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Research Grants 2015


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

2015 Grants - Deyts

Targeting APP-CTF as Potential Disease Modifier to Reduce Abeta Burden

Carole Deyts, Ph.D.
The University of Chicago
Chicago, Illinois

2015 New Investigator Research Grant

How do amyloid precursor protein carboxy terminal fragments (APP-CTFs) affect brain levels of beta amyloid and nerve cell function?

Background
Beta-amyloid (also known as Abeta) is a protein fragment at the focus of research into understanding the causes of Alzheimer’s disease. It can accumulate into clumps called amyloid plaques, a hallmark of Alzheimer’s in the brain. Beta-amyloid is produced by the cutting of its parent protein, amyloid precursor protein (APP). In addition to producing beta-amyloid, this cutting process also generates protein fragments known as APP carboxy terminal fragments (APP-CTFs).

Although beta-amyloid has been a main focus of research in Alzheimer’s disease, scientists have recognized that APP-CTFs may play important roles in the disease process. These fragments activate signaling pathways (a series of chemical reactions) in nerve cells, although how this activation affects nerve cell function is not well understood.

Research Plan
Carole Deyts, Ph.D., and colleagues have proposed experiments to study the signaling pathways activated by APP-CTFs. In initial studies, the researchers found evidence that activation of these pathways may promote the growth and protection of nerve cells. Dr. Deyts and colleagues will use molecular techniques to increase levels of APP-CTFs in the brains of Alzheimer’s-like mice and examine the effects on nerve cell structure and function. They will also determine if activation of APP-CTF pathways can prevent the production and accumulation of beta-amyloid in the brain. In addition, the researchers will modify specific regions of the APP-CTF molecule to precisely determine which regions are essential for its effects on cellular function.

Impact
These studies will improve our understanding of the signaling pathways activated by APP-CTFs and how these pathways may reduce or prevent nerve cell damage related to beta-amyloid. The results may also uncover targets for potential new drugs to slow or prevent brain damage in Alzheimer’s disease.


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

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