysfunction and language issues.

The researchers noted an association between these cognitive issues and loss of smell but not with the severity of the initial SARS-CoV-2 infection.

According to Dr. Erausquin, [we are] starting to see clear connections between COVID-19 and problems with cognition months after infection.

[It is] imperative we continue to study this population, and others around the world, for a longer period of time to further understand the long-term neurological impacts of COVID-19.

In another study presented at the conference, Prof. Thomas M. Wisniewski, professor of neurology, pathology, and psychiatry at New York University Grossman School of Medicine, and his colleagues explored the possible links between COVID-19 and clinical signs of Alzheimers disease.

The researchers took blood plasma samples from 310 people who had been admitted to hospital with COVID-19. Of those, 158 had neurological symptoms associated with COVID-19 most frequently, confusion while 152 did not.

In the patients who did not have cognitive issues prior to developing COVID-19 but then did develop neurological symptoms, the researchers found an increase in biological markers associated with Alzheimers disease, brain injury, and neuroinflammation, compared with the patients who did not have neurological symptoms.

These included total tau, neurofilament light, glial fibrillary acid protein, phosphorylated tau, and ubiquitin carboxyl-terminal hydrolase L1. The researchers also noted a correlation between some of these markers and C-reactive peptide.

Prof. Wisniewski explains: These findings suggest that patients who had COVID-19 may have an acceleration of Alzheimers-related symptoms and pathology. However, more longitudinal research is needed to study how these biomarkers impact cognition in individuals who had COVID-19 in the long term.

Researchers also presented findings looking at the relationship between cognitive issues linked to COVID-19, and peoples physical condition and blood oxygen levels.

Dr. George D. Vavougios, a postdoctoral researcher for the University of Thessaly in Greece, and his colleagues recruited 32 people who had been hospitalized with mild or moderate COVID-19 and then discharged 2 months later.

Just over half of the participants had issues with cognitive decline, including short-term memory impairment as well as multidomain impairment without short-term memory issues.

The researchers found a correlation between worse levels of cognitive scores and being older, having a larger waist circumference, and a higher waist-to-hip ratio.

The participants also took a 6-minute walking test. After accounting for sex and age, the researchers found a link between worse memory and thinking scores and lower blood oxygen levels.

Dr. Vavougios says: A brain deprived of oxygen is not healthy, and persistent deprivation may very well contribute to cognitive difficulties. These data suggest some common biological mechanisms between COVID-19s dyscognitive spectrum and post-COVID-19 fatigue that have been anecdotally reported over the last several months.

The research presented at the conference is also supported by a new study published in The Lancet, which drew on data from over 80,000 participants. Having accounted for a range of factors, the researchers behind this study found that people who had recovered from COVID-19 had significant cognitive issues, compared with a control group.

Speaking to Medical News Today, Dr. Adam Hampshire, of the Department of Brain Sciences, Dementia Research Institute, Care Research and Technology Centre, Imperial College London in the United Kingdom, and the corresponding author of the study, said the study emerged out of ongoing research he was conducting when the pandemic took hold.

By coincidence, when the pandemic accelerated in the U.K., I was in the process of collecting one of the largest online surveys of cognitive abilities to have been conducted.

He went on to say: Several peers wrote to me noting that the study could be extended to address questions about the potential impact of the virus, and of the pandemic more broadly, on cognition and mental health. I had been thinking along similar lines so decided to try and help address this important question.

Dr. Hampshire said that the findings make clear a link between cognitive dysfunction and COVID-19 but that more research needs to be done to confirm these findings, explore them in more detail, and understand what, if any, causal mechanisms may be underlying them.

We have identified a worrying association between [COVID-19] illness and cognitive deficits. We also have ruled out many potentially confounding factors.

What is needed is a combination of longitudinal studies that determine how long these deficits last and to disentangle causality, as well as brain imaging studies to understand the underlying neural basis. Such work is underway, and some of those studies are using our assessment software, which I have made available for this purpose.

Dr. Adam Hampshire

For live updates on the latest developments regarding the novel coronavirus and COVID-19, click here.

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New research links COVID-19 and signs of Alzheimer's disease - Medical News Today

Memory Effects Of Long COVID-19 Can Resemble Alzheimer’s : Shots – Health News – NPR

Posted: at 1:54 am

Medical staff members check on a patient in the COVID-19 Intensive Care Unit at United Memorial Medical Center in Houston last November. Doctors are now investigating whether people with lingering cognitive symptoms may be at risk for dementia. Go Nakamura/Bloomberg via Getty Images hide caption

Medical staff members check on a patient in the COVID-19 Intensive Care Unit at United Memorial Medical Center in Houston last November. Doctors are now investigating whether people with lingering cognitive symptoms may be at risk for dementia.

Before she got COVID-19, Cassandra Hernandez, 38, was in great shape both physically and mentally.

"I'm a nurse," she says. "I work with surgeons and my memory was sharp."

Then, in June 2020, COVID-19 struck Hernandez and several others in her unit at a large hospital in San Antonio.

"I went home after working a 12-hour shift and sat down to eat a pint of ice cream with my husband and I couldn't taste it," she says.

The loss of taste and smell can be an early sign that COVID-19 is affecting a brain area that helps us sense odors.

Hernandez would go on to spend two weeks in the hospital and months at home disabled by symptoms including tremors, extreme fatigue and problems with memory and thinking.

"I would literally fall asleep if I was having a conversation or doing anything that involved my brain," she says.

Now, researchers at UT Health San Antonio are studying patients like Hernandez, trying to understand why their cognitive problems persist and whether their brains have been changed in ways that elevate the risk of developing Alzheimer's disease.

The San Antonio researchers are among the teams of scientists from around the world who will present their findings on how COVID-19 affects the brain at the Alzheimer's Association International Conference, which begins Monday in Denver.

What scientists have found so far is concerning.

For example, PET scans taken before and after a person develops COVID-19 suggest that the infection can cause changes that overlap those seen in Alzheimer's. And genetic studies are finding that some of the same genes that increase a person's risk for getting severe COVID-19 also increase the risk of developing Alzheimer's.

Alzheimer's diagnoses also appear to be more common in patients in their 60s and 70s who have had severe COVID-19, says Dr. Gabriel de Erausquin, a professor of neurology at UT Health San Antonio. "It's downright scary," he says.

And de Erausquin and his colleagues have noticed that mental problems seem to be more common in COVID-19 patients who lose their sense of smell, perhaps because the disease has affected a brain area called the olfactory bulb.

"Persistent lack of smell, it's associated with brain changes not just in the olfactory bulb but those places that are connected one way or another to the smell sense," he says.

Those places include areas involved in memory, thinking, planning and mood.

COVID-19's effects on the brain also seem to vary with age, de Erausquin says. People in their 30s seem more likely to develop anxiety and depression.

"In older people, people over 60, the foremost manifestation is forgetfulness," he says. "These folks tend to forget where they placed things, they tend to forget names, they tend to forget phone numbers. They also have trouble with language; they begin forgetting words."

The symptoms are similar to those of early Alzheimer's, and doctors sometimes describe these patients as having an Alzheimer's-like syndrome that can persist for many months.

"Those people look really bad right now," de Erausquin says. "And the expectation is that it may behave as Alzheimer's behaves, in a progressive fashion. But the true answer is we don't know."

Another scientist who will present research at the Alzheimer's conference is Dr. Sudha Seshadri, founding director of the Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases at UT Health San Antonio.

The possibility that COVID-19 might increase the risk of Alzheimer's is alarming, Seshadri says. "Even if the effect is small, it's something we're going to have to factor in because the population is quite large," she says.

In the U.S. alone, millions of people have developed persistent cognitive or mood problems after getting COVID-19. It may take a decade to know whether these people are more likely than uninfected people to develop Alzheimer's in their 60s and 70s, Seshadri says.

Studies of people who have had COVID-19 may help scientists understand the role infections play in Alzheimer's and other brain diseases. Previous research has suggested that exposure to certain viruses, including herpes, can trigger an immune response in the brain that may set the stage for Alzheimer's.

"If one understands how the immune response to this virus is accelerating [Alzheimer's] disease, we may learn about the impact of other viruses," Seshadri says.

Meanwhile, people like Cassandra Hernandez, the nurse, are simply trying to get better. More than a year after getting sick, she says, her brain is still foggy.

"We were at dinner and I forgot how to use a fork," she says. "It was embarrassing."

Even so, Hernandez says she's improving slowly.

"Before this I was working on my master's," she says. "Now I can do basic math, addition and subtraction, I can read at a fifth-grade level. I'm still working hard every day."

Hernandez has been working with Dr. Monica Verduzco-Gutierrez, chair of the department of physical medicine and rehabilitation at UT Health and director of the COVID-19 recovery clinic.

Verduzco-Gutierrez says her practice used to revolve around people recovering from strokes and traumatic brain injuries. Now she spends some days seeing only patients recovering from COVID-19.

The most common complaint is fatigue, Verduzco-Gutierrez says. But these patients also frequently experience migraine headaches, forgetfulness, dizziness and balance issues, she says.

Some of these patients may never recover fully, Verduzco-Gutierrez says. But she's hopeful for Hernandez.

"She's made so much improvement and I would love for her to go back to nursing," Verduzco-Gutierrez says. "But again, we don't know what happens with this disease."

More here:
Memory Effects Of Long COVID-19 Can Resemble Alzheimer's : Shots - Health News - NPR

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