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Skip Navigation LinksHome > Research > Disease Research Areas > Alzheimer's Disease
Alzheimer's Disease 
 
A progressive brain disease, Alzheimer’s disease is the most common cause of dementia. It gradually destroys a person’s ability to reason, remember, learn, make judgments, and carry out daily activities. In late stages, Alzheimer’s patients need total care. The rate of progression can vary greatly from one person to the next. The average time to death after diagnosis is eight years.

 Hope Center Scientists and Clinicians who Work on Alzheimer's Disease

Randall Bateman M.D.
Assistant Professor of Neurology

Alzheimer's disease: Pathophysiology, biomarkers, predictive diagnostics and treatments

Guojun Bu Ph.D.
Professor of Pediatrics and Cell Biology & Physiology

LDL receptor family members in human disease

Nigel Cairns Ph.D., MRCPath
Research Associate Professor of Neurology and Pathology & Immunology; Director, Betty Martz Laboratory for Neurodegenerative Research

Protein misfolding, inclusion formation and neurodegeneration in Frontotemporal Dementias

Hans H. Dietrich Ph.D.
Research Assistant Professor of Neurological Surgery

Regulatory mechanisms of cerebrovascular microcirculation

Anne M. Fagan Niven Ph.D.
Research Associate Professor of Neurology

Biomarkers, and mechanisms of apoE4 action in Alzheimer's Disease

Carl Frieden Ph.D.
Professor of Biochemistry & Molecular Biophysics

Protein folding, structure

James E. Galvin M.D., M.P.H.
Assistant Professor of Neurology

Clinical and pathological correlates of neurodegenerative disease

Alison M. Goate D.Phil.
Samuel and Mae S. Ludwig Chair in Psychiatry; Professor of Neurology and Genetics; Hope Center Steering Committee

Linkage and association studies to uncover genetic susceptibility to neuropsychiatric disease.

David M. Holtzman M.D.
Andrew B. and Gretchen P. Jones Professor and Chairman of Neurology; Professor of Molecular Biology; Hope Center Steering Committee

Cellular/Molecular/Biomarkers studies of Alzheimer's disease and neonatal brain injury.

Eugene M. Johnson Ph.D.
Professor of Neurology and Developmental Biology; Hope Center Steering Committee

Biological function and pharmacological potential of GFL neurotrophic factors

Vitaly Klyachko PhD
Assistant Professor of Biomedical Engineering and Cell Biology and Physiology

Raphael Kopan Ph.D.
Professor of Internal Medicine and Developmental Biology

Studies of cell fate determination in mammalian system with focus on Notch mediated signal transduction.

Jin-Moo Lee M.D., Ph.D.
Associate Professor of Neurology

Understanding the molecular pathogenesis of spontaneous intracerebral hemorrhage

Rohit V. Pappu Ph.D.
Associate Professor of Biomedical Engineering

Alzheimer's disease; biophysics; mathematical modeling; thermodynamics

B. Joy Snider M.D., Ph.D.
Assistant Professor of Neurology

Mechanisms of protein degradation and intracellular calcium homeostasis in neurodegenerative disorders

Heather L. True-Krob Ph.D.
Assistant Professor of Cell Biology & Physiology

Protein misfolding and aggregation of prion proteins

Gregory J. Zipfel M.D.
Assistant Professor of Neurological Surgery and Neurology

Role of amyloid-B peptide and cerebral amyloid angiopathy in neurovascular dysfunction, ischemic brain injury and subarachnoid hemorrhage

 

 Read about Hope Center research on Alzheimer's Disease

Randall Bateman 
Through clinical studies with volunteers such as Carl Garrett, researcher Randall J. Bateman, MD, and colleagues are studying the body’s production and clearance rates of the protein fragments that collect and impair the brains of Alzheimer’s patients.

Washington University Sites

Information about Alzheimer's Disease

No single cause is known. The most common form is late-onset Alzheimer’s, affecting adults over 65. By age 85, the risk of Alzheimer’s is 50%.

A rare form of familial Alzheimer’s, linked to a specific gene, has been found in several hundred families around the world. Members of these families are virtually certain to get the disease, sometimes by their 30’s or 40’s.

What happens in Alzheimer’s?

The brains of Alzheimer’s patients show at least two abnormal features: “plaques,” or abnormal buildups between brain cells of a fatty protein called amyloid beta; and “tangles,” or twisted strands of another protein within brain cells.

We’re not sure what role these features play in Alzheimer’s, but they are associated with a decline in a chemical called acetylcholine, a neurotransmitter necessary for cognitive function.

How is Alzheimer’s diagnosed?

There is no single diagnostic test for Alzheimer’s. However, a skilled physician can diagnose it with 90% accuracy. Diagnosis is based on a thorough medical exam, tests of mental function, family history, and exclusion of other conditions or possible causes of dementia, such as vascular dementia, or brain damage due to constriction or disruption of blood flow to the brain. Some of these other conditions can coexist with Alzheimer’s in a “mixed dementia.” Since some of them are reversible, it’s important to rule them out. It’s believed that brain cell damage caused by Alzheimer’s begins years before symptoms show. Symptoms can include more than ordinary forgetfulness, mood changes including depression, and sudden changes in ordinary routines such as sleep patterns. Alzheimer’s symptoms are often first spotted by family or household members.

What are some active areas of investigation in Alzheimer’s?

Washington University scientists recently announced an important discovery about the rate at which amyloid beta builds up and is cleared from brain tissue. The Hope Center for Neurological Disorders conducts laboratory and patient research, and works collaboratively across disciplines to find causes and treatments for neurodegenerative and cerebrovascular diseases.

Although many Hope Center faculty are physicians, the Hope Center itself does not provide direct medical care.

To schedule an appointment with a specialist in Alzheimer's Disease, please contact the WU Department of Neurology.   

U.S. Government Sites

 Associations and Foundations