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Research Grants - 2011


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Research Grants 2011


To view an abstract, select an author from the vertical list on the left.

2011 Grants - Teich

Beta-Amyloid42 Positively Regulates Alpha7-Cholinergic Receptors

Andrew Teich, M.D., Ph.D.
Columbia University Medical Center
New York, New York

2011 New Investigator Research Grant

In Alzheimer's disease, brain levels of the protein fragment beta-amyloid become abnormally high. Beta-amyloid accumulations have been shown to disrupt cell-to-cell communication in the brain and cause brain cell death. However, other research has shown that the protein fragment may promote brain cell activity in animals and humans. Recent studies, in fact, have found that the brain requires small concentrations of beta-amyloid to maintain the health of synapses — the tiny channels through which brain cells communicate with one another — and to support memory functions.

Andrew Teich, M.D., Ph.D., and colleagues have studied the role of beta-amyloid in promoting activity of cholinergic neurons. These neurons use a chemical messenger called acetylcholine to communicate with one another, and they are a vital component of the brain's communication network. Acetylcholine binds to specific receptors, or docking sites, on cholinergic neurons. The researchers have found in animal studies using mice, that those lacking beta-amyloid tend to lose key cholinergic receptors called alpha7-cholinergic receptors. Such losses likely compromise the healthy functioning of cholinergic neurons.

Based on this finding, Dr. Teich and colleagues hypothesize that low brain concentrations of beta-amyloid can help maintain cognitive health by regulating the activity of alpha7-cholinergic receptors. This study will seek to test this hypothesis in mice. The researchers also hope to determine precisely where and how amyloid-induced cholinergic regulation occurs. Results of these studies could shed new light on how beta-amyloid may promote healthy brain activity. The data generated might also indicate novel mechanisms related to how the protein fragment becomes overproduced in Alzheimer's disease.