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Mobile app allows early detection of Alzheimers disease – The Jakarta Post – Jakarta Post

Posted: September 22, 2020 at 3:53 am


At least 1 million Indonesians suffered from Alzheimer's disease in 2013 alone, and the number is estimated to grow twofold in2030 and fourfold in 2050, according tothe Indonesian Neurological Association (PERDOSSI).

A lack of public awareness and understanding [about Alzheimers] has led to stigmatization and challenges in diagnosing and treating patients, PERDOSSI chairman Dodik Tugasworo recently told a virtual press conference.

Alzheimers is the most common form of dementia, asyndrome in which sufferers experience deterioration in memory, thinking, behavior and the ability to perform everyday activities.

Contrary to popular belief, people of productive agecan suffer from this disease, which results in them having a lower life quality and continuousdependenceon other people to perform familiar activities.

According to PERDOSSI's head of neurobehavior study Astuti, among the most common symptoms of Alzheimers diseaseare memory loss, difficulty in doing routine tasks, disorientation, trouble communicating, social withdrawal and changes in behaviors. Sufferers also can be sensitive, easily offended and agitated, she added.

People whose family members suffer from Alzheimers may have a higher chance of developing the disease. Also at risk are people who have experienced a head injury, people who have down syndrome or diabetes, or those who have had a low quality education.

Alzheimers is currently incurable. The symptoms get progressively worse over time, particularly without early and proper treatment.

Early detection is crucial for people with Alzheimers as they will be treated in advance, therefore the diseases progression can be slowed down, said Astuti.

Those who need such early screening can use the E-Memory Screening (EMS) app launched by PT Eisai Indonesia, a subsidiary of Japan-based pharmaceutical company Eisai Co., Ltd., in collaboration with PERDOSSI. It is currently available on the Google Play Store.

Hopefully this app can be one strategy to contain dementia, said neurologistPukovisa Visa Prawiroharjo. The app provides three main features, namely a reliablescreening [process], a compilation of valid information from the experts and a trusted referral directory.

Visa added that the app could also help users find "the nearest hospital within a 50-kilometer radius of their location." (kes)

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Mobile app allows early detection of Alzheimers disease - The Jakarta Post - Jakarta Post

Organizations help bring awareness to Alzheimer’s disease – WTHITV.com

Posted: at 3:53 am


TERRE HAUTE, Ind. (WTHI) - September is Alzheimers Awareness month.

One local organization is helping bring more attention to the disease through teddy bears.

And, alpacas and llamas are doing there part to spread the word, too.

In Terre Haute, teddy bears were dropped off at Sycamore Place Saturday for a picnic.

A senior Education Ministries representative says the stuffed animals are known to improve the quality of life for Alzheimers and Dementia patients.

They help to stimulate memories and improve communication.

One intern says they are working hard to break the stigma surrounding the disease.

"The importance of getting this information out for people with alzheimer's awareness is to let people know what people with alzheimer's are going through and also to help people within our community who experience alzheimer's dementia and things as is," said the stduent Quenn Davis.

The teddy bears donated at the drive thru event will be delivered to local patients Sunday.

And Alpacas and Llamas lent a helping hand over at Saint Mary of the Woods College Saturday!

Check this out!

This was at the White Violet Center.

The Vigo County 4-H Alpaca and Llama Club an Sister of Providence got the animals out to mingle and take a walk.

This was all to raise money and awareness of Alzheimer's disease.

Children and adults got to love on the gentle animals, too.

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Organizations help bring awareness to Alzheimer's disease - WTHITV.com

Global Alzheimer’s Platform Foundation Selects IXICO for Innovative Bio-Hermes Trial – PRNewswire

Posted: at 3:53 am


LONDON, Sept. 21, 2020 /PRNewswire/ -- IXICO plc, the data analytics company delivering insights in neuroscience, today announced that it has been selected by the Global Alzheimer's Platform Foundation (GAP) to support GAP's planned Bio-Hermes trial. IXICO will apply its expertise to collect Positron Emission Tomography (PET) brain scans in qualifying imaging centres participating in Bio-Hermes and provide analysis of the scans.

Bio-Hermes' core purpose is development of a bio-sample database to investigate biomarkers on a head-to-head basis in conjunction with medical history elements. The Bio-Hermes trial will include 1,000 volunteers over the age of 60 screened for Preclinical Alzheimer's Disease, Prodromal AD, or Mild Dementia AD. Observational biomarker studies consistently suggest that amyloid deposition and tau deposition in neurofibrillary tangles in the brain may be the sentinel events in Alzheimer's Disease pathology. In the Bio-Hermes trial, Avid Pharmaceuticals' Amyvid will be used as the radioactive diagnostic agent to estimate -amyloid neuritic plaque density.

Giulio Cerroni, Chief Executive Officer of IXICO, commented:

"We are delighted to be selected by GAP as their prime choice for the analysis of PET scans in the Bio-Hermes trial. With a reinvigorated level of interest in Alzheimer's disease, we are excited about the prospects of long-term collaborationwith our colleagues at GAP who share our own commitment to reducing the time, cost, and risk for Alzheimer's Disease trials. The support provided by IXICO staff on Bio-Hermes is an important commercial development in enhancing IXICO's market position in neuroimaging for Alzheimer's Disease clinical trials."

John Dwyer, President of Global Alzheimer's Platform Foundation (GAP), commented:

"Our collaboration with IXICO for neuroimaging and AI is a key element of GAP's innovative Bio-Hermes trial, which is taking a novel approach to provide digital and blood biomarker results for comparison across cognitively normal and impaired individuals. We've also committed to ground-breaking levels of minority participation so that future treatment breakthroughs can benefit everyone impacted by Alzheimer's."

For further information please contact:

IXICO plc Giulio Cerroni, Chief Executive Officer Grant Nash, Chief Financial Officer +44 (0)20 3763 7498

Global Alzheimer's Platform Foundation Media Pamela Larkin +1408-466-5952 or [emailprotected]

About the Global Alzheimer's Platform Foundation (GAP)

The Global Alzheimer's Platform Foundation (GAP) is a patient-centric nonprofit dedicated toacceleratingthe delivery of innovative therapies for neurological disorders by reducing thedurationand cost of clinical trials. Research centersacross the US and Canadaare part of the growing GAP Network (GAP-Net). GAP supportsGAP-Net research centers by assisting withstudy start up and recruitment activities,promotingdiversity in research studies, andofferingnational programsthatchampion brain health and the citizen scientists who make research possible.

About IXICO

IXICO is dedicated to delivering insights in neuroscience. Our purpose is to advance medicine and human health by turning data into clinically meaningful information, providing valuable new insights in neuroscience and our goal is to be a leading proponent of artificial intelligence in medical image analysis. We will achieve this by developing and deploying breakthrough data analytics, at scale, through our remote access technology platform, to improve the return on investment in drug development and reduce risk and uncertainty in clinical trials for our pharmaceutical clients.

More information is available on http://www.IXICO.com.

SOURCE IXICO

https://ixico.com

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Global Alzheimer's Platform Foundation Selects IXICO for Innovative Bio-Hermes Trial - PRNewswire

Does Cassava Sciences Have the Alzheimer’s Disease Drug We’ve Been Waiting For? – The Motley Fool

Posted: at 3:53 am


Shares of Cassava Sciences (NASDAQ:SAVA) rocketed higher last week in response to compelling results from a clinical trial with sumifilam, an experimental treatment for Alzheimer's patients. This disease affects roughly one in 10 adults over 65, and there still aren't any effective treatment options that curtail its progression.

Recently released results from a midstage clinical trial with mild to moderate stage Alzheimer's disease (AD) patients are compelling, but we've been here before. Here's what investors should know about sumifilam, the potential new AD drug from Cassava Sciences, and potential pitfalls the company's peers have stumbled into before.

Image source: Getty Images.

There still aren't any available treatments that curtail progressive mental deterioration brought on by the disease. In the past decade, we've seen AD candidates from Pfizer,Roche, Eli Lilly, andBiogen (NASDAQ:BIIB) exhibit signs of efficacy in early stage clinical trials only to disappoint in larger and exponentially more expensive phase 3 trials.

While there aren't available AD treatments at the moment, there could be one before the end of the year. The FDA is currently reviewing a controversial application from Biogen for its AD candidate, aducanumab.

There's a chance the FDA will decide that the hazy benefit Biogen reported outweighs clear health risks seen among patients who received regular infusions of aducanumab. In a far more likely scenario, there will still be an enormous unmet need for effective AD drugs years from now when Cassava's ready to present phase 3 results for its AD candidate.

Sumiflam's a first-in-class small-molecule drug that's designed to fix misfunctioning filamin A, a scaffolding protein associated with higher concentrations of protein fragments that form plaques in the brains of AD patients. Successful results from phase 2 suggest it works as expected.

In a randomized controlled phase 2 trial, investigators split 64 patients with mild-to-moderate AD into three groups, two that received pills containing 50 milligrams or 100 milligrams of sumifilam twice daily and a third that received a placebo.

After 28 days of treatment, researchers examined samples of the fluid that was bathing their brains and spinal cords for signs of tau, amyloid-beta, and several other biomarkers associated with AD and other forms of dementia. Across all biomarkers measured, patients in the sumifilam groups showed reductions that were significantly lower than the placebo group.

Image source: Getty Images.

Biomarker reductions are all fine and good, but the FDA wants to see proof that a drug can improve outcomes before approving it to treat millions of relatively healthy people. Patients treated with sumifilam tested higher when asked to remember new information, but the difference wasn't strong enough to be considered statistically significant. Remember, this was a small study, funded by the National Institutes of Health, that enrolled just 64 patients and observed them after only four weeks of treatment.

The cognitive symptoms associated with Alzheimer's disease progress so slowly that we can't realistically expect measurable cognitive benefits after just 28 days. The results Cassava reported in this NIH sponsored phase 2 trial, though, suggest sumifilam's doing something right.

If a sumifilam can repeat it's recent success in a larger study designed to measure long term cognitive benefits, it could eventually become the top-selling drug of its time. Anyone considering an investment in Cassava, though, needs to understand there's still a long road ahead.

In a nutshell, Cassava Sciences isn't equipped to run a pivotal AD trial with thousands of patients and dozens of study locations. At the end of June, the company had just $25 million in cash, no reliable sources of revenue, and hardly enough employees to fill a small conference room.

One way or another, Cassava's going to need capital to run a phase 3 study with sumifilam. This could come in the form of a collaboration agreement with a larger pharmaceutical company or a complete buyout offer. At the moment, the company sports an extremely modest $251 million market cap that puts the company well within reach of dozens of potential suitors.

Investors should know that sumifilam was Cassava's last hope just a couple of years ago, when the company was still called Pain Therapeutics. You may remember, Pain Therapeutics shifted gears in 2018 after receiving multiple rejections from the FDA for Remoxy ER, an abuse-deterrent opioid.

The data we've seen so far from sumifilam clearly warrants further study, but Cassava's still run by Remi Barber, the same CEO who spent years convincing shareholders Remoxy ER was a good bet. If you're going to take a chance on Cassava Sciences stock, don't risk anything you can't afford to lose.

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Does Cassava Sciences Have the Alzheimer's Disease Drug We've Been Waiting For? - The Motley Fool

Respecting Your Elders in the Fight vs. Alzheimer’s Disease – TAPinto.net

Posted: at 3:53 am


As Grandparents Day fell on this past weekend, I reflected on what my mother used to tell me as a child. Respect your elders. When she said that, she meant respect them when in their presence.

Together with like-minded volunteers and Ambassadors for The Alzheimers Association Greater New Jersey Chapter I respect our elders even if I dont know them, by fighting Alzheimers disease with tenacity and fortitude.

My father-in-law, Lorenzo Malanga, had a seven-year battle with Alzheimers, finally succumbing to the disease two years ago. Seeing him decline and fade away is what inspired me and my family to get involved with The Alzheimers Association, volunteering as chairs for the Walk to End Alzheimers, attending training sessions, fundraising in many different ways, journeying to DC for Forum, and traveling to The Alzheimers annual Summit.

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Of course, I did these things not only for self reward, but to honor those who have passed from or who are currently suffering with dementia.

We can be part of something bigger than ourselves as we volunteer and advocate for laws such as the Elder Abuse Act.

In the future, if we are lucky, we will all be the elders. It is in our own self interest to revere and respect our elders, as we may be there soon. We are not only fighting for now, but for the future. Our future.

I urge Congresswoman Mikie Sherrill to support The Promoting Alzheimers Awareness to Prevent Elder Abuse Act (S.3703/H.R.6813) which will enable all Americans to have a brighter future.

Lets work together, help each other, and do everything we can to end this terrible affliction. To do nothing is passive, but to do something is massive.

Dave Whetton

Caldwell resident

Ambassador for The Greater NJ Chapter of The Alzheimers Association

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Respecting Your Elders in the Fight vs. Alzheimer's Disease - TAPinto.net

Brookdale Communities Take Part in Virtual Walk to End Alzheimer’s Events Across the Country – PRNewswire

Posted: at 3:53 am


NASHVILLE, Tenn., Sept. 21, 2020 /PRNewswire/ -- While this year's Walk to End Alzheimer's events will be different, they continue to be deeply meaningful. They continue to help raise awareness about the sixth-leading cause of death in the United States. They continue to help raise funds that make a difference in the lives of those facing Alzheimer's. Brookdale Senior Living Inc. continues to be one of the largest corporate supporters of the Walk to End Alzheimer's. This year, thousands of Brookdale associates, residents, and patients are participating in or supporting virtual walks across the country. Many will share the impacts this disease has had on their families and friends. More importantly, they'll also show that those living with dementia still have much to live for.

"It is essential to do what we can to combat this disease," said Brookdale President and CEO Lucinda M. Baier. "We know the walks will be different this year due to the COVID-19 pandemic, but we believe in the importance of these events as part of the fight against Alzheimer's."

September 21st is World Alzheimer's Day, and people across the globe do what they can to raise awareness and challenge the common stigmas that surround Alzheimer's and other forms of dementia. Since 2008, Brookdale's associates, residents, families and business partners have raised almost $17 million for the Walk to End program through the Alzheimer's Association.In many of these years, Brookdale surpassed an annual $2 million mark for the Walk to End program as a Diamond National Team. The company's efforts are not just about donations, they are about making a difference. Brookdale is the nation's largest operator of memory care communities, and has developed innovative programs that take a person-centered approach to care.

"According to the World Health Organization, there are around 50 million people worldwide living with dementia and unfortunately Alzheimer's Disease International reports that two out of every three people globally believe there is little or no understanding of dementia in their countries," said Juliet Holt Klinger, gerontologist and expert on dementia care at Brookdale. "That astounds me. The impact of World Alzheimer's Month is growing, but the stigmatization and misinformation that surrounds dementia remain a global problem that require that all of us pay attention. At Brookdale, we strive to support people living with dementia to live their best life possible. We believe that working to decrease the stigma around the dementia diagnosis is a big part of that."

About Brookdale

Brookdale Senior Living Inc. is the leading operator of senior living communities throughout the United States. The Company is committed to providing senior living solutions primarily within properties that are designed, purpose-built, and operated to provide the highest-quality service, care, and living accommodations for residents. Brookdale operates and manages independent living, assisted living, memory care, and continuing care retirement communities, with 737 communities in 44 states and the ability to serve approximately 65,000 residents as of June 30, 2020. The Company also offers a range of home health, hospice, and outpatient therapy services to over 17,000 patients as of that date. For more Brookdale news, go to brookdalenews.com.

SOURCE Brookdale Senior Living

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Brookdale Communities Take Part in Virtual Walk to End Alzheimer's Events Across the Country - PRNewswire

Not being able to visit loved ones with dementia takes a toll, advocates say – News-Leader

Posted: at 3:52 am


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Mark Applegate and his stepfather John Alexander visit with Brenda Alexander, Mark's mom and John's wife, who has been in a Greene County nursing home with Alzheimer's disease since 2018. Applegate used to be able to stop by and visit with his mom several times a week but due to COVID-19, he can only visit with her once a week and from six feet away.(Photo: Nathan Papes/Springfield News-Leader)

The pandemic has taken a devastating toll on residents and staff in nursing home and long-term care facilities. So far in Greene County, there have been more than 30 deaths associated with long-term care facilities.

Early on in the pandemic, facilities put a pause on visits from family and friends.

Mark Applegate and his stepfather John Alexander visit with Brenda Alexander, Mark's mom and John's wife, who has been in a Greene County nursing home with Alzheimer's disease since 2018. Applegate used to be able to stop by and visit with his mom several times a week but due to COVID-19, he can only visit with her once a week and from six feet away.(Photo: Nathan Papes/Springfield News-Leader)

An unfortunate consequence of this has been the social isolation andloneliness for residents, as well as the potential for cognitive decline among those with dementia and Alzheimer's disease.

Mark Applegate's mom,Brenda Alexander, has end-stage Alzheimer's disease and hasbeen in a Greene County nursing home since 2018.

Before the pandemic, Applegate would stop by and visit with his mom several times a week. Alexander's husband, John, used to stop by three times a day to visit and feed Brenda.

Mark Applegate visits with his mom Brenda Alexander who has been in a Greene County nursing home with Alzheimer's disease since 2018. Applegate used to be able to stop by and visit with his mom several times a week but due to COVID-19, he can only visit with her once a week and from six feet away.(Photo: Nathan Papes/Springfield News-Leader)

Due to COVID-19, theycan now only visit with her once a week sitting outside for 15 to 20 minuteswith at least six feet between them.

Applegate called the dilemma a "catch-22."

"(Nursing homes) would love to be open, but they also would love to not get (COVID-19) and not have the patients get it," Applegate said. "They've got to do the best they can to keep it out of the building."

Applegatevolunteers with the Alzheimer's Association and shares his family's story on his blog, digitalcornbread.com.

Jerry Dowell, vice president of public policy for the Missouri chapter of the Alzheimer's Association, said it's important for individuals with dementia to have routines and social interactions. But with the pandemic, that's not really happening.

"Whenever there's an outbreak inside a facility, they've got to be socially isolated from everybody. There's no more congregate meals," Dowell said. "There's no more games or enjoying different areas of the facility. It will affect their cognition because they are not understanding why that's occurring."

Another negative consequence of not having face-to-face visits with family members is residents don't have that extra set of eyes on them to notice when something may be going on with their physical health.

"A lot of these individuals with dementia have other comorbidities," Dowell said. "As individuals progress with dementia, they become less verbal. So maybe they are feeling terrible or they've got something wrong with them, but they are not able to share that with anybody because they can't verbalize pain."

Applegate said he worries about this with his mother. From six feet away, he can see she has gained a considerable amount of weight. She seems happy every time they visit.

But he knows from past experience, he can usually tell when something is wrong with his mother's health before the nursing home staff can.

Mark Applegate and his stepfather John Alexander visit with Brenda Alexander, Mark's mom and John's wife, who has been in a Greene County nursing home with Alzheimer's disease since 2018. Applegate used to be able to stop by and visit with his mom several times a week but due to COVID-19, he can only visit with her once a week and from six feet away.(Photo: Nathan Papes/Springfield News-Leader)

Applegate recalled a time last year when he was the one who noticed her stomach was distended a bit.

"I could tell she was constipated," he said. "The more you are around someone, the more you recognize stuff like that. And when you are used to being kind of apartial caregiver, not being able to see them makes it very uncertain. It's challenging, for sure."

Dowell said the Alzheimer's Association is urging state and federal lawmakers to implement new policies to address the immediate and long-term issues such facilities are facing during the pandemic.

Rapid point-of-care testing the kind used at the White House is at the top of the association's wish list. With this sort of testing, results are back within 15 to 20 minutes.

"In order to end social isolation and ensure every long-term care community has access and opens up is that we need to ensure that you do rapid testing on all residents, all staff and any visitors that enter a facility," Dowell said.

"As with what we are seeing with the school kids going back to school, in person or otherwise, there is a toll that's been taken on our kids," he said. "The same is with our individuals with dementia that have been socially isolated. We need to do everything we can to get things back to normal."

The Alzheimer's Association is also advocatingfor more accurate and immediate reporting and for the creation of a central, publicly-accessible web platform that is searchable down to the facility level to makedata available immediately upon reporting.

"One of the most important things is getting their loved ones back in contact," Dowell said. "It's not only been hard on those that suffer from dementia inside of these facilities. It's been hard on the loved ones that have not been able to be part of their care plan and taking care of them."

Learn more atalz.org/greatermissouri.

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Not being able to visit loved ones with dementia takes a toll, advocates say - News-Leader

A journey in Alzheimer’s disease documented during travels in Minnesota – Grand Forks Herald

Posted: September 18, 2020 at 9:57 am


Dressed in a bright red jacket and wearing red lipstick that contrasts with her strikingly beautiful white hair, Colleen is ready for the days adventure thats part of a unique mother-and-son journey.

Its a journey with two purposes: to relive old memories, and make new memories while Colleen travels down the tough road of Alzheimers disease.

John, who had been living in Arizona while working for an international travel company, moved back to his hometown of Willmar, Minn., two years ago to care for his parents. His father, Donald, died in November 2018. Since then hes been focused on caring for his mother.

The family has always had a love for traveling, and John said rather than sitting at home with his mother, he decided to take her on jaunts around Minnesota, including traveling to nearly all of the state parks.

Colleen Kellen stands near one of the photos in her son's collection at WEAC that documents her journey with Alzheimer disease and their journey together to sites throughout Minnesota. A virtual tour of the display is available through October. Photo courtesy of John Kellen

To manage the challenges of caring for a parent with increasing dementia, John renewed an interest in photography and joined the Little Crow Photography Club, where he was encouraged to take photos of the things he saw while taking trips with his mother.

Photos of wildlife, landmarks and poignant shots of his mother are part of Kellens collection of 25 photographs on display at the Willmar Education and Arts Center through October. Because of COVID-19, the display can be viewed only through a virtual tour.

The solo exhibit, called A Picture is Worth a Thousand Words the Language of Photography, was made possible through an emerging artist grant from the Southwest Minnesota Arts Council that Kellen received, in collaboration with the Willmar Area Arts Council.

While taking his mother on trips around Minnesota, John Kellen captures photos of wildlife that are part of his display at WEAC. Because of COVID, the display can only be seen through a virtual tour. Photo courtesy of John Kellen

While his mothers ability to express herself verbally is declining, Kellen said its easy to tell when shes happy and excited and connecting with places, people and memories. It might be on one of the many trips they take to cemeteries where family members are buried, or being on the lookout for deer and ducks when driving through state parks.

One of the photos in the collection shows Colleen standing at the grave of her husband at Fort Snelling as she holds a photo of him as a young man in his military uniform. Theres a photo of mother and son standing by a float plane as part of a once-in-a-lifetime, three-day trip to Isle Royale National Park in Michigan, and one of Colleen holding a nice fish on the end of a fishing pole.

This photo of Colleen Kellen captures her love of fishing and dogs. "At this stage in her life I'm committed to providing as good of a quality of life as possible for Mutti while she is still able to enjoy and experience those activities that light her up," writes John Kellen in a description of the scene he caputred. Photo courtesy of John Kellen

The collection includes detailed and touching narratives that provide the background for the photos, like the one where Colleen, who is called Mutti by Kellen, is holding a light diffuser while Kellen photographed a native Prairie Smoke flower.

The photo captures Colleen being helpful, which Kellen said is important to his mother, who still wants to be able to contribute something of value.

Being outdoors and watching nature is a passion that mother and son share. Stunning photos of waterfowl, water, rocks and prairie flowers were selected because they have some current significance for his mother that brings her joy, Kellen said.

Colleen Kellen, holding a light reflector, serves as a photography assistant for her son, John Kellen, during one of their many journeys around the state. Photo courtesy of John Kellen

A photo of a cardinal has a special meaning because Donald Kellen worked for many years as a counselor in the Willmar School District home of the Cardinals.

A photo of a goldfinch is included even though Colleen is no longer able to say the name but is able to say yellow one, said Kellen, who mourns his mothers loss of language but tries to not focus on whats missing but on what she still has.

Kellen said hes determined to give his mother quality-of-life experiences as long as Im able to do it.

I see it as a gift, Kellen said of being his mothers caretaker and travel companion. But its certainly not for the faint of heart.

Technically and artistically the photos of his mother are not his best, Kellen said. But theyre an important part of the story hes telling in the exhibit about the value of spending time and being in the moment with people you love.

Its the story of mom, he said.

To experience John Kellens virtual tour of his solo photography show, A Picture is Worth a Thousand Words The Language of Photography go to the Willmar Area Arts Councils webpage at http://www.willmarareaartscouncil.org and click on the gallery heading. The tour will be available through October.

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A journey in Alzheimer's disease documented during travels in Minnesota - Grand Forks Herald

Teams will drive rather than walk for Alzheimer’s Resource Center fundraiser – Dothan Eagle

Posted: at 9:57 am


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Adam Jones, far left, and Marilyn Barnes talk about the upcoming fundraiser, A Drive to Remember for Alzheimer's disease as Curtis Barnes looks on at the Alzheimer's Resource Center on Sept. 9. The three are co-chairs for this year's event, which has been changed to A Drive to Remember this year due to the pandemic.

There are many things Marilyn Barnes misses about her mother.

Her mother, Jimmie Stubbs Skipper, loved to sing and dance and even taught Marilyn how to do the Jitterbug. Skipper was active in her church choir and loved having all her family together for Thanksgiving and Christmas.

But Barnes especially misses the phone calls shed get from her mother around 10 p.m., just before bedtime.

She called me almost every night, Barnes said. It took me awhile to get over that.

Jimmie Stubbs Skipper, known simply as Mimi by family, began showing signs of Alzheimers disease around 2008. She died in 2015.

My mother loved to talk, loved to laugh, Marilyn Barnes said. She was always dressed to a T. She didnt go to her mailbox without lipstick and earrings on. Thats just the way she was. She went to the beauty parlor every week to have her hair done, and we continued that when she was sick.

Marilyn and her husband, Curtis Barnes, and her son Adam Jones are co-chairs of the 2020 fundraiser for the Alzheimers Resource Center in Dothan. Normally called A Walk to Remember, this years event is A Drive to Remember due to the ongoing coronavirus pandemic. Instead of walking, teams will decorate their vehicles and drive in a convoy through Westgate Park on Saturday, Oct. 3. Other COVID-19 restrictions, such as masks and social distancing, will also be in place.

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Teams will drive rather than walk for Alzheimer's Resource Center fundraiser - Dothan Eagle

How a Factor on the X Chromosome May Offer Resilience to… : Neurology Today – LWW Journals

Posted: at 9:57 am


Article In Brief

A protective mechanism on the X chromosome may make females more resilient to Alzheimer's disease, explaining why they live longer than men with the disease.

Scientists at University of California, San Francisco (UCSF) have identified a factor on the X chromosome that protects against Alzheimer's disease (AD). The study was conducted in animal models of AD and cell cultures, but the factor is also present on the human X chromosome and may help explain why women live longer than men with the disease and have a less severe cognitive course early on, scientists told Neurology Today.

The findings were reported in the August 26 issue of Science Translational Medicine.

Dena B. Dubal, MD, PhD, FAAN, associate professor of neurology and the David Coulter endowed chair in aging and neurodegenerative disease at UCSF, has long been interested in sex differences in AD, and she and her colleagues have used powerful tools in sex biology to begin to identify differences between males and females and vulnerability or resilience to the disease.

If we can understand what makes one sex more vulnerable or resilient to Alzheimer's we can target new pathways for treatment, she said.

Dr. Dubal's interest in sex differences in AD began a decade ago. When she and her colleagues began looking at the literature from around the world it was pretty clear that males had an increased risk of dying earlier than women with AD. She had just believed the epidemiology that pointed to more women having AD. In fact, men and women have an equal risk until very old age, but men die sooner than women. The question was why.

The scientists turned to the mutant human amyloid precursor protein (APP) mouse model to determine the answer. They quickly discovered that male mice progressed faster to death than the female APP mice. The scientists decided to take away hormones (by removing their gonads) in males and females and see what happens. (Note that mice do not lose hormones as they age, as humans do.) Again, the males progressed faster with increased cognitive deficits even with equal levels of amyloid-beta, and they died earlier than the females.

What was it about the sex chromosomes that were conferring this risk? They used two different models that both pointed to sex chromosomes, and they were able to identify a specific factor that seemed to be the missing resilience factor.

For the first study, they produced APP mice that were XX female and made mice that were XX male. They grew up male (with testes and testosterone) but had the female sex chromosomes. They used a genetic technique to delete the Y chromosome but transpose its Sry gene that makes a protein that gives instructions on masculinizing an organism onto another chromosome. So the males were still male but were XX.

The APP XX males lived longer and had less cognitive deficits compared to the APP mice that were XY. All the mice that were XX, whether they had ovaries or testes, lived longer and showed more resilience against AD toxicity, explained Dr. Dubal.

To understand the next study, Dr. Dubal provided short course on sex chromosome biology. All female mammals have two X chromosomes but the second copy is inactivated or silenced. This mechanism is called lyonization and was first described by British geneticist Mary Lyon in the 1970s.

This innate mechanism prevents female cells from having twice as much gene product from the X chromosome as males do. As it turns out, the one copy that was inactivated wasn't so quiet after all. There are still a few genesfive, in fact that slip by this mechanism and are active in brains of both mice and humans.

Is there something about the gene dosing on the second X chromosome that is helpful or hurtful? They set out to cross the APP mouse with another mouse model that alters the dose of sex chromosomes. (Normally, the X and Y chromosomes do not recombine but there is a technique to trick the X and Y chromosomes to recombine and this allows for a different dose of the sex chromosomes. It creates an XY male with an extra X chromosome. You can also take an XX female and remove one X chromosome and create an XO female, in which one of the two X chromosomes were completely absent.

When they back-crossed these mice with the APP mouse that extra X turned out to be very important to living longer and having fewer cognitive deficits. It basically rescued their mortality. They now lived almost as long as the XX females and adding the extra X dose reduced their cognitive problems. There was 90 percent survival at eight months. (Normally, XY survival was about 75 percent.) By contrast, the XO animals did much worse. Their survival was around 40 percent.

All of the animals tested had their gonads removed in adulthood to keep the hormonal playing field even and model human reproductive aging.

We had no idea what was going to happen when we conducted these experiments, said Dr. Dubal. We would have gone wherever the science took us.

So here we were, wondering why having two copies of the X chromosome would matter compared to one X chromosome, especially since in humans one copy is inactivated, Dr. Dubal recalled.

She and her colleagues turned to the internet searching every database for clues as to what is escaping from the silent X chromosome? They identified a handful in mice and even fewer in humans and there were five shared between them. One of them stood outa gene called KDM6A. People born with a mutation in the gene have a rare condition called Kabuki syndrome and while there are a range of symptoms one important hallmark is intellectual disability and developmental delays. It was a clue worth following.

They read everything they could about KDM6A and discovered that it was expressed more in women and female mice. They went back to the lab and added it to neuronal cell cultures exposed to amyloid-beta and they found that the neurons became resilient to the toxic protein. Then, they used a genetic editing technique to increase the genetic factor in APP transgenic males to the same level found in females, and it improved the animal's cognitive deficits.

They then asked UCSF geneticist Jennifer Yokoyama, PhD, an associate professor of neurology at the UCSF Memory and Aging Center to look at the gene in humans. She found that there is one variant of the gene that codes for more KDM6A so that more of the gene product is made in the brain. She conducted longitudinal research on people with AD and other forms of dementia and found that people with this variant have less cognitive decline over a ten-year period than those who do not have that variant. And women with this variant have an even higher dose, given the activity that slips through the silencing mechanism of the second X chromosome.

So what does it all mean? It means that KDM6A is relevant to human brain health, said Dr. Dubal. It's exciting on so many levels. Most importantly, it establishes a role for sex chromosomes in Alzheimer's disease. Then, knowing a protective mechanism on the X chromosome opens up the possibility of targeting new therapeutic pathways. It is not about masculinity or femininity but about cognitive function that might be improved by enhancing this genetic factor. One of the main roles of the gene is to work in the nucleus to unwind DNA and this opens the door to more gene expression, she added.

Her group is now looking at the other four shared factors between mice and humans, and also looking into samples from their human research subjects to see whether the genetic factor is involved in other types of dementia.

This is an elegant study with interesting speculation on the genetic contributions to sex differences but one cannot ignore lifestyle differences between the sexes, said Ronald C. Petersen, MD, PhD, FAAN, director of the Mayo Alzheimer's Disease Research Center and the Mayo Clinic Study on Aging. That is, men generally have a greater cerebrovascular burden than women which could contribute to genetic vulnerability, especially for mild cognitive impairment and dementia, and perhaps for AD itself.

His colleague, Nilfer Ertekin-Taner, MD, PhD, professor of neurology and neuroscience at Mayo Clinic in Jacksonville, FL, added that this research is an important example of studying sex as a biological variable and dissecting numerous aspects of sex including chromosomal vs. gonadal effects. It highlights the necessity to not only include models from both sexes, but also to evaluate different aspects of sexual biology to bring a nuanced understanding of this variable in human health and disease. Performance of gonadectomy provides an essential control for hormonal effects, but the need to specifically test for hormonal effects in different study designs should be emphasized.

Discovery of KDM6A as a potential resilience gene in AD is certainly interesting, Dr. Ertekin-Taner said. Nonetheless many questions remain, as expected from this novel finding: KDM6A encodes a histone H3K27 demethylase.

Histone modifications are known to have myriad effects on the expressions of other genes and biological pathways, she explained. Given this, whether the effects seen in the model systems and human data are due to KDM6A or genes/pathways influenced by this gene remains to be established. For the same reason, the potential of KDM6A as a therapeutic agent in AD or aging is questionable. On the one hand therapies that target epigenetic pathways may be deemed a dirty approach with potentially multiple undesirable effects. On the other hand, complex diseases, such as AD, may benefit from therapies that can beneficially influence multiple biological pathways.

She said that future studies should focus on additional mouse models to replicate these findings in the context of different backgrounds and AD-related pathologies.

Biological consequences of KDM6A require in-depth investigations to determine the molecules that can confer resilience and be leveraged as therapies in AD, Dr. Ertekin-Taner said. Finally, additional factors that may play a role in disease risk and survival between males and females, including vascular risk and social factors need to be continually explored. This study provides a solid approach and intriguing questions for the field and gives sex as a biological variable its long-neglected attention.

Dr. Dubal has consulted for AbbVie Inc. data monitoring committee and serves on the scientific advisory board for Vigorous Minds Inc. Drs. Petersen and Ertekin-Taner have no relevant disclosures.

WHAT IT IS

Female mammals typically have two X chromosomes and male mammals have one X and one Y chromosome. Scientists have been able to manipulate sex chromosome dosing using a genetic trick to increase the amount of gene dosing by adding a second X chromosome in males.

HOW IT WORKS

There are several mutant mice with atypical sex chromosomes that have allowed the UCSF scientists to carry out these experiments. The testis-determining factor, Sry, causes testes to form and shapes male brain and behavior. Without Sry, ovaries develop. In one mouse model, scientists can delete Sry on the Y-chromosome and replace it with a transgenic copy of the gene that is inserted into an autosome. They can do this in XX and XY mice so either testes or ovaries can develop in both sexes. This does not alter the hormonal milieu so XX and XY mice that develop with testes still behave as males and vice versa. In another mouse model, they can also add an X chromosome to XY males and even knock out the second X chromosome in XX females. and look for any differences that would suggest that either the second X chromosome or the Y chromosome governed a sex chromosome effect.

HOW IS IT APPLIED

The scientists used these techniques to make a variety of mutant mice with atypical sex chromosomes that led to their discovery. With these techniques, they were able to determine if a sex difference in hAPP mice was due to sex chromosomes or to gonads. When they found that sex chromosomes largely governed the sex difference, they dissected whether it was the second X chromosome or the Y chromosome that contributed to the sex difference.

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Alzheimer’s Disease Patients Market 2020 | Know the Latest COVID19 Impact Analysis And Strategies of Key Players: Forest Laboratorie, Eisai, H….

Posted: at 9:57 am


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Alzheimer’s Disease Isn’t the Only Cause of Dementia – Discover Magazine

Posted: September 9, 2020 at 5:57 pm


Growing old is a natural part of life. Our hair will turn gray and our skin will wrinkle. Our bones and muscles will weaken, and our blood vessels will get stiff. But many of us will also lose our minds, and that is something that's not supposed to happen.

Half of people age 80 or older have some form of dementia. The older someone is, the more their risk goes up. Significant declines in brain function may seem inevitable because of how common it is. But most experts believe that dementia is not a normal part of aging and that it can somehow be stopped. For that day to come, a better understanding of the nuances of the dementia subtypes and their underlying pathologies is crucial, says Peter Nelson, a neuropathologist at theSanders-Brown Center on Aging at the University of Kentucky.

Theres still a tendency to lump all dementia patients into what Nelson calls a grab bag of Alzheimers disease. Some older people who are experiencing impairments to their thinking, memory and judgment might not have Alzheimer's, but another form of dementia. Other brain diseases associated with old age can be just as devastating and more common than you might think. A greater emphasis on non-Alzheimer's dementias not only would help patients get better care, but it could move research forward. Until diseases are correctly named, defined and understood, finding ways to treat and prevent them is pretty much next to impossible.

Its just like the many other fields where it turns out that its important to differentiate the symptom like shortness of breath from the disease, like pneumonia and asthma, Nelson says. This is a real explanation for why a lot of previous clinical trials didnt work. The samples were hopelessly muddy. If youre trying to treat a bunch of people with pneumonia, but youre only using therapies for people with asthma, youre not going to win.

Alzheimer's is the most common type of dementia, accounting for roughly 60 to 80 percent of all cases. But Alzheimer's is a specific disease, whereas dementia is not. Rather, dementia is an umbrella term that refers to declines in a persons memory and cognition that become serious enough to interfere with daily activities.

In some ways, saying someone has dementia is similar to saying they have a cold. Some 200 viruses, each genetically different, can attack the respiratory system. Many of the symptoms are alike coughing, sneezing, a sore throat but that doesnt tell you much about the underlying causes or how to fix them.

Every organ has dozens and dozens of diseases and dysfunctions as you age. The brain is entirely more complicated than the other ones, and yet, we have this view that only one disease can affect it with aging, Nelson says.

Something many dementias have in common is that they're caused by a buildup of harmful proteins in the brain. Why these proteins start to misfold and clump together is poorly understood. But the end result is brain damage that gets worse over time. Glops of misshapen proteins prevent neurons from communicating with each other. Eventually, neurons lose function and wither away, causing the brain to literally shrink.

"The glop literally destroys the cells around it, and they get taken away in a persons blood. And you end up losing a big physical portion of your brain. It just melts away as this glop accumulates, Nelson said. That brain has gone from a 4-pound brain to a 3-pound brain. Youve literally lost 30 percent of the weight of your brain. Its been demolished.

According to Nelson, the gloppy proteins that wreak havoc on the brain vary based on the type of dementia someone has. With Alzheimers disease, its well-established that tau and beta-amyloid proteins are the culprit. Initially, the damage appears to take place in the hippocampus, the part of the brain essential in forming memories, before becoming more widespread.

Its different from what youd see in the brain of someone with LATE, another common form of dementia thats often mistaken for Alzheimers disease. The acronym LATE stands for limbic-predominant age-related TDP-43 encephalopathy. The syndrome's name indicates the area of the brain affected, as well as the protein responsible for deterioration, called TDP-43.

Nelson was a member of the international team that published the first definition for LATE in 2019. He says researchers are learning that LATE is very common among older adults, affecting about a quarter of those over age 80.

Another type of dementia thats often confused with Alzheimers is Lewy body dementia. Accounting for roughly 10 percent of all dementia cases, the disease shares similarities with both Alzheimer's and Parkinson's, as it affects both mental abilities and movement. Notably, around 80 percent of people with the disease also experience hallucinations. This type of dementia is caused by an accumulation of alpha-synuclein proteins, which form into clumps known as Lewy bodies.

But Nelson said that not all dementias are caused by misfolded proteins. Vascular dementia, for instance, can be caused by a major stroke, a series of small strokes or clogged blood vessels that reduce blood flow to the brain over time. Nelson says this form of dementia is often the most unpredictable in its symptoms, as it depends on which part of the brain has been damaged.

Complicating matters even further is the fact that most people with dementia tend to have more than one underlying disease affecting their brain. In particular, there seems to be a lot of overlap between LATE and Alzheimers, and that can make outcomes worse for the person, Nelson says.

A lot of people have both LATE and Alzheimers disease ... and were still struggling with how to deal with that, Nelson says. People with Alzheimers get impairment and dementia, and its a horrible disease. People with LATE also get impairment and dementia, but its a subtler and slower disease. However, for many people ... that have both, the severity of their dementia and the swiftness of their decline is greater than either LATE or Alzheimers in the pure form.

The brain changes that cause dementia begin years even decades before symptoms reveal themselves. By the time a person receives a diagnosis, their brain is probably too damaged to fix, Nelson says. Thats why the field has shifted away from finding a cure and is now focusing on uncovering ways to keep the brain healthy.

But first, researchers must establish biomarkers for Alzheimer's and other dementia subtypes. Biomarkers are biological indicators that signal whether a person is at risk for a disease, or if it's already present. A biomarker test would give doctors the ability to catch diseases in their early stages and prevent them from getting worse. Biomarkers also would pave the way for more effective medications, providing concrete ways to measure how effective a drug is.

To find biomarkers, researchers are studying cognitively healthy people to better understand what's happening in the body before the symptoms appear. But recruiting clinical trial volunteers whether theyre healthy or sick has long been a challenge in dementia research, Nelson explained. According to the University of Southern Californias Leonard D. Schaeffer Center for Health Policy & Economics, nearly 99 percent of eligible Alzheimers patients are never asked to consider participating in a trial.

In cancer, theyve been more vigorous about saying, youre a patient, you have cancer, it has a bad prognosis, you have a choice to treat or not treat, and the treatment involves enrolling in a clinical trial. And thats how we bent the curve of survival for cancer. Not so in dementia, Nelson says. In part, that is because people in my field have been much more timid not in terms of generating theories, but in terms of providing adult people with the choice.

It's even more difficult to recruit people who arent yet sick, who likely hold the answers that can help the rest of us. Nelson says the field desperately needs people who are 75 or older to step forward and join studies, such as those listed on ClinicalTrials.gov.

I would have my mom do it, which is my clinical criteria for ethics, Nelson says. Its just a no brainer, you go in, and you have a chance. That is what would move the field forward.

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Alzheimer's Disease Isn't the Only Cause of Dementia - Discover Magazine

Oliver: Yearly visit to neurologist confirms the toll Alzheimer’s disease takes – Northwest Herald

Posted: at 5:57 pm


Every year at this time, the fissure in my heart gets a little bigger.

Thats because we go to see Tonys neurologist to track the progress of his Alzheimers disease, something he was diagnosed with in 2015.

Its not as if I dont know where we are in the progression of the disease, which we have named Fred to make a distinction between it and the man I adore. I live with Fred every day, and these days I see far more of Fred than I do of Tony, which is a cause of frustration for both Tony and me.

In the beginning, I found the series of questions that were asked at the neurologists office to be a bit unfair, but in those days Tony could answer most of them. In fact, he even did better in Year 2 because I knew what would be asked, and I went over it with him beforehand. Then again, his short-term memory was better then, too.

The doctors assistant asks what day it is, what year it is, what season it is, what county we are in and what floor the doctors office is on, among other things. Tony also is asked to repeat a list of three items and then come back to it in a few minutes and say them again. He is asked to identify a pen. He is asked to read a sentence (Close your eyes) and then do it. Hes asked to copy a couple of hexagons and to write a sentence.

From the get-go, Tony had forgotten the name of our county and what season it is. And because his main complaint was lack of short-term memory, the list items were never correct.

Each year a few more things have fallen off, which is to be expected. Ive learned to brace myself and try not to help. When Tonys sentence was I love my wife last year, I broke down in tears.

This year, however, those tears were more for being made to face what I already know: Tonys Alzheimers disease has gotten a lot worse.

He couldnt answer the day, date or year question. He could not answer the town and county questions. He wrote gibberish for his sentence, although it still was perfectly printed.

Amazingly, he actually got two items out of the list of three on the short-term memory quiz. Which just goes to show you how fickle Alzheimers can be.

Worst of all, he could not identify a pen. Now, Im sure not getting anything right before that probably had something to do with it, since frustration usually derails Tonys ability to think clearly.

Still, it was disheartening, but not unexpected. After all, I see this sort of thing every single day.

When the doctor said that there was nothing more that we could do for Tony, well, I saw that coming, too. I know that hes on every drug that he can be and taking doctor-recommended supplements to try to slow down this speeding train, but it is what it is.

Alzheimers is what takes my darling husband away from me piece by piece. It is what eventually will make me a widow. It breaks my heart.

One more year in. Twelve more months of little losses.

Still, I realize that I cant dwell on that. I have to find a way to do the best I can to make every one of Tonys days the best they can be for as long as we have. I have to find a way to not let Fred get the best of me, as much as I want to scream and rail against him.

This wonderful man I married still is in there, although sometimes hes harder to see.

Yet, I made a promise to stand by him no matter what. Weve had the better, now were dealing with the worse. Im not going anywhere.

For me, a promise is a promise. And Im good for my word.

Joan Oliver is the former Northwest Herald assistant news editor. She has been associated with the Northwest Herald since 1990. She can be reached at jolivercolumn@gmail.com.

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Peter Davies, Beloved Giant of Alzheimer’s Disease Research, Dies at 72 – Alzforum

Posted: at 5:57 pm


04 Sep 2020

When Peter Davies passed away on August 26, the Alzheimers research community lost a brilliant mind, and a truly generous human being. Davies died at age 72, after a long battle with cancer.

His discoveries paved the way for the first Alzheimers drugs and uncovered the startling complexity of the tau protein and its role in Alzheimers and other tauopathies. In their tributes on Alzforum, fellow scientists particularly recalled Davies generous sharing of antibody reagents and spirited conversations with him about the pathophysiology of AD, as much as they saluted his scientific achievements.

Peter Davies

Peter was clearly one of the greatest investigators in the pantheon of Alzheimers researchers. I knew him as a dear friend and valued mentor since the 80s. I always valued his great balance of scientific objectivity and empathy, especially for young investigators, Rudy Tanzi of Massachusetts General Hospital wrote to Alzforum.

Davies grew up in Wales, and studied biochemistry at the University of Leeds in northern England. After completing postdoctoral work at the University of Edinburgh, he joined the staff of the Medical Research Council Brain Metabolism Unit there in 1974. It was in Edinburgh that Davies began to explore Alzheimers disease.

Published on Christmas Day in 1976, his first AD paper turned out to be a gift to the field. He reported that the cholinergic system took a severe hit in the disease, a discovery that led to the development of acetylcholinesterase inhibitors, the first FDA-approved treatments for the disease (Davies and Maloney, 1976; Alzforum timeline).

His move, in 1977, to Albert Einstein College of Medicine in the Bronx, New York, brought him under the tutelage of the two great (and late) Bobs of early Alzheimers research in the U.S.Katzmanand Terry. Terry had recruited the young hotshot from England. In 2006, Davies became the scientific director of the Litwin-Zucker Center for Research on Alzheimers disease at theFeinstein Institute for Medical Research,North Shore-LIJ Health System, Long Island.

Peter Davies, Robert D. Terry, and Robert Katzman. Image credit: Peter Davies

Davies is perhaps best known for his work on the myriad forms of tau. He helped lay bare the devilish complexity of this microtubule-binding, tangle-forming protein. Starting with the development of Alz50, the first antibody to latch onto misfolded tau, Davies group went on to develop many more such antibodiesincluding MC-1and PHF-1trained against different forms the protein (Wolozin et al., 1986; Greenberg and Davies, 1990;Jicha et al., 1999).

Davies readily shared these reagents with other researchers. If you ever wanted to obtain and utilize any of the very useful antibodies that his laboratory created and you sent him an email, a few days later the antibody would just appear in your lab, recalled David Holtzman of Washington University in St. Louis. Throughout the field, Davies antibodies proved essential to pivotal discoveries about tau pathobiology (for detail, see Michel Goedert and Maria Grazia Spillantinis tribute below). The neuroscience community, and I especially, will be forever grateful for Peters generosity in sharing his wonderful library of antibodies and his boundless excitement for scientific discovery, wrote Ralph Nixon of New York University.

Over more than three decades, Davies published some 250 papers on tau, from its phosphorylation to truncation (Jicha et al., 1999;Weaver et al., 2000; Espinoza et al., 2008; dAbramo et al., 2013).

He kept an eye toward targeting toxic forms of the protein with therapeutics, and Zagotenemab,a derivative of his MC-1 antibody developed by Lilly, is currently finishing a Phase 2 trial in 285 people with early AD.

Davies also generated mouse models, including the hTau mice expressing all six isoforms of human tau (Duff et al., 2000; Nov 2001 news;May 2011 conference news).

Davies received numerous awards for his scientific achievements, including two MERIT awards from the National Institutes of Health, a Lifetime Achievement Award from the International Congress on Alzheimers Disease (ICAD), and the Potamkin Prize for Research in Picks, Alzheimers, and Related Diseases (Apr 2015 news).

For some years, Davies emphasis on the role of tau pathology in AD put him at odds with those who centered their research on amyloid. He was a witty voice for the tauist side during the fields sometimes truculent, and long past, period of division into baptist-versus-tauist camps. But for all Davies zest for tau, he pursued a broad understanding of the disease.

Publicly, Peter kept faith as a tauist and championed taus role in AD and related disorders, recalled Todd Golde of the University of Florida in Gainesville. In a more private setting though, Peter always had a quite encompassing view of the complexities of AD.

For him, tau was worthy of defense, but it was not a religion, noted Nixon. His ecumenicism as a scientist allowed him to embrace varied viewpoints on AD pathogenesis and to convey this broader understanding to junior scientists.

Davies was a skilled debater. He energetically questioned entrenched assumptions in the field (e.g., Mar 2006 webinar;Jul 2004 conference news).We had many friendly and interesting discussions about presenilin, wrote Bart De Strooper of KU Leuven in Belgium.Despite me being in the amyloid wing of thedebates in the field, he liked my work and his comments were, for mea young scientist at the timevery encouraging and helpful.

Daviess deep understanding of the disease made him a sought-after advisor, noted Benjamin Wolozin of Boston University. Indeed, chatting with Peter into the evening was always an immense pleasure because he always offered a challenging view of the pathophysiology of Alzheimers disease.

Throughout his career, Davies mentored budding researchers, many of whom are still working in the field. Peter was one of the first people Mike Hutton and I talked to about our JNPL3 tau model,and he did some of the first characterization of the mice, Jada Lewis of the University of Florida, Gainesville, wrote to Alzforum (Lewis et al. 2000). Peter believed in our model well before I did. At the time, I was brand-new to the field and had no clue what an honor it was to have Peter involved.I credit this initial collaboration and his subsequent generosity with his resources in helping buildmy career, wrote Lewis. He was a great scientist and mentor, but also a kind and generous human being, wrote Nikolaos Robakisof Mount Sinai Medical Center in New York.

Perhaps less well known to this audience is that Davies was actively interested in human suffering from schizophrenia. He published around 10 studies on psychosis, in tau transgenic mice, in human cohorts, and at the level of human synaptic neuropathology (Koppel et al,., 2018; Gabriel et al., 1997).

Davies received the inaugural Alzforum Mensch Award in 2002, a more light-hearted time during this websites early years, when Alzheimerologists used to get together during the Society for Neuroscience meeting for a sometimes raucous hour of comedy, karaoke, and dance shared over beers (Nov 2002 conference news).

More seriously, Davieshas been a dear, and always kind, friend of Alzforum from the get-go. Peter was a founding scientific advisor. During the sites early years, Peter penned conference dispatches for Alzforum (e.g., Sept 2002 conference news). Subsequently, he contributed 25 written commentaries plus countless in-person tips on where the field was headed. He left too soon, and will be missed.

Do you have special memories of Peter? How did he influence your work and career? Found a fun photo? To add to our collective tribute, email gstrobel@alzforum.org or type into the comment field below. Jessica Shugart and Gabrielle Strobel

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Peter Davies, Beloved Giant of Alzheimer's Disease Research, Dies at 72 - Alzforum

Ryan Blaney Family Foundation working to make an impact and raise awareness for brain health – WCNC.com

Posted: at 5:56 pm


The Blaney family was directly affected by Alzheimers disease after their family member Lou Blaney passed away from complications of the disease.

CHARLOTTE, N.C. For Ryan Blaney, his sister Erin and the rest of their family the passion for raising awareness for brain health comes from watching their own grandfather Lou Blaney battle Alzheimer's disease. Now the Blaney family hopes to use their platform and foundation to educate and assist others.

"It being 11 years ago now that he passed away, I think even then the people around him didn't have as much education about the disease and it wasn't as talked about back then. A huge part of why we want to raise so much awareness is to just normalize that it happens and just help people understand it," Erin Blaney said.

As the foundation works to educate and provide support for those affected by Alzheimers, including forming Team Blaney in this years Walk to End Alzheimers, which you can find more information on or joinhere, concussions are another topic that is close to the Blaney family and the sport of NASCAR.

"A few years back my dad got a really bad concussion through Sprint Car racing and was pretty messed up for a minute. Dale Jr. actually recommended that he go to this concussion center and it completely changed his life and since then he's recommended it to other drivers and other friends and tying it in with brain health, we knew that's something we also wanted to be correlated with."

While the Blaney family's bond is strong on the track, now it's focus is also helping other families worldwide with their foundation.

"I feel like it's continuing to grow because we're all so close and to see Ryan make an impact not only on the platform he has, but for the greater good has just been really inspiring and really inspires us to keep this foundation growing and becoming stronger."

The foundation just launched a T-shirt series with Flag & Anthem with 100% of the proceeds going back to the foundation to their Fund A Fellow program, which will fund an individuals schooling through UPMC's Sports Med concussion program. Additionally, it will then help the individual selected open their own clinic in Charlotte, NC.

For more on the Ryan Blaney Family Foundation follow them on Instagram or Twitter.

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Ryan Blaney Family Foundation working to make an impact and raise awareness for brain health - WCNC.com

Sleeping patterns of a person may help predict when will Alzheimer’s disease begin: Study – Devdiscourse

Posted: at 5:56 pm


By observing one's sleeping patterns, neuroscientists, to some extent can estimate a time frame for when Alzheimer's is most likely to strike in a person's lifetime, according to a recent study. Their findings suggest one defence against this virulent form of dementia - for which no treatment currently exists - is deep, restorative sleep, and plenty of it.

The research was led by UC Berkeley neuroscientists Matthew Walker and Joseph Winer that was published in the journal Current Biology. "We have found that the sleep you're having right now is almost like a crystal ball telling you when and how fast Alzheimer's pathology will develop in your brain," said Walker, a UC Berkeley professor of psychology and neuroscience and senior author of the paper."The silver lining here is that there's something we can do about it," he added. "The brainwashes itself during deep sleep, and so there may be a chance to turn back the clock by getting more sleep earlier in life."

Walker and fellow researchers matched the overnight sleep quality of 32 healthy older adults against the buildup in their brains of the toxic plaque known as beta-amyloid, a key player in the onset and progression of Alzheimer's, which destroys memory pathways and other brain functions and afflicts more than 40 million people worldwide. Their findings show that the study participants who started out experiencing more fragmented sleep and less non-rapid eye movement (non-REM) slow-wave sleep were most likely to show an increase in beta-amyloid over the course of the study.

Although all participants remained healthy throughout the study period, the trajectory of their beta-amyloid growth correlated with baseline sleep quality. The researchers were able to forecast the increase in beta-amyloid plaques, which are thought to mark the beginning of Alzheimer's. "Rather than waiting for someone to develop dementia many years down the road, we are able to assess how sleep quality predicts changes in beta-amyloid plaques across multiple timepoints. In doing so, we can measure how quickly this toxic protein accumulates in the brain over time, which can indicate the beginning of Alzheimer's disease," said Winer, the study's lead author and a PhD student in Walker's Center for Human Sleep Science at UC Berkeley.

In addition to predicting the time it is likely to take for the onset of Alzheimer's, the results reinforce the link between poor sleep and the disease, which is particularly critical in the face of a tsunami of ageing baby boomers on the horizon.While previous studies have found that sleep cleanses the brain of beta-amyloid deposits, these new findings identify deep non-REM slow-wave sleep as the target of intervention against cognitive decline.And though genetic testing can predict one's inherent susceptibility to Alzheimer's, and blood tests offer a diagnostic tool, neither offers the potential for a lifestyle therapeutic intervention that sleep does, the researchers point out."If deep, restorative sleep can slow down this disease, we should be making it a major priority," Winer said. "And if physicians know about this connection, they can ask their older patients about their sleep quality and suggest sleep as a prevention strategy." The 32 healthy participants in their 60s, 70s and 80s who are enrolled in the sleep study are part of the Berkeley Aging Cohort Study headed by UC Berkeley public health professor William Jagust, also a co-author on this latest study. The study of healthy ageing was launched in 2005 with a grant from the National Institutes of Health.

For the experiment, each participant spent an eight-hour night of sleep in Walker's lab while undergoing polysomnography, a battery of tests that record brain waves, heart rate, blood-oxygen levels and other physiological measures of sleep quality. Over the course of the multi-year study, the researchers periodically tracked the growth rate of the beta-amyloid protein in the participants' brains using positron emission tomography, or PET scans and compared the individuals' beta-amyloid levels to their sleep profiles.

Researchers focused on brain activity present during deep slow-wave sleep. They also assessed the study participants' sleep efficiency, which is defined as actual time spent asleep, as opposed to lying sleepless in bed. The results supported their hypothesis that sleep quality is a biomarker and predictor of the disease down the road.

"We know there's a connection between people's sleep quality and what's going on in the brain, in terms of Alzheimer's disease. But what hasn't been tested before is whether your sleep right now predicts what's going to happen to you years later," Winer said. "And that's the question we had."And they got their answer: "Measuring sleep effectively helps us travel into the future and estimate where your amyloid buildup will be," Walker said. As for next steps, Walker and Winer are looking at how they can take the study participants who are at high risk of contracting Alzheimer's and implement methods that might boost the quality of their sleep.

"Our hope is that if we intervene, then in three or four years the buildup is no longer where we thought it would be because we improved their sleep," Winer said."Indeed, if we can bend the arrow of Alzheimer's risk downward by improving sleep, it would be a significant and hopeful advance," Walker concluded. (ANI)

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Sleeping patterns of a person may help predict when will Alzheimer's disease begin: Study - Devdiscourse

Alzheimer’s Disease Therapeutics and Diagnostics Market to Witness Robust Expansion by 2026 with Top Key Players like Namenda, Aricept, Exelon,…

Posted: at 5:56 pm


Alzheimers Disease Therapeutics and Diagnostics Marketresearch is an intelligence report with meticulous efforts undertaken to study the right and valuable information. The data which has been looked upon is done considering both, the existing top players and the upcoming competitors. Business strategies of the key players and the new entering market industries are studied in detail. Well explained SWOT analysis, revenue share and contact information are shared in this report analysis.

Alzheimers Disease Therapeutics and Diagnostics Market is growing at a High CAGR during the forecast period 2020-2026. The increasing interest of the individuals in this industry is that the major reason for the expansion of this market.

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The report gathers the essential information including the new strategies for growth of the industry and the potential players of the global Alzheimers Disease Therapeutics and Diagnostics Market. It enlists the topmost industry player dominating the market along with their contribution to the global market. The report also demonstrates the data in the form of graphs, tables, and figures along with the contacts details and sales of key market players in the global Alzheimers Disease Therapeutics and Diagnostics Market.

Global Alzheimers Disease Therapeutics and Diagnostics Market Segmentation:

Market Segmentation by Type:

BiomarkersCholinesterase inhibitorsNMDA receptor antagonistsBrain imagingBlood tests

Market Segmentation by Application:

Drugs MarketDiagnostics Market

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Table of Contents

Global Alzheimers Disease Therapeutics and Diagnostics Market Research Report 2020

Chapter 1 Alzheimers Disease Therapeutics and Diagnostics Market Overview

Chapter 2 Global Economic Impact on Industry

Chapter 3 Global Market Competition by Manufacturers

Chapter 4 Global Production, Revenue (Value) by Region

Chapter 5 Global Supply (Production), Consumption, Export, Import by Regions

Chapter 6 Global Production, Revenue (Value), Price Trend by Type

Chapter 7 Global Market Analysis by Application

Chapter 8 Manufacturing Cost Analysis

Chapter 9 Industrial Chain, Sourcing Strategy and Downstream Buyers

Chapter 10 Marketing Strategy Analysis, Distributors/Traders

Chapter 11 Market Effect Factors Analysis

Chapter 12 Global Alzheimers Disease Therapeutics and Diagnostics Market Forecast

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Alzheimer's Disease Therapeutics and Diagnostics Market to Witness Robust Expansion by 2026 with Top Key Players like Namenda, Aricept, Exelon,...

Peter Davies, Beloved Giant of Alzheimer’s Disease Research, 72 – Alzforum

Posted: September 5, 2020 at 11:52 pm


04 Sep 2020

When Peter Davies passed away on August 26, the Alzheimers research community lost a brilliant mind, and a truly generous human being. Davies died at age 72, after a long battle with cancer.

His discoveries paved the way for the first Alzheimers drugs and uncovered the startling complexity of the tau protein and its role in Alzheimers and other tauopathies. In their tributes on Alzforum, fellow scientists particularly recalled Davies generous sharing of antibody reagents and spirited conversations with him about the pathophysiology of AD, as much as they saluted his scientific achievements.

Peter Davies

Peter was clearly one of the greatest investigators in the pantheon of Alzheimers researchers. I knew him as a dear friend and valued mentor since the 80s. I always valued his great balance of scientific objectivity and empathy, especially for young investigators, Rudy Tanzi of Massachusetts General Hospital wrote to Alzforum.

Davies grew up in Wales, and studied biochemistry at the University of Leeds in northern England. After completing postdoctoral work at the University of Edinburgh, he joined the staff of the Medical Research Council Brain Metabolism Unit there in 1974. It was in Edinburgh that Davies began to explore Alzheimers disease.

Published on Christmas Day in 1976, his first AD paper turned out to be a gift to the field. He reported that the cholinergic system took a severe hit in the disease, a discovery that led to the development of acetylcholinesterase inhibitors, the first FDA-approved treatments for the disease (Davies and Maloney, 1976; Alzforum timeline).

His move, in 1977, to Albert Einstein College of Medicine in the Bronx, New York, brought him under the tutelage of the two great (and late) Bobs of early Alzheimers research in the U.S.Katzmanand Terry. Terry had recruited the young hotshot from England. In 2006, Davies became the scientific director of the Litwin-Zucker Center for Research on Alzheimers disease at theFeinstein Institute for Medical Research,North Shore-LIJ Health System, Long Island.

Peter Davies, Robert D. Terry, and Robert Katzman. Image credit: Peter Davies

Davies is perhaps best known for his work on the myriad forms of tau. He helped lay bare the devilish complexity of this microtubule-binding, tangle-forming protein. Starting with the development of Alz50, the first antibody to latch onto misfolded tau, Davies group went on to develop many more such antibodiesincluding MC-1and PHF-1trained against different forms the protein (Wolozin et al., 1986; Greenberg and Davies, 1990;Jicha et al., 1999).

Davies readily shared these reagents with other researchers. If you ever wanted to obtain and utilize any of the very useful antibodies that his laboratory created and you sent him an email, a few days later the antibody would just appear in your lab, recalled David Holtzman of Washington University in St. Louis. Throughout the field, Davies antibodies proved essential to pivotal discoveries about tau pathobiology (for detail, see Michel Goedert and Maria Grazia Spillantinis tribute below). The neuroscience community, and I especially, will be forever grateful for Peters generosity in sharing his wonderful library of antibodies and his boundless excitement for scientific discovery, wrote Ralph Nixon of New York University.

Over more than three decades, Davies published some 250 papers on tau, from its phosphorylation to truncation (Jicha et al., 1999;Weaver et al., 2000; Espinoza et al., 2008; dAbramo et al., 2013).

He kept an eye toward targeting toxic forms of the protein with therapeutics, and Zagotenemab,a derivative of his MC-1 antibody developed by Lilly, is currently finishing a Phase 2 trial in 285 people with early AD.

Davies also generated mouse models, including the hTau mice expressing all six isoforms of human tau (Duff et al., 2000; Nov 2001 news;May 2011 conference news).

Davies received numerous awards for his scientific achievements, including two MERIT awards from the National Institutes of Health, a Lifetime Achievement Award from the International Congress on Alzheimers Disease (ICAD), and the Potamkin Prize for Research in Picks, Alzheimers, and Related Diseases (Apr 2015 news).

For some years, Davies emphasis on the role of tau pathology in AD put him at odds with those who centered their research on amyloid. He was a witty voice for the tauist side during the fields sometimes truculent, and long past, period of division into baptist-versus-tauist camps. But for all Davies zest for tau, he pursued a broad understanding of the disease.

Publicly, Peter kept faith as a tauist and championed taus role in AD and related disorders, recalled Todd Golde of the University of Florida in Gainesville. In a more private setting though, Peter always had a quite encompassing view of the complexities of AD.

For him, tau was worthy of defense, but it was not a religion, noted Nixon. His ecumenicism as a scientist allowed him to embrace varied viewpoints on AD pathogenesis and to convey this broader understanding to junior scientists.

Davies was a skilled debater. He energetically questioned entrenched assumptions in the field (e.g., Mar 2006 webinar;Jul 2004 conference news).We had many friendly and interesting discussions about presenilin, wrote Bart De Strooper of KU Leuven in Belgium.Despite me being in the amyloid wing of thedebates in the field, he liked my work and his comments were, for mea young scientist at the timevery encouraging and helpful.

Daviess deep understanding of the disease made him a sought-after advisor, noted Benjamin Wolozin of Boston University. Indeed, chatting with Peter into the evening was always an immense pleasure because he always offered a challenging view of the pathophysiology of Alzheimers disease.

Throughout his career, Davies mentored budding researchers, many of whom are still working in the field. Peter was one of the first people Mike Hutton and I talked to about our JNPL3 tau model,and he did some of the first characterization of the mice, Jada Lewis of the University of Florida, Gainesville, wrote to Alzforum (Lewis et al. 2000). Peter believed in our model well before I did. At the time, I was brand-new to the field and had no clue what an honor it was to have Peter involved.I credit this initial collaboration and his subsequent generosity with his resources in helping buildmy career, wrote Lewis. He was a great scientist and mentor, but also a kind and generous human being, wrote Nikolaos Robakisof Mount Sinai Medical Center in New York.

Perhaps less well known to this audience is that Davies was actively interested in human suffering from schizophrenia. He published around 10 studies on psychosis, in tau transgenic mice, in human cohorts, and at the level of human synaptic neuropathology (Koppel et al,., 2018; Gabriel et al., 1997).

Davies received the inaugural Alzforum Mensch Award in 2002, a more light-hearted time during this websites early years, when Alzheimerologists used to get together during the Society for Neuroscience meeting for a sometimes raucous hour of comedy, karaoke, and dance shared over beers (Nov 2002 conference news).

More seriously, Davieshas been a dear, and always kind, friend of Alzforum from the get-go. Peter was a founding scientific advisor. During the sites early years, Peter penned conference dispatches for Alzforum (e.g., Sept 2002 conference news). Subsequently, he contributed 25 written commentaries plus countless in-person tips on where the field was headed. He left too soon, and will be missed.

Do you have special memories of Peter? How did he influence your work and career? Found a fun photo? To add to our collective tribute, email gstrobel@alzforum.org or type into the comment field below. Jessica Shugart and Gabrielle Strobel

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Peter Davies, Beloved Giant of Alzheimer's Disease Research, 72 - Alzforum

UAB study targets gene associated with Alzheimer’s disease – The Mix

Posted: at 11:52 pm


The UAB team identified how the poorly understood BIN1 gene might be player in Alzheimers disease.

The neurons in this image are stained blue, indicating the presence of the BIN1 protein. Points of direct interaction between BIN1 and calcium channels are in purple.Researchers at the University of Alabama at Birmingham are on the track of a gene that might play a role in the development of Alzheimers disease. The research team is studying a gene called BIN1, which was first linked to Alzheimers disease in 2009.

In a paper recently published online in eLife, the team shows that BIN1 helps to regulate the activity of neurons. This may be significant, as too much neuronal activity, known as hyperexcitability, is associated with Alzheimers disease. BIN1 becomes the first gene to be linked to hyperexcitability as a driver of Alzheimers disease.

BIN1 was identified as a risk factor for Alzheimers following large scale studies called genome wide association studies, which looked at the genomes of thousands of people with and without Alzheimers disease.

These genetic studies showed that variants of BIN1 were present in many of the study participants who had Alzheimers, said Erik Roberson, M.D., Ph.D., the Rebecca Gale Professor in the Department of Neurology, School of Medicine, and lead author of the study. The problem was that nobody had a clear idea what BIN1 does in the brain.

Using different ways of increasing BIN1 and measuring neuronal activity, members of Robersons lab found that neurons with higher BIN1 levels fired more often and were more prone to hyperexcitability.

We think thats important because hyperexcitability is now recognized as a feature of early Alzheimers, said Roberson, who is director of the UAB Alzheimers Disease Center and the Center for Neurodegeneration and Experimental Therapeutics. The neurons fire too often, which appears to lead to damage.

Prior studies had linked BIN1 to the Tau protein, which has long been associated with Alzheimers as one of the hallmarks of the disease.

Importantly, we found a key role for Tau in the hyperexcitability caused by BIN1, said Yuliya Voskobiynyk, a senior graduate student in Robersons lab who led the work. Reducing Tau made neurons resistant to the effects on BIN1 on neuronal hyperexcitability. Along with BIN1 and Tau, a third factor is involved: channels that allow calcium into the neuron, which are important for neuronal firing. We found that calcium channels form a complex along with BIN1 and Tau, and reducing Tau not only blocked neuronal hyperexcitability, but also reduced the formation of this complex.

Erik Roberson, M.D., Ph.D.Roberson is quick to point out that this research, conducted in animal models and cell cultures, is very preliminary. Tau is a major research focus for investigators worldwide; but the role of BIN1, and its interactions with Tau and calcium channels, is only starting to be explored.

It seems clear that something about this gene has a role to play in Alzheimers, Roberson said. At this point, we dont know if that role is driven by too much BIN1 protein, too little, or by more subtle changes in the type of BIN1 being made in people with Alzheimers disease.

Roberson says next steps will include digging deeper into the genes normal function within the brain, and then working to understand what happens in Alzheimers disease. His lab was already working to develop drugs that would block the binding between Tau and proteins like BIN1 as potential therapies.

This study helps to establish that there is a connection between Tau, BIN1 and calcium channels, Roberson said. But we need to learn more. We need to understand how they bind and how binding affects their function. If we can zero in on the molecular details of these interactions, we may be able to find new targets for intervention.

The research was supported by the National Institutes of Health grants RF1AG059405, R01NS075487, R01MH114990, T32NS095775 and T32NS061788; the

Alzheimers Association; and the Weston Brain Institute.

Co-authors are Jonathan R. Roth, J. Nicholas Cochran, Travis Rush, Jacob S. Mesina, Mohammad Waqas and Rachael Vollmer, of the UAB Center for Neurodegeneration and Experimental Therapeutics, Alzheimers Disease Center and Evelyn McKnight Brain Institute; Nancy V.N. Carullo and Jeremy Day, Ph.D., UAB Department of Neurobiology; and Lori McMahon, Ph.D., UAB Department of Cell, Developmental and Integrative Biology.

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UAB study targets gene associated with Alzheimer's disease - The Mix

ALZHEIMER’S ASSOCIATION INVITES WESTERN WI RESIDENTS TO JOIN 2020 WALK TO END ALZHEIMER’S ON SEPTEMBER 19 – The Baldwin Bulletin

Posted: at 11:52 pm


Participants Will Continue to Walk as Individuals, Families or Small Teams on Sidewalks, Tracks and Trails across Western WI in Wake of COVID-19

The Alzheimers Association is inviting Western WI residents to join the fight to end Alzheimers by participating in the Alzheimers Association Walk to End Alzheimers on Saturday, September 19.

The Walk to End Alzheimers continues, but instead of hosting a large gathering, the Alzheimers Association is encouraging participants to walk as individuals or in small groups on sidewalks, tracks and trails across Western WI. The Walk is chaired by Cassie Cook, Life Enrichment and Volunteer Director, Presbyterian Homes - Woodland Hill.

This years Walk to End Alzheimers will be everywhere, said Wendy Vizek, vice president, constituent events at the Alzheimers Association. The pandemic is changing how we walk, but it doesnt change the need to walk. This year, more than ever, we need to come together to support all those affected by Alzheimers and other dementia. With the dollars raised, the Alzheimers Association can continue to provide care and support to families during these difficult times while also advancing critical research toward methods of treatment and prevention.

Time-honored components of the Walk to End Alzheimers are being replicated. On Walk day, an online Opening Ceremony beginning at 9:00 a.m., will feature local speakers and a presentation of Promise Flowers to honor the personal reasons participants join together to fight Alzheimers and all other dementia, all delivered to participants' smartphones, tablets and computers. A small group of Alzheimers Association staff and volunteers will create the iconic Promise Garden in a view only format on Walk day at the St. Croix County Services Center, 1752 Dorset Lane in New Richmond to honor all those impacted by Alzheimers. The garden will be on display from 9:00 a.m. to 1:00 p.m.

To enhance the participant experience leading up to the event and on Walk day, new features are being added to the Walk to End Alzheimers mobile app to create an opportunity for the community to connect. Participants can use the app and new Walk Mainstage'' to track their steps and distance, follow a virtual Walk path, manage their Facebook fundraisers, and access information and resources from the Association and Walk sponsors to help individuals and families affected by the disease. A new audio track is available to encourage participants along the way and to congratulate them upon completion of their Walk.

Alzheimers is not taking a hiatus during COVID-19 and neither are we, said David Grams, Executive Director, Alzheimers Association Wisconsin Chapter. We must continue Walk to End Alzheimers, and we are working with all participants to ensure they have a powerful and moving experience that is felt when we are together. Many of our constituents are at higher risk when it comes to COVID-19 and we know that our volunteers and participants appreciate our commitment to keeping all involved healthy and safe.

More than 5 million Americans are living with Alzheimer's disease the sixth-leading cause of death in the United States. Additionally, more than 16 million family members and friends provide care to people living with Alzheimers and other dementias. In Wisconsin alone, there are more than 120,000 people living with the disease and 195,000 caregivers.

Participants can register, support another walker and get information online at http://www.alz.org/walk. For questions or assistance, please call 800-272-3900.

The Alzheimers Association Wisconsin Chapter thanks the numerous volunteers and sponsors of the Walk to End Alzheimers, including National Presenting Sponsors - Edward Jones and CVS Health and local sponsors including, the ADRC of Pierce County, the ADRC of St. Croix County, and Holiday Vacations.

Alzheimer's Association Walk to End Alzheimers

The Alzheimers Association Walk to End Alzheimers is the worlds largest event to raise awareness and funds for Alzheimers care, support and research. Since 1989, the Alzheimers Association mobilized millions of Americans in the Alzheimers Association Memory Walk; now the Alzheimers Association is continuing to lead the way with Walk to End Alzheimers. Together, we can end Alzheimers.

Alzheimer's Association

The Alzheimers Association is a worldwide voluntary health organization dedicated to Alzheimers care, support and research. Its mission is to lead the way to end Alzheimer's and all other dementia by accelerating global research, driving risk reduction and early detection, and maximizing quality care and support. Visit alz.org or call 800.272.3900.

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ALZHEIMER'S ASSOCIATION INVITES WESTERN WI RESIDENTS TO JOIN 2020 WALK TO END ALZHEIMER'S ON SEPTEMBER 19 - The Baldwin Bulletin

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