Alzheimer's Assocation Research only
All of
  • Go to
  • Research Center
  • AAIC
  • Journal
  • Grants
  • TrialMatch
  • Press
  • Donate
  • Contact Us
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 2008

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

2008 Grants - Yan

Cyclophilin D as a Mitochondrial Target of Alzheimer's Disease

Shi Du Yan, M.D.
The University of Kansas Center for Research, Inc.

2008 Investigator-Initiated Research Grant

Mitochondria are compartments inside of every living cell that act as the energy-producing "powerhouse" of the cell. Mitochondrial dysfunction is one of the early features of Alzheimer's disease in nerve cells.

Cyclophilin D, an enzyme that exists within mitochondria, may play a role in "programmed cell death," a kind of self-destruct function that, normally, is intended to eliminate faulty cells. When cyclophilin D associates with mitochondrial membrane, it contributes to the formation of pores in the membrane, causing dysfunction of the mitochondria and possibly the death of the cell.

Shi Du Yan, M.D., and colleagues are studying the function of cyclophilin D and how that function is changed in brain cells affected by Alzheimer's disease. They have found evidence that levels of cyclophilin D are increased in regions of the brain affected by the disease. They have also observed that cyclophilin D levels are increased in mice that have been genetically engineered to express high levels of amyloid precursor protein, a key protein involved in the development of Alzheimer pathology. Finally, the researchers have found that nerve cells lacking cyclophilin D are less susceptible to the detrimental effects of beta-amyloid, which is produced from amyloid precursor protein and is a leading cause of nerve cell death in Alzheimer's.

Dr. Yan and colleagues plan to extend their studies of cyclophilin D and its role in mitochondrial dysfunction and nerve cell death in Alzheimer's disease. They will use genetic engineering techniques to reduce or eliminate cyclophilin D from mitochondria of mouse brain cells. This experimental model will then enable them to study whether beta-amyloid requires cyclophilin D to mediate its toxicity and how cyclophilin D contributes to the normal function of brain cells. These studies may also help to determine whether cyclophilin D is a potential target for therapies to reduce the toxic effects of beta-amyloid in Alzheimer's disease.

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

Abstract Submissions Now Open

The Scientific Program Committee is now accepting submissions for poster
presentations, oral presentations and featured research sessions.