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Research Grants 2008

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

2008 Grants - Rosi

Altered Neuronal-Microglia Communication Impacts Neuronal Function

Susanna Rosi, Ph.D.
University of California, San Francisco
San Francisco, California

2008 New Investigator Research Grant

Nerve cells (neurons) in the brain interact with each other by the process of synaptic transmission, by which rapid signals are transmitted, endowing the brain with many of its unique abilities. In addition to neurons, several other cell types exist in the brain, the most common of which are glial cells. One type of glial cell, microglia, is an important mediator of inflammation. Studies have found that microglia are activated in key parts of the brain in individuals with early signs of Alzheimer's disease, possibly contributing to neuronal damage and synaptic dysfunction.

Susanna Rosi, Ph.D., and colleagues are studying interactions between neurons and microglia, especially how activated microglia can disrupt synaptic transmission and synaptic plasticity. Synaptic plasticity is the process by which repeated transmissions result in neuronal changes that make transmission more efficient—a function of memory formation and learning. Dr. Rosi and colleagues have found evidence that activation of microglia changes the pattern of gene expression associated with synaptic plasticity. These findings suggest that inflammation, such as that found in the brain of persons with early Alzheimer's disease, may disrupt the activity of neurons, possibly explaining some of cognitive deficits of the disease.

Dr. Rosi and colleagues plan to continue studying how neurons and micro-
glia interact, and how microglia-mediated inflammation causes neuronal dysfunction. One focus of their study is a group of genes called immediate early genes, which undergo rapid changes in expression in response to the appropriate stimulus. Immediate early genes are known to play key roles in synaptic plasticity. These studies may improve our understanding of the molecular and cellular mechanisms of cognitive dysfunction in persons with Alzheimer's disease and may suggest new targets for therapy.

Alzheimer's Association International Conference | July 16-20, 2017, London, England

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