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Research Grants 2015

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

2015 Grants - Morales

Contribution of Peripheral Amyloid-Beta Over Brain Pathology in Alzheimer’s Disease

Rodrigo Morales, Ph.D.
The University of Texas Health Science Center at Houston
Houston, Texas

2015 New Investigator Research Grant to Promote Diversity

How does beta-amyloid enter the brain from the body and does this contribute to the onset or progression of Alzheimer’s disease?

Beta-amyloid is a protein fragment at the focus of research into the causes of Alzheimer’s disease. A characteristic feature of Alzheimer’s disease is the progressive brain accumulation of abnormal beta-amyloid into amyloid plaques. The molecular mechanisms that may trigger the accumulation of beta-amyloid remain unclear. Recent evidence has shown that abnormal beta-amyloid is present in organs other than the brain in people with Alzheimer’s disease, but it is not known how this may contribute to the disease process.

In previous studies, Rodrigo Morales, Ph.D., and colleagues found that injecting small amounts of beta-amyloid into the body (periphery) of Alzheimer’s-like mice caused an increase in the accumulation of beta-amyloid throughout their brains. More research is needed to better understand how beta-amyloid in the blood or peripheral organs may affect the formation of amyloid plaques in the brain.

Research Plan
For their current studies, Rodrigo Morales, Ph.D., and colleagues will explore how abnormal beta-amyloid can move from the body into the brain. They will place a traceable form of beta-amyloid into the bodies of mice and track the length of time and different routes it takes to reach the brain. The research team will also use a novel technique to measure beta-amyloid levels in non-brain tissues collected from individuals that had Alzheimer’s disease. They will administer small amounts of these tissue samples to the mice and determine how this impacts beta-amyloid levels in the brain and memory function.

These studies suggest that Alzheimer’s disease may involve, or possibly start with, the movement of abnormal beta-amyloid from the periphery into the brain. The results will provide novel information on how beta-amyloid found in non-brain tissues may affect the progression of Alzheimer’s disease. This work could also lead to the development of new diagnostic tests for Alzheimer’s disease that measure amyloid levels in body tissues and novel ways to prevent or treat the disease.

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

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