Alzheimer's Assocation Research only
All of alz.org
  • Go to Alz.org
  • Research Center
  • AAIC
  • ISTAART
  • Journal
  • Grants
  • TrialMatch
  • Press
  • Donate
  • Contact Us
Home
Science and Progress
Clinical Trials
Funding and Collaboration
You can Help
Stay Current
Video and Resources

Text Size

Small text Medium text Large text

Research Grants 2007


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

2007 Grant - Kuan

Vascular Effects of Beta-Amyloid Peptide via Rac GTPase in Ischemia-Hypoxia

Chia-Yi Kuan, M.D., Ph.D.
Cincinnati Children's Hospital Medical Center
Cincinnati, Ohio

2007 New Investigator Research Grant

In the Alzheimer brain, beta-amyloid protein fragments aggregate, or assemble themselves into structures. Studies suggest that small aggregates of just a few beta-amyloid molecules are particularly toxic to neurons. Additional evidence suggests that small aggregates of beta-amyloid also have damaging effects on the blood vessels in the brain, possibly causing or contributing to the progression of dementia. One possible mechanism for this action involves beta-amyloid activation of a protein known as Rac GTPase. Such activation in turn activates a series of cellular events that lead to the damage from toxic oxygen molecules, or oxidative stress.

Chia-Yi Kuan, M.D., Ph.D., and colleagues plan to test this idea using a mouse model that has been genetically altered to express beta-amyloid and that exhibits many features of Alzheimer pathology. Using this model, they will induce a stroke-like event in the blood circulation of the brain. Then they will test whether animals expressing beta-amyloid experience increased oxidative stress and impaired ability to recover, as compared with normal healthy animals. The researchers will then test whether inhibitors of Rac GTPase alleviate the damaging effects of beta-amyloid.

These studies may help to clarify our understanding of how beta-amyloid damages the brain. They may also provide initial evidence for drugs that could be used to slow or halt the progression of beta-amyloid-induced toxicity in Alzheimer's disease.