To view an abstract, select an author from the vertical list on the left.
2011 Grants - Pena
Disruption of Interneuronal Networks by Beta-Amyloid
Fernando Pena, Ph.D.
Neurobiology Institute at the National Autonomous University of Mexico
2011 New Investigator Research Grant
The protein fragment beta-amyloid, a key suspect in Alzheimer's disease, is thought to disrupt cell-to-cell communication in the brain and cause brain cell death. Many research teams have been searching for the biological mechanisms underlying amyloid toxicity. One of the first brain regions to be damaged by beta-amyloid is the hippocampus, a region important for learning and memory. Such damage often occurs among a group of hippocampal brain cells called interneurons. These cells help transport chemical messages among other groups of neurons through tiny channels called synapses. Amyloid-related damage to such interneuronal networks may play a key early role in Alzheimer's disease progression.
In preliminary studies with cultured brain cells, Fernando Pena, Ph.D., and colleagues have used sophisticated methods of analyzing the electrical and physiological activity of interneuronal networks — and the effects that beta-amyloid has on them. Their results so far suggest that beta-amyloid may disrupt the activity of highly active brain cells called fast-spiking interneurons.
For this grant, the researchers plan to expand on their earlier research. Using their analytical methods, they hope to characterize more completely the effects of beta-amyloid on interneuronal networks. Such efforts will involve studying how amyloid affects the activities of interneurons, especially their role in transmitting chemical messages across synapses. A greater understanding of these toxic mechanisms could lead to the identification of therapies to prevent them — and prevent the onset of Alzheimer's disease.