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Research Grants 2015

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

2015 Grants - Baglietto-Vargas

Molecular Mechanisms of Synaptic Degeneration in Alzheimer’s Disease

David Baglietto-Vargas
University of California, Irvine
Irvine, California

2015 New Investigator Research Grant

How do beta-amyloid and tau proteins hinder the structure and function of synapses and promote memory loss in Alzheimer’s disease?

For the brain to function properly, nerve cells need to communicate effectively with one another. Nerve cells communicate by sending chemical messages across specialized regions called synapses. In Alzheimer’s disease, synapses become damaged which can hinder nerve cell communication and may lead to problems with memory and other forms of cognition. Scientists, however, do not know exactly how synaptic damage occurs in Alzheimer’s.

Research Plan
David Baglietto-Vargas, Ph.D., and colleagues have been studying the function of synapses in mice engineered to develop Alzheimer’s-like brain changes. They found that two molecules implicated in Alzheimer’s disease — the protein fragment beta-amyloid and an abnormal form of tau protein — tend to accumulate around synapses. Beta-amyloid and abnormal tau appear to disrupt the activity of another protein called actin, which normally helps maintain synaptic structure and function.

For their current studies, the research team will examine how beta-amyloid and tau interfere with actin and promote synaptic damage. They will use Alzheimer’s-like mice and employ novel molecular techniques to increase the levels of beta-amyloid either (1) within the nerve cells or (2) outside of the nerve cells. This will allow them to assess whether the location of toxic beta-amyloid determines its effects on the function of actin and the health of synapses. In addition, the researchers will examine whether beta-amyloid and tau need to “work together” to promote synaptic damage and cognitive loss.

The results of this effort may shed new light on the earliest molecular changes that lead to the clinical symptoms of Alzheimer’s disease. These findings could also promote the development of Alzheimer’s drug therapies that target beta-amyloid and tau in the synaptic regions.

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

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