2026 Alzheimer’s Public Educational Forum: Summary

Friday, May 1, 2026
Virtual Forum

Presented by The Wien Center for Alzheimer’s Disease and Memory Disorders, Mount Sinai Medical Center, and the 1Florida ADRC, with support from Eli Lilly and Company, University of Florida, and the Florida Department of Elder Affairs

Forum Chair: Ranjan Duara, MD, FAAN

The 2026 Alzheimer’s Public Educational Forum brought together clinicians, biomarker scientists, dementia specialists, and brain-aging researchers to help patients, families, caregivers, and community members understand one of the fastest-changing areas in medicine: how Alzheimer’s disease is now detected, diagnosed, treated, and understood.

The Forum was designed for the public, but it did not dilute the science. Instead, it translated it. Across three sessions, the faculty addressed the questions that patients and families now face with increasing urgency: What can a blood test actually tell us? When should memory changes be evaluated? Who may benefit from anti-amyloid treatment? What are the risks? How do infection, inflammation, diabetes, sleep, obesity, and other whole-body factors affect brain health?

One theme ran through the entire program: Alzheimer’s disease care is entering a new era, but better tools do not automatically make decisions easier. Biomarkers, scans, genetic information, and disease-modifying therapies can provide powerful information, but they must be interpreted carefully, explained clearly, and used in the context of the whole person. The brain, inconveniently but truthfully, does not live alone in a glass case.

The Forum was organized into three sessions:

Session I focused on biomarkers and what tests can, and cannot, tell us about memory.

Session II examined disease-modifying therapies, including current anti-amyloid treatments and future therapeutic strategies.

Session III explored infection, inflammation, immune function, and what these forces may mean for dementia risk and prevention.

Together, the presentations gave the audience a grounded view of hope: real scientific progress, real treatment options, real limits, and real opportunities for people to take action today.

Opening remarks

Dr. Ranjan Duara opened the Forum by welcoming attendees and outlining the three major themes of the program: biomarkers, disease-modifying therapies, and infection/inflammation. He emphasized the purpose of the Forum as an educational program for the public, designed to connect current Alzheimer’s disease research with the questions patients and families bring into clinics, homes, and conversations with loved ones.

He also acknowledged the organizations and supporters making the Forum possible, including Mount Sinai Medical Center, the 1Florida Alzheimer’s Disease Research Center, University of Florida, Eli Lilly and Company, the Florida Department of Elder Affairs, and the late Marilyn and Myers Gersh.

Chair: Breton Asken, PhD
University of Florida

Session I began with a fundamental clarification: biomarkers are powerful tools, but they do not replace clinical evaluation.

Dr. Breton Asken opened the session by explaining the difference between the symptoms a person experiences and the biological processes that may be causing them. Memory loss, cognitive change, behavior change, psychiatric symptoms, or movement changes are clinical features. Alzheimer’s disease, vascular disease, Lewy body disease, and other brain disorders are possible underlying causes.

That distinction matters. A biomarker can help identify whether a specific disease process may be present in the brain. It may help explain why someone is having symptoms. It may help rule out certain causes. It may help guide prognosis or treatment eligibility. But a biomarker alone cannot determine whether someone has memory loss, dementia, or cognitive impairment. Those conclusions still require a careful clinical evaluation.

Dr. Asken offered one of the clearest practical messages of the Forum: biomarkers help explain the “why,” but they do not, by themselves, define the “what.” The patient’s symptoms, functioning, history, and clinical examination remain essential.

Sid O’Bryant, PhD
UNT Health Fort Worth

Dr. Sid O’Bryant presented research from the Health & Aging Brain Study – Health Disparities, or HABS-HD, one of the largest and most comprehensive studies of Alzheimer’s disease biology across diverse populations.

His central argument was direct: precision medicine is not precision medicine if the science does not include everyone.

Dr. O’Bryant explained that major advances now allow clinicians and researchers to detect Alzheimer’s disease biology during life, using brain scans and blood tests. This is a major change from the era when Alzheimer’s disease could only be confirmed definitively at autopsy. These advances matter because the field now has disease-modifying therapies that target amyloid in the brain. Patients should not receive such therapies unless the relevant biology is actually present.

But he also emphasized a major concern: much of the research used to develop and validate biomarker tools has historically been conducted in populations that were not fully representative of the broader community. His work examines how Alzheimer’s disease biomarkers may differ across Hispanic, Black, and non-Hispanic white populations, and how genetics, medical comorbidities, environment, sociocultural factors, and systemic disease may influence risk, presentation, and biomarker interpretation.

Dr. O’Bryant highlighted several findings from HABS-HD. Genetic risk factors, including APOE-related risk, may function differently across communities. Brain amyloid levels may differ across groups. The relationship between amyloid plaques, tau tangles, neurodegeneration, and cognitive decline may not follow exactly the same pattern in every population. Medical comorbidities, especially diabetes, may play a powerful role in brain aging and cognitive decline.

One of the most important practical points concerned diabetes. Dr. O’Bryant explained during discussion that diabetes may not be strongly linked to amyloid plaques themselves, but it appears to be linked to neurodegeneration and memory loss. In a person who already has Alzheimer’s disease biology, diabetes may worsen the clinical picture. In a person without Alzheimer’s disease biology, diabetes may still contribute to memory problems. That makes diabetes not merely a background condition, but a possible entry point for prevention and intervention.

He closed with a tangible recommendation: improve sleep. Sleep is not a decorative lifestyle accessory. It is part of the brain’s maintenance system. During sleep, the brain clears waste products, including molecules related to Alzheimer’s disease. Better sleep may therefore support better brain health.

Claire Erickson, PhD, MPA
Banner Alzheimer’s Institute

Dr. Claire Erickson focused on the rapidly changing landscape of Alzheimer’s disease blood biomarkers and the practical challenges of using these tools in primary care.

She began by defining biomarkers as ways to identify and track disease. In Alzheimer’s disease, common biomarker approaches include PET scans, lumbar punctures, and blood or plasma tests. PET imaging remains a gold standard for detecting amyloid and tau in the brain, but it is expensive, resource-intensive, and not widely available in every community. Blood biomarkers are therefore especially important because they may offer a lower-cost, more accessible way to begin the diagnostic process.

Dr. Erickson reviewed several major blood biomarker categories. The Aβ42/40 ratio can provide information about amyloid biology, although amyloid is difficult to measure in blood. Phosphorylated tau, especially p-tau217, has emerged as a particularly useful marker because it is more closely tied to Alzheimer’s disease pathology. GFAP reflects a more general brain-injury or inflammatory response and is not specific to Alzheimer’s disease. MTBR tau 243 is a newer biomarker that may help reflect tau tangle pathology and disease stage, though it remains under validation.

A major message of her talk was that blood biomarkers are promising, but they are not magic. They may be useful as first-line screening tools, particularly in people over 55 who have cognitive symptoms. A negative result may be reassuring in some contexts. A positive result may require confirmatory testing, often with PET imaging or other evaluation, especially if treatment is being considered.

Dr. Erickson also addressed a major access problem. Specialty memory clinics are difficult to reach for many patients, and the United States has a shortage of dementia specialists. Primary care clinicians are often the first point of contact for memory concerns, and many dementia diagnoses first appear in primary care records. Yet primary care visits are short, and many clinicians report limited confidence in diagnosing and communicating dementia-related conditions.

Her conclusion was practical and policy-oriented: if Alzheimer’s blood tests are going to reach the people who need them, primary care will need investment. That means clinician education, collaborative care models, nurse practitioners, social workers, better payment structures, and more time for meaningful conversations. The test may be simple. The system around it is not.

The Session I discussion centered on how biomarkers should be used, when memory concerns should prompt evaluation, and how patients can advocate for themselves.

Drs. Asken, O’Bryant, and Erickson discussed the current role of blood biomarkers. At present, these tests are primarily used in specialty settings, though the field is moving toward broader use. p-tau217 was discussed as a particularly useful screening tool, especially when interpreted carefully. However, the panel emphasized that a positive blood test may still require confirmatory testing, particularly before disease-modifying therapy is considered.

The panel also addressed APOE testing. APOE status may help estimate risk, but its immediate clinical importance is especially strong when anti-amyloid treatment is being considered, because APOE4 status affects the risk of amyloid-related imaging abnormalities, or ARIA.

A particularly important public-facing message came from Dr. O’Bryant: memory loss is not simply normal aging. Processing speed and attention may change with age, but significant memory loss should not be dismissed. If a person or their loved ones notice meaningful changes, they should raise the concern with a physician.

Dr. Erickson added that early detection provides more runway. A person may not always recognize their own cognitive changes, so input from family members and close friends can be important. The panel also discussed cultural barriers to diagnosis, including situations where questioning an elder’s memory may feel disrespectful or where the word “dementia” may carry stigma or mistranslation.

The advice to patients was clear: come prepared. Write down the symptoms. Give examples. Ask what the test is intended to answer. Ask what a positive or negative result would change. A biomarker should not be ordered just because it exists. Even shiny tools need a reason to be taken out of the drawer.

Session II: Changing the Course: Disease-Modifying Therapies Today and Tomorrow

Chair: Steven DeKosky, MD
University of Florida

Session II shifted from diagnosis to treatment. Dr. Steven DeKosky introduced the session by framing the progress and complexity of Alzheimer’s disease therapeutics. The session focused on what current disease-modifying therapies can do, what they cannot do, who is most likely to benefit, and what risks must be considered.

The overarching message was measured but hopeful. Alzheimer’s disease treatment is no longer limited to symptomatic medications. Anti-amyloid therapies can slow disease progression in appropriately selected patients. But they are not cures, they do not generally improve symptoms, and they require careful evaluation, monitoring, and risk counseling.

Ranjan Duara, MD, FAAN
Mount Sinai Medical Center

Dr. Ranjan Duara presented a clear explanation of the amyloid hypothesis and how it relates to current anti-amyloid therapies.

He described Alzheimer’s disease as a long biological process that often begins many years before memory symptoms appear. Beta-amyloid accumulates first. Tau pathology follows. Neurodegeneration then develops, leading eventually to measurable changes in cognition, memory, language, and daily functioning. This progression can take 15 to 20 years from the earliest amyloid deposition to the appearance of symptoms.

Dr. Duara explained how PET imaging and blood tests can detect different pieces of this process. Amyloid PET can detect amyloid plaques. Tau PET can detect tau deposition, which tends to track more closely with cognitive symptoms. MRI can show neurodegeneration, such as shrinkage of the hippocampus. Blood tests can detect amyloid-related changes, phosphorylated tau, GFAP, and neurofilament light, each reflecting different aspects of disease or injury.

He then distinguished between symptomatic and disease-modifying treatments. Symptomatic treatments, such as cholinesterase inhibitors and memantine, may help the brain function more efficiently for a period of time, but they do not address the underlying pathology. Disease-modifying treatments, such as lecanemab and donanemab, target amyloid pathology and aim to slow future progression.

Dr. Duara emphasized that disease-modifying therapies should not be expected to reverse Alzheimer’s disease or produce dramatic improvement. Their goal is slowing progression. Stability may be a very meaningful outcome.

He also reviewed factors that influence the likely benefit of anti-amyloid therapy. Tau burden is especially important: lower tau levels are associated with better response. Earlier clinical stage matters. Younger age may be associated with greater efficacy. APOE4 status affects both risk and treatment considerations. Amyloid burden also matters because very high amyloid may take longer to clear. Comorbidities, especially vascular disease and other age-related conditions, may reduce the visible benefit of amyloid removal.

The practical message was simple and consequential: earlier diagnosis matters because these treatments appear to work best before the disease is too advanced.

Dr. Duara also emphasized lifestyle interventions as part of brain health. Diet, physical activity, mental engagement, social connection, vascular risk reduction, oral health, and management of systemic inflammation are not side notes. They are part of the whole plan.

Lawrence S. Honig, MD, PhD, FAAN
Columbia University

Dr. Lawrence Honig reviewed currently approved and investigational Alzheimer’s disease therapies, placing today’s treatments in the longer history of Alzheimer’s disease research.

He explained that the two marketed disease-modifying therapies, lecanemab and donanemab, are monoclonal antibodies designed to bind beta-amyloid and remove it from the brain. Clinical trials have shown that these drugs can clear amyloid and slow clinical worsening in people with mild cognitive impairment or mild dementia due to Alzheimer’s disease.

Dr. Honig emphasized that the clinical benefit is real but modest. These therapies slow decline; they do not stop the disease, restore lost cognition, or cure Alzheimer’s disease. Their benefit appears stronger when treatment begins earlier, and ongoing studies are examining whether longer treatment, earlier intervention, or newer antibodies may produce greater effects.

He also discussed the major safety concern: ARIA, or amyloid-related imaging abnormalities. ARIA can involve swelling or fluid accumulation in the brain, called ARIA-E, or small hemorrhages, called ARIA-H. Many ARIA cases are asymptomatic, but some can produce headache, visual symptoms, language disturbance, or other neurological symptoms. APOE4 status is a major risk factor, especially in individuals with two copies of APOE4.

Dr. Honig compared lecanemab and donanemab, noting that both show similar overall efficacy and share similar categories of risk. One important distinction is that donanemab appears to be used for a time-limited strategy tied to plaque removal, while lecanemab may continue to have rationale beyond visible plaque clearance because of its activity against other amyloid forms.

He also reviewed future therapeutic directions, including anti-tau therapies, approaches targeting neuroinflammation, strategies aimed at neurodegeneration, and possible genetic or APOE-related interventions. The treatment pipeline is expanding beyond amyloid, though amyloid-lowering antibodies remain the only disease-modifying approach with proven clinical efficacy at this time.

The Session II discussion focused on treatment selection, treatment timing, asymptomatic Alzheimer’s disease, cognitive reserve, white matter disease, and the risks and uncertainties of anti-amyloid therapy.

A major question concerned whether cognitively normal people with positive amyloid biomarkers should be treated. The panel was cautious. Dr. Honig explained that anti-amyloid therapies have not yet been conclusively tested in asymptomatic Alzheimer’s disease populations, though prevention trials are ongoing. Dr. DeKosky added an important warning: many people with amyloid positivity do not necessarily go on to develop clinical Alzheimer’s disease symptoms. Treating all amyloid-positive individuals would expose many people to treatment risk without clear evidence of benefit. The field needs safer therapies, better prediction tools, or both.

The panel also discussed cognitive reserve. Some people may perform normally on cognitive testing despite underlying Alzheimer’s pathology because they began with higher cognitive capacity or have more compensatory ability. This makes the boundary between “normal” and “symptomatic” more difficult than it appears on paper.

Another question concerned white matter disease or small vessel disease on MRI. The discussion distinguished between safety and efficacy. Moderate white matter changes may not automatically rule out anti-amyloid treatment, but if a patient’s cognitive decline is primarily driven by vascular disease rather than Alzheimer’s disease, amyloid treatment may offer less benefit. The panel emphasized individualized interpretation.

The discussion reinforced a major Forum theme: disease-modifying therapy is not a yes-or-no button. It is a clinical pathway requiring diagnosis, biomarkers, MRI, genetics, safety monitoring, patient goals, and honest conversation.

Session III: Infection, Inflammation, and the Brain: What You Need to Know

Chair: Leonard Sokol, MD
Mount Sinai Medical Center

Session III broadened the conversation beyond amyloid and tau to examine how infection, inflammation, immune function, and systemic health may shape dementia risk.

Dr. Leonard Sokol introduced the session by explaining that inflammation is not merely a secondary reaction to brain damage. Increasing evidence suggests that immune dysfunction and inflammatory processes may be part of the Alzheimer’s disease cascade itself. These processes may operate both inside and outside the central nervous system, linking the brain to the rest of the body’s immune response.

The session made a clear point: dementia research is no longer just about what happens inside the brain. The rest of the body keeps calling, and sometimes the brain picks up.

Keenan Walker, PhD
National Institute on Aging

Dr. Keenan Walker presented an overview of how inflammation, immune function, and infectious exposures may relate to dementia and cognitive decline.

He began by defining inflammation as part of the immune system’s response to injury, infection, and threat. In the short term, inflammation is protective. It helps the body fight infection and repair damage. But chronic or excessive inflammation can become harmful, especially when inflammatory signals persist over time.

Dr. Walker explained that the brain has its own immune cells, including microglia, which help monitor and respond to injury or disease. When systemic inflammation occurs outside the brain, through infection, chronic disease, obesity, stress, or other insults, those signals may influence the brain’s immune environment. Over time, chronic inflammatory signaling may contribute to neurodegeneration and cognitive decline.

He reviewed evidence that inflammatory proteins and severe infections are associated with increased dementia risk. Acute infections such as pneumonia, COVID-19, and other severe inflammatory events may be followed by delirium or cognitive changes. Chronic inflammatory diseases may also contribute to long-term risk. At the same time, Dr. Walker was careful not to overstate the evidence. The field does not yet have infection-specific biomarkers that reliably predict future neurodegenerative disease risk.

The discussion also addressed anti-inflammatory treatments and vaccination. Dr. Walker noted evidence suggesting that treatment of some inflammatory diseases with TNF blockers may be associated with lower Alzheimer’s disease risk. He also discussed shingles vaccination, including evidence suggesting that herpes zoster vaccination may reduce dementia risk by approximately 20% over seven years. The mechanisms remain under investigation and may include prevention of viral reactivation, immune modulation, or reduction in inflammatory burden.

On lifestyle, Dr. Walker identified diet and adiposity, particularly visceral adiposity, as major drivers of chronic inflammation. Obesity, especially fat around the gut, can be a persistent source of inflammatory proteins. Reducing adiposity through diet, exercise, and weight management may therefore plausibly reduce dementia risk by lowering chronic inflammation.

He also addressed biomarkers after acute infection. While no specific post-infection dementia-risk biomarker is ready for routine clinical use, general inflammatory markers such as C-reactive protein may provide some indication of the severity of the inflammatory response. A very high C-reactive protein level after infection may suggest a more severe inflammatory insult, though whether that translates into future dementia risk remains uncertain.

Dr. Walker’s message was balanced: inflammation matters, infection may matter, and prevention matters, but the field still needs better tools to determine who is at risk, when risk is highest, and which interventions work best.

Session III discussion

The Session III discussion focused on what members of the public can do now, and what remains uncertain.

Dr. Sokol and Dr. Walker discussed chronic inflammation, obesity, diet, infection, and immune health. The panel emphasized that people should not try to suppress the immune system indiscriminately after infection. The body needs inflammation to fight infection. The goal is not to shut down immunity, but to reduce chronic, unnecessary inflammatory burden.

Practical strategies included physical activity, healthier diet, weight management, vaccination where appropriate, management of chronic diseases, and attention to overall health after serious infections. Dr. Duara emphasized exercise as one of the most important practical interventions for older adults. Dr. Walker highlighted the role of diet and adiposity in inflammation-related dementia risk.

The discussion also returned to biomarkers. Blood-based Alzheimer’s biomarkers such as Aβ42/40 and p-tau217 show promise for screening and diagnosis in the right context, but they are not yet proven tools for monitoring treatment response or predicting post-infection dementia risk in everyday clinical care.

The session closed the Forum on a broader biological note: Alzheimer’s disease is not only a disease of plaques and tangles. It is also shaped by aging, immunity, inflammation, vascular health, metabolism, infection history, genetics, and resilience. The story is bigger than one protein. Science, at last, is catching up with the messiness of real life.

Dr. Ranjan Duara is the Medical Director of the Wien Center for Alzheimer’s Disease and Memory Disorders at Mount Sinai Medical Center and holds the Denis C. Cole Family Chair in Alzheimer’s Disease Research. In addition, Dr. Duara serves the Associate Director and leader of the Clinical Core of the 1Florida Alzheimer’s Disease Research Center, a research collaboration between four university medical centers and Mount Sinai Medical Center in Florida. Dr. Duara is a Courtesy Professor of Neurology at the University of Florida College of Medicine, Gainesville, Florida, and the Herbert Wertheim College of Medicine, Florida International University, Miami, Florida. He serves as the Principal Investigator of the State of Florida Dementia Brain Bank Program.

Dr. Duara is a clinical neurologist with a special interest in the use of brain imaging for the diagnosis and treatment of Alzheimer’s disease and other causes of Adult Cognitive Disorders. Through his research in this area, he has helped to enhance what is known about the biology of Alzheimer’s disease.
He completed his undergraduate medical education at Christian Medical College, Vellore, South India, completed two years of neurology residency with Dr. Noshir Wadia at Grant Medical College in Bombay, India, followed by residencies in internal medicine and neurology in the United Kingdom, and in neurology at Thomas Jefferson University Hospital in Philadelphia. He then completed a four-year fellowship in neuroscience and neuroimaging of aging, with Dr Stanley Rapaport at the National Institute on Aging (National Institutes of Health, Bethesda, MD).

Dr. Duara’s research has focused primarily on early diagnosis of Alzheimer’s disease and other dementias, neuroimaging, genetic epidemiology, and the methodology for staging the transition from normal cognitive aging to dementia. He has contributed to more than 250 articles in peer-reviewed scientific journals and has been an investigator in observational studies on aging, as well as clinical trials of novel agents for the treatment of Alzheimer’s Disease. Dr. Duara is also the chair and organizer of the Mild Cognitive Impairment Symposium, which is held annually in Miami Beach.

Dr. Sid O’Bryant is the Executive Director of the Institute for Translational Research and Dr. Joe and Peggy Schooler Endowed Chair in Pharmacology and Neuroscience.

He is the principal investigator of the Health & Aging Brain Study – Health Disparities (HABS-HD), which is the most comprehensive study of Alzheimer’s disease among the three largest racial/ethnic groups in the U.S. ever conducted – African Americans, Hispanics, non-Hispanic whites. The goal of the HABS-HD program is to understand the life course factors, including biological, sociocultural, environmental, and behavioral, that impact risk for Alzheimer’s disease in late life. This work will ultimately lead to population-specific precision medicine approaches to treating and preventing Alzheimer’s disease (i.e., “treating your Alzheimer’s disease”).

In addition to being a global leader in health disparities in cognitive aging, Dr. O’Bryant is a global expert in the use of blood-based biomarkers for the generation of a precision medicine approach to novel diagnostic and therapeutic strategies for Alzheimer’s disease, Parkinson’s disease, Dementia with Lewy Bodies and Alzheimer’s disease among adults with Down Syndrome.  

Dr. Keenan Walker is a Senior Investigator at the National Institute on Aging (NIA) Intramural Research Program, and he is Chief of the Multimodal Imaging of Neurodegenerative Disease Section (MINDS).

He received his Ph.D. in clinical psychology from St. John’s University and completed his pre-doctoral internship in clinical neuropsychology at the University of California San Diego/VA San Diego Healthcare System before beginning an NIH-funded postdoctoral fellowship at Johns Hopkins University School of Medicine. Shortly thereafter he began his career as a Tenure-Track Investigator at NIA.

Dr. Walker currently runs a research program focused on identifying biomarkers and therapeutic targets for Alzheimer’s disease and related dementias.

Breton Asken, PhD, ATC, is an Assistant Professor in the Department of Clinical and Health Psychology at the University of Florida. He is a Fixel Scholar in the Normal Fixel Institute for Neurological Diseases and a member of the Clinical Core of the 1Florida Alzheimer’s Disease Research Center. Additional affiliations include the UF McKnight Brain Institute, Center for Cognitive Aging and Memory, and the UF Brain Injury, Rehabilitation, and Neuroresilience (BRAIN) Center.

Dr. Asken completed bachelor’s degrees at the University of North Carolina at Chapel Hill (Exercise & Sport Science – Athletic Training, Psychology) and was a research assistant in the Matthew Gfeller Sport-Related Traumatic Brain Injury Research Center. He then earned his doctorate in Clinical Psychology (Neuropsychology track) from the University of Florida and completed his clinical internship in neuropsychology at Brown University. Dr. Asken completed a postdoctoral fellowship in neuropsychology at the UCSF Memory and Aging Center.

Dr. Asken’s research integrates multimodal biomarkers with cognitive and behavioral evaluations to study the complex associations between neuropathological changes and clinical phenotypes among patients with Alzheimer’s disease and related dementias. His sub-focus is studying the role that lifetime head trauma plays in later-life neurodegenerative disease, specifically looking at hippocampal and limbic network vulnerability to developing neuropathological changes with aging.

Dr. Asken is an active clinical neuropsychologist in the UF Memory Disorders Clinic and specializes in evaluation of patients with suspected neurodegenerative disease.

Dr. Steven DeKosky, a prominent Alzheimer’s disease and traumatic brain injury researcher and UF alumnus, came to UF in July 2015 as the institute’s deputy director and professor of neurology in the College of Medicine.

Prior to joining the McKnight Brain Institute, Dr. DeKosky was vice president and dean of the University of Virginia School of Medicine from 2008 to 2013, and was then appointed emeritus professor of neurology . Prior to becoming dean at UVA, he spent 18 years at the University of Pittsburgh in roles that included chair of the department of neurology and director of the Alzheimer’s Disease Research Center.

As a researcher, Dr. DeKosky focused on understanding the neurochemistry, neuroimaging, treatment and prevention of Alzheimer’s disease in both his laboratory and in clinical research. He also co-authored the first report of the dementia associated with traumatic brain injuries among professional football players and published extensively in basic research of TBI..

At UF, Dr. DeKosky did graduate work in psychology and neuroscience, received a medical degree in 1974 and following an internship at The Johns Hopkins Hospital, returned to UF to complete a residency in neurology, followed by a fellowship in neurochemistry at the University of Virginia Center for Neurosciences.