CUIMC Newsroom

Evolution is usually equated with advancement, but the most useful biological innovations aren’t always found in the “highest” organisms.

Zebrafish, for example, can continually generate new neurons in their brains, which protects these vertebrates from the ravages of neurological disease and injury. Adult humans, on the other hand, can only make a meager number of new neurons, mostly in the hippocampus (the brain’s memory center), and diseases like Alzheimer’s suppress this production even further.

Fortunately, zebrafish are giving up their secrets.

Columbia University researchers have discovered a mechanism that promotes neurogenesis in the zebrafish brain and has the potential to be activated in people.

“It’s possible that by activating neurogenesis in people with Alzheimer’s disease, we could slow the disease’s progression,” says study leader Caghan Kizil, PhD, associate professor of neurological sciences (in neurology and in the Taub Institute). [read more]

WYPL Memphis Public Library Radio

Dr. Carol Troy, professor of pathology and cell biology and neurology (in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain) at Columbia University, discusses how experimental eye drops in mice have been more effective in treating retinal vein occlusion than using eye injections. [podcast] Editor's Note: Dr. Troy's segment of the 8/13/2023 Podcast begins at 4:50.

NewYork-Presbyterian Health Matters

Lecanemab, a therapy that targets amyloid proteins thought to cause Alzheimer’s disease, has been granted full approval by the Food and Drug Administration (FDA), a decision that will result in greater access to the treatment.

“Lecanemab, marketed as Leqembi, is the first drug for Alzheimer’s disease to receive approval on the basis of clinically slowing the progression of Alzheimer’s disease,” says Dr. Lawrence S. Honig, a neurologist at NewYork-Presbyterian/Columbia University Irving Medical Center. “Full approval is a major step forward.”

The Centers for Medicare & Medicaid Services (CMS) has indicated that the medication will be covered after this latest approval as long as the prescribing physician and clinical team provide information about patients in a privacy-protected registry, “a database designed to collect information about how the drug works in the real world,” adds Dr. Honig. [read more]

CNN

Dr. Lawrence S. Honig is a neurologist at NewYork-Presbyterian/Columbia University Irving Medical Center. He is a professor of neurology at the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, and the Gertrude H. Sergievsky Center, where he directs the New York State funded Center of Excellence for Alzheimer’s Disease.  Honig was an investigator for the study that led to the FDA’s approval of Leqembi and has been an investigator for, received research funding from, and consulted for Eisai, the pharmaceutical company developing lecanemab, and other pharmaceutical companies. The opinions expressed in this commentary are his own. 

In early July, the US Food and Drug Administration granted traditional full approval of Leqembi (lecanemab-irmb) for the treatment of Alzheimer’s disease (AD). This is the first approved medication proven to slow the progression of AD’s clinical symptoms. A phase three trial among 50- to 90-year-old patients with early AD showed that it can do so by about 27% over an 18-month period. While we cannot extrapolate beyond 18 months, this represents about a six-month delay in progression of AD symptoms.

The drug functions by removing the amyloid beta protein that accumulates in the form of plaques in the brains of people with AD. A second disease-slowing drug, donanemab, has recently shown similar effects and may get FDA approval by the end of the year.

The development of Leqembi, building on two decades of research, is a notable success for medical science in that a disease previously impervious to any disease-modifying medical intervention now has an available, effective treatment. However, paraphrasing Winston Churchill, this is not the beginning of the end but the end of the beginning. The drug does not reverse disease symptoms or prevent progression, it slows progression. And there are considerations that make it inappropriate for many patients with AD.

It does, however, lay the groundwork for future AD medications that could alleviate suffering from this devastating disease for generations to come. [read more]

Donanemab, Second Alzheimer’s Drug to Slow Disease’s Progression May Be Approved in the U.S. This Year

CNN Online

“Donanemab was very effective at eliminating its target, cerebral amyloid, but the clinical effect was comparatively weak,” Jennifer Manly, of Columbia University Irving Medical Center, and Kacie Deters, of the University of California, Los Angeles, wrote in one editorial.

Dr. Lawrence Honig, a professor of neurology at Columbia University Irving Medical Center who had not yet seen the full donanemab results, argued that it’s scientifically and medically “unrealistic to think that the Alzheimer process will be stopped by six to 18 months of antibody treatment.” “Alzheimer’s is a chronic disease involving slow, gradual accumulation of amyloid beta forms in the brain,” he wrote to CNN in an email. “It is not likely that removing plaques over some months will prevent the disease process from progressing.” [read more]

This story was also covered by: HealthDay

Eli Lilly Expects FDA Approval of its Alzheimer’s Drug This Year

The Hill

“Given the wide availability of these drugs following US Food and Drug Administration approval and the disproportionate burden of cognitive impairment and dementia due to Alzheimer disease in many of these groups, it is critical that clinicians, patients, and families understand the limits of what is known,” Jennifer Manly, of Columbia University Irving Medical Center, and Kacie Deters, of the University of California, Los Angeles, wrote in the editorial. [read more]

Second Alzheimer’s Drug in Pipeline Can Slow the Disease by a Few Months but With Safety Risk

Associated Press

Another concern: More than 90% of the study’s participants were white, leaving little data about how other populations might respond, Alzheimer’s specialist Jennifer Manly of Columbia University wrote in JAMA. [read more]

CUIMC Newsroom

A new study suggests that eye drops developed by Columbia University researchers could be a more effective–and comfortable–therapy for a common eye disease currently treated with injections into the eye.

Retinal vein occlusion (RVO), an eye disease that affects up to 2% of people over age 40, occurs when a vein in the eye’s retina becomes blocked, leading to swelling in the eye, inflammation, damage to the retina, and vision loss.

Standard therapy involves injecting into the eye a vascular endothelial growth factor inhibitor (anti-VEGF) that reduces swelling. The therapy can improve vision but patients with significant retinal damage due to impaired blood flow often have poor outcomes.

“Anti-VEGF therapy has helped a lot of people with RVO, but the fear factor—having to get a needle in the eye—causes many people to delay treatment, which can lead to retinal damage,” says Carol M. Troy, MD, PhD, professor of pathology & cell biology and of neurology at Columbia University Vagelos College of Physicians and Surgeons. “There’s an opportunity to help more people with this disease that is a leading cause of blindness worldwide.” [read more]

Dr. Lawrence Honig spoke with CNN Health and Gray Television Washington News Bureau following the FDA’s announcement that lecanemab (sold by Eisai as "Leqembi"), the first drug proven to slow the progression of Alzheimer’s disease (AD) in early stage patients, would be shifted to their traditional approval process. According to Dr. Honig, while many patient considerations remain, this “important advance” marks the beginning of a “new treatment era” for patients with AD.

Fortune

“The improvement among study participants with low-flavanol diets was substantial and raises the possibility of using flavanol-rich diets or supplements to improve cognitive function in older adults,” Adam M. Brickman, PhD, professor of neuropsychology at Columbia University Vagelos College of Physicians and Surgeons and co-leader of the study, said in a press release about the study.

“Age-related memory decline is thought to occur sooner or later in nearly everyone, though there is a great amount of variability,” said the study’s senior author, Dr. Scott A. Small, the Boris and Rose Katz Professor of Neurology at Columbia University Vagelos College of Physicians and Surgeons, in the press release. [read more]

CNN Online

At the end of the first year, people in the study who took the daily 500-milligram pill and who had tested in the bottom tier of flavanols “normalized” their levels of flavanols, said study co-author Dr. Scott Small, professor of neurology and director of the Alzheimer’s Disease Research Center at Columbia University in New York City. In those people, the flavanols also “restored” their age-related mental decline to levels similar to people who “had high flavanols at baseline,” he said. [read more]

Also covered by: CBS News Baltimore (video), UPI, The Guardian, New York Post, The Times (UK), and Independent (UK).

CUIMC Newsroom

Taking a daily multivitamin supplement can slow age-related memory decline, finds a large study led by researchers at Columbia University and Brigham and Women’s Hospital/Harvard.

“Cognitive aging is a top health concern for older adults, and this study suggests that there may be a simple, inexpensive way to help older adults slow down memory decline,” says study leader Adam M. Brickman, PhD, professor of neuropsychology at Columbia University Vagelos College of Physicians and Surgeons.

Many older people take vitamins or dietary supplements under the assumption that they will help maintain general health. But studies that have tested whether they improve memory and brain function have been mixed, and very few large-scale, randomized trials have been done. [read more]

Associated Press

Millions of American adults take daily multivitamins, even though the pills have not been shown to prevent ailments like heart disease or cancer and experts say it’s better to get nutrients from food.

The latest research looks at whether taking a daily vitamin can have an effect on memory. The study found multivitamins may boost memory function in some people, by the equivalent of three years of normal, age-related memory loss.

While the study isn’t comprehensive enough to warrant broad recommendations to take vitamins, it provides important information about their use, said Adam Brickman, the Columbia University professor of neuropsychology who led the study. “Well-designed research studies are showing that there might indeed be some benefits ” to taking multivitamins, he said. [read more]

Editor's Note: This story was also covered by The Washington Post, Good Morning America, CNN Online, Fortune, New York Post, Independent, and NBC News.

Columbia University Irving Medical Center

Have you thought about your memory lately?

According to the CDC, 11% of people over age 45 have subjective cognitive decline, a form of cognitive impairment that can be one of the earliest noticeable symptoms of Alzheimer's disease and related dementias. That’s 1 in 9. And while all these people are aware of the decline, few discuss it with health care providers.

Subjective cognitive decline is exactly what it sounds like. It's subjective, meaning a person notices a worsening of thinking abilities and memory, but the decline cannot be verified by standard tests.

“Neurocognitive decline is a growing public health issue, and neurologists in this area of memory care are concerned,” says Columbia gynecologist Mary Rosser, MD, PhD, who is working with Stephanie Cosentino, PhD, a Columbia neuropsychologist, to develop screening tools to detect subjective cognitive decline and more advanced forms of memory loss, including dementia, among her older patients. [read more]

Columbia University Irving Medical Center

A study of more than 2,200 adults who attended U.S. high schools in the early 1960s found that those who attended higher-quality schools had better cognitive function 60 years later.  

Previous studies have found that the number of years spent in school correlates with cognition later in life, but few studies have examined the impact of educational quality. 

“Our study establishes a link between high-quality education and better late-life cognition and suggests that increased investment in schools, especially those that serve Black children, could be a powerful strategy to improve cognitive health among older adults in the United States,” says Jennifer Manly, PhD, professor of neuropsychology at Columbia University Vagelos College of Physicians and Surgeons and senior author of the study. [read more]

The New York Times

Speaking two languages provides the enviable ability to make friends in unusual places. A new study suggests that bilingualism may also come with another benefit: improved memory in later life.

Studying hundreds of older patients, researchers in Germany found that those who reported using two languages daily from a young age scored higher on tests of learning, memory, language and self-control than patients who spoke only one language.

The findings, published in the April issue of the journal Neurobiology of Aging, add to two decades of work suggesting that bilingualism protects against dementia and cognitive decline in older people.

“It’s promising that they report that early and middle-life bilingualism has a beneficial effect on cognitive health in later life,” said Miguel Arce Rentería, a neuropsychologist at Columbia University who was not involved in the study. “This would line up with the existing literature.” [read more]

CUIMC Newsroom

Columbia University neurologists are investigating a set of blood tests that, used in combination with memory tests, may help physicians correctly diagnose Alzheimer disease in low-resource environments, where 58% of people worldwide living with dementia reside.

In a new study, Columbia researchers in collaboration with local physicians recruited 746 older adults (average age of 71 years) from the Dominican Republic and the Dominican community of northern Manhattan.

“Alzheimer’s disease is one form of dementia and as more treatments emerge, developing an accurate blood test will be essential in finding people who will benefit from treatment, particularly those who lack access to more advanced diagnostic tools,” says Richard Mayeux, MD, chair of the Department of Neurology at Columbia University Vagelos College of Physicians and Surgeons and one of the study’s senior authors. [read more]

CUIMC Newsroom

An analysis of human brain cells provides new evidence in support of the “amyloid hypothesis,” the prevailing idea that Alzheimer's is caused by the accumulation of beta-amyloid proteins in the brain.

In the study(link is external and opens in a new window), Columbia University researchers found that amyloid sparks an alliance between two proteins in the brain’s neurons and this pairing is linked to about half of the gene changes that are known to occur in the disease, triggering the rapid accumulation of tau proteins, a primary driver of neurodegeneration in the disease.

“This protein pair seems very central to the disease, and because it does not appear to have another function in the brain, it is a good target for a new therapy,” says the study’s senior author, Ulrich Hengst, PhD, associate professor of pathology and cell biology (in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain) at the Columbia University Vagelos College of Physicians and Surgeons. [read more]

Health Matters

Taub faculty member Dr. James Noble spoke with NewYork-Presbyterian Health Matters about "What to Know About Frontotemporal Dementia," the most common form of dementia for people under the age of 60. As Dr. Noble explains, "Among the causes of dementia, FTD is unique in that about one-third of all people with FTD will have a family history, which is suggestive of a genetic link. Several genes have been implicated in FTD, and genetic testing is more often discussed and considered in FTD than in other dementias." [read more]

MedPage Today

Of all the possible contributors, intense physical activity was the likely disease-modifying factor, Davangere Devanand, MD, of Columbia University Irving Medical Center in New York City, and co-authors wrote in Alzheimer's & Dementia. [read more]

Pictured: Chris Haynes and Janine Schiavi

The sixth annual Laugh to Remember event, led by Chris Haynes and Janine Schiavi of Broadacre Financial, was held June 8 at Gotham Comedy Club to benefit Columbia’s Taub Institute for Research on Alzheimer’s Disease and the Aging Brain. The event raised $250,000 to support medical research for neurodegenerative disorders, such as Alzheimer’s, Parkinson’s, ALS, and frontotemporal dementia.

Navigating Life with Dementia, written by Dr. James M. Noble, an associate professor of neurology and dementia specialist in the Division of Aging and Dementia, is the latest title in the American Academy of Neurology's Brain & Life® Book series, published with Oxford University Press. In an engaging interview now featured on the Brain & Life website, Dr. Noble explains that he wrote the book “to create something that patients and their families could read at their own pace for additional information and resources, other patients' experiences, and some sense of the road ahead."

A team of investigators from the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at NewYork-Presbyterian/Columbia University Irving Medical Center (NYP/CUIMC) have joined a major international initiative, directed by the John P. Hussman Institute for Human Genomics (HIHG) at the University of Miami Miller School of Medicine, to build a resource that will expand Alzheimer’s disease genetic studies in the underrepresented African ancestry populations and Hispanic/Latinx groups. This five-year, multisite initiative also includes investigator teams from Case Western Reserve University, Wake Forest University, the University of Pennsylvania, and the University of Ibadan as the lead institution for the African Dementia Consortium (AfDC). [read more]

CUIMC Newsroom

For more than 20 years, scientists have known that people with hypertension, diabetes, high cholesterol, or obesity have a higher likelihood of developing Alzheimer’s disease.

The conditions can all affect the brain, damaging blood vessels and leading to strokes. But the connection between vascular disease in the brain and Alzheimer’s has remained unexplained despite the intense efforts of researchers.

Now, a study led by researchers at Columbia University's Vagelos College of Physicians and Surgeons has uncovered a possible mechanism. The study found a gene called FMNL2 links cerebrovascular disease and Alzheimer’s and suggests changes in FMNL2 activity caused by cerebrovascular disease prevent the efficient clearance of toxic proteins from the brain, eventually leading to Alzheimer’s disease.

The finding could lead to a way to prevent Alzheimer’s in people with hypertension, diabetes, obesity, or heart disease.

“Not only do we have a gene, but we have a potential mechanism,” says senior author Richard Mayeux, MD, chair of neurology at Columbia and NewYork-Presbyterian/Columbia University Irving Medical Center. “People have been trying to figure this out for a couple of decades, and I think we have our foot in the door now. We feel there must be other genes involved and that we've just scratched the surface.”

Mayeux and his colleagues found FMNL2 in a genome-wide hunt designed to uncover genes associated with both vascular risk factors and Alzheimer’s disease. The search involved five groups of patients representing different ethnic groups. [read more]

The Wall Street Journal

The amyloid hypothesis, posited in the 1990s, proposes that amyloid-plaque formation leads to a cascade of negative effects including the accumulation of tau, inflammation, cell death and the loss of synapses, the junctions through which nerve cells known as neurons communicate with each other. “It was so compelling that it triggered the pharmaceutical industry to act,” said Scott Small, director of the Alzheimer’s Disease Research Center at Columbia University. [read more]
Editor's Note: Accessing this article requires a WSJ subscription.

NEW YORK – When Alzheimer's disease first attacks the brain, it doesn't strike randomly. The damage tends to begin in the entorhinal cortex, a tiny hub especially connected to other parts of the brain. Why this area would be particularly vulnerable is a puzzle that scientists have been trying to work out for decades.

Researchers at Columbia University may finally have a solution, one that backs a new approach to developing treatments for this devastating neurodegenerative disease. Seven years of step-by-step sleuthing has implicated retromers: microscopic mail carriers that help package, ship and recycle molecules inside of cells. The scientists report their findings December 28 in Cell Reports.

“Efforts to treat Alzheimer’s disease have focused on what Dr. Alois Alzheimer observed more than a hundred years ago, but we have come a long way since then. Retromers offer a new direction and a new hope,” said Scott Small, MD, director of the Alzheimer’s Disease Research Center at Columbia University, the Boris and Rose Katz Professor of Neurology at Columbia University’s Taub Institute and Vagelos College of Physicians and Surgeons, and an affiliate member of Columbia’s Zuckerman Institute. 

Starting with the Fundamentals

Sabrina Simoes, PhD, wasn't thinking about Alzheimer's when she first began exploring retromers as an associate research scientist in Dr. Small's lab. She had been reading about how, in organisms ranging from yeast to humans, every cell contains the retromer VSP26a. But only neurons, a type of brain cell, possess a different paralog of this retromer, VSP26b. As a scientist fascinated by the fundamental biology of cells, she found her curiosity piqued.

“I thought, 'This can't be a fluke, there must be some reason neurons need this second version of this retromer,'” said Dr. Simoes, who is now an Assistant Professor of Neurology at Columbia University’s Vagelos College of Physicians and Surgeons and Taub Institute. “So I took a closer look.”

Dr. Simoes grew and stimulated neurons in a dish. Under a microscope, she saw that the 26b paralog tended to hang out in cellular compartments used to recycle molecules inside brain cells: that is, to move molecules to and from the surfaces of neurons to regulate the cells’ electrical activity. The researcher wondered what role 26b plays in different brain regions. So she started working with mice from the University of Science & Technology in Korea that had been genetically modified to disable the Vps26b gene. And she teamed up with Jia Guo, PhD, an expert in the brain scanning technology functional magnetic resonance imaging at Columbia’s Zuckerman Institute.

A Surprising Scan

Dr. Guo used fMRI machines specially made for small animals to noninvasively scan the brains of the modified lab mice. He noticed something peculiar: a lack of activity in one small, sharply defined area in their brains, as compared to the brains of normal mice.

“I have never seen an fMRI imaging result in humans or other animals that was so striking, such a focused spot,” said Dr. Guo, an assistant professor in Columbia's Department of Psychiatry. “Normally, the differences in brain activity we see are fuzzy and diffuse.”

That spot coincided with a sliver of the entorhinal cortex brain region. When the researchers then directly measured the electrical activity of neurons in that area using electrodes, they found deficits, confirming the fMRI results. The mice also had trouble completing memory-related tasks known to involve the entorhinal cortex. Reintroducing working copies of Vps26b into the mice completely fixed these problems.

With all signs pointing to a link between the retromer and the entorhinal cortex, Simoes' fundamental cell biology work had been connected with Alzheimer's disease. That’s because neurological diseases have different hallmarks. Parkinson's starts in the substantia nigra, a brain region important for controlling the body. Huntington's first affects the striatum, related to rewards. And Alzheimer's, as has been known for decades, tends to set its sights on the entorhinal cortex.

“The evidence built up that this retromer variant, linked to cellular recycling, was crucial for proper brain function in the entorhinal cortex,” said Dr. Simoes. “This brain region's role in Alzheimer's led us to investigate whether the paralog could be related to the disease.”

Introducing SORL1

While the researchers were hard on the retromer's trail, another clue emerged. In 2007, a team that included Columbia’s Richard Mayeux, MD, MSc, chair of neurology at Columbia University Vagelos College of Physicians and Surgeons, had found a new gene connected to Alzheimer's. Mutations in this SORL1 gene were associated with late-onset Alzheimer's, which afflicts people over the age of 65, and SORL1 has emerged as one of the most damaging genes in the disease. Dr. Small and colleagues first found that the SORL1 protein is part of the same molecular shipping system associated with retromers.

Hoping to further connect this gene to their retromer variant, Dr. Small and his team checked their mice and found a deficiency of SORL1 in the entorhinal cortex. The scientists also examined brains donated by people diagnosed with Alzheimer’s and found a striking pattern: Tissues in the entorhinal cortex were depleted in both SORL1 and Vps26b.

Putting all these pieces together suggests that Alzheimer’s might begin with problems with a neuron’s ability to move molecules around. Scientists know the entorhinal cortex, a hub in the brain, forms an unusually large number of connections with other parts of the brain. These connections and the activity they generate could stimulate a lot of molecular recycling, making the entorhinal cortex especially susceptible to disruptions in these processes. For Dr. Small, these results hold promise for developing new treatments.

“Anchored in genetics and revealing that retromer dysfunction and SORL1 deficiency can explain the regional vulnerability we see in Alzheimer’s disease, this work validates the idea that retromer-enhancing drugs are worth pursuing for Alzheimer's disease therapeutics,” he said.

###

“Alzheimer’s vulnerable brain region relies on a distinct retromer core dedicated to endosomal recycling” appeared on December 28 in Cell Reports. Authors are Sabrina Simoes, Jia Guo, Luna Buitrago, Yasir H. Qureshi, Xinyang Feng, Milankumar Kothiya, Etty Cortes, Vivek Patel, Suvarnambiga Kannan, Young-Hyun Kim, Kyu-Tae Chang, Alzheimer’s Disease Neuroimaging Initiative, S. Abid Hussaini, Herman Moreno, Gilbert Di Paolo, Olav M. Andersen, and Scott A. Small.

The authors declare competing financial interests: Scott Small is a co-founder of Retromer Therapeutics, has equity in the company, and is a paid consultant to the company. In addition, Scott Small has equity in Imij Technologies, an MRI-based company. Gilbert Di Paolo is a full-time employee of Denali Therapeutics, Inc. Olav M. Andersen has commercial interests in Retromer Therapeutics. Lastly, Scott Small, Sabrina Simoes, and Yasir H. Qureshi are listed as co-inventors on Columbia University-owned patents that relate to retromer biomarkers and retromer drug discovery targets.

This study was partly supported by NIH R01 grants AG034618, AG035015, and P30AG066462 to S.A.S., NS056049 to G.D.P. and AG051556 to H.M. Human MRI data collection and sharing for this project were funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) (NIH Grant U01 AG024904) and Department of Defense 409 ADNI (award number W81XWH-12-2-0012). Data collection and sharing for this project was partially funded by the ADNI (National Institutes of Health Grant U01 411 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-412 0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer's Association; Alzheimer's Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.;Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer's Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.

Source: Columbia Zuckerman Institute

Prevention

The Wall Street Journal

STAT

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