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2010 Grants - Slutsky
Initiation of Alzheimer's Disease: From Amyloid-Beta Release to Synaptic Failure
Inna Slutsky, Ph.D.
2010 New Investigator Research Grant
Accumulation in the brain of beta-amyloid, a protein fragment, is thought to play a major role in initiating Alzheimer's disease. Studies have found that a certain form of amyloid called beta-amyloid 42 is particularly toxic in Alzheimer's. Within diseased brains, levels of this amyloid form may overtake levels of a less harmful type called beta-amyloid 40. Such increases in harmful beta-amyloid likely cause damage to synapses, the tiny channels through which brain cells communicate with one another. However, the biological mechanisms underlying dysregulation of harmful beta-amyloid—as well as amyloid's role in synaptic dysfunction—are unclear.
Inna Slutsky, Ph.D., and colleagues hypothesize that altered brain cell activity patterns may lead to harmful beta-amyloid release and the resulting synaptic damage. They will test this hypothesis with cultured brain cells and brain slices. The researchers will use sophisticated imaging technology to study amyloid release at synaptic sites. They will also study electrical patterns that indicate changes in brain cell activity.
Results of this effort could elucidate how synaptic deficits are initiated at the earliest stages of Alzheimer's. Such findings could lead to strategies for preventing the disease.