2008 Grants - Ninan

Modulation of Synaptic Neurotransmission by Physiological Amyloid-Beta

Ipe Ninan, Ph.D.
New York University School of Medicine
New York, New York

2008 New Investigator Research Grant

Beta-amyloid (also known as amyloid-beta) is a protein fragment strongly implicated in the neurodegeneration observed in persons with Alzheimer's disease. Although low levels of beta-amyloid are found in the brains of healthy individuals, higher levels in persons with Alzheimer's disease have been shown to be associated with impairments in synaptic plasticity, a key function of nerve cells responsible for some forms of learning and memory.

Ipe Ninan, Ph.D., and colleagues are studying how normal, healthy levels of beta-amyloid ("physiological" levels) affect nerve cells, especially synaptic transmission, the process by which nerve cells rapidly transmit signals throughout the nervous system. Using animal models, the researchers have already found evidence that physiological levels of beta-amyloid increase synaptic transmission between nerve cells in a region of the brain called the hippocampus.

Dr. Ninan and colleagues plan to extend their studies by using electrical and biochemical methods to study synaptic transmission between nerve cells of the hippocampus in animal models. They will also study how the effects of beta-amyloid are mediated by interactions with the structural components of the nerve cells. These studies may shed light on how beta-amyloid affects nerve cell function in healthy individuals and suggest how disease-related levels of beta-amyloid contribute to dysfunction.