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2008 Grants - Tampellini
Study of the Relation Between Synaptic Activity and Beta-Amyloid
Davide Tampellini, Ph.D.
Joan & Sanford I. Weill Medical College of Cornell University
New York, New York
2008 New Investigator Research Grant
The protein fragment beta-amyloid is believed to disrupt cell-to-cell communication in Alzheimer's disease. Research has found that beta-amyloid can damage synapses, or tiny channels through which brain cells send and receive chemical messages. Specifically, the fragment may inhibit the activities of proteins and other molecules that are vital to synaptic health.
Previous efforts to determine the exact relationships between synaptic activity and beta-amyloid have yielded paradoxical results. Some studies have found that reducing beta-amyloid levels in the brain can prevent synaptic damage, and ultimately improve cognitive health. But other studies have found that increases in synaptic activity actually enhance the secretion of beta-amyloid.
For this study, Davide Tampellini, Ph.D., and colleagues hope to identify more clearly how synaptic activity and beta-amyloid production are related. Their preliminary research suggests that increased synaptic activity may promote the transport of beta-amyloid, but reduce overall beta-amyloid levels. The investigators hypothesize that by modulating synaptic activity among brain cells, they can affect both the production and transport of beta-amyloid within these cells. The team also believes that changes in synaptic activity may affect the levels of synaptic proteins. Dr. Tampellini and colleagues will test these hypotheses using cultured cells and animals engineered to produce Alzheimer-like symptoms.
The results of this study could shed new light on the biological processes underlying beta-amyloid's role in Alzheimer's disease.