To view an abstract, select an author from the vertical list on the left.
2007 Grant - Perry
Mitochondrial Abnormalities in Alzheimer's Disease
George Perry, Ph.D.
Case Western Reserve University
Candidate for 2007 Zenith Fellows Award
Mitochondria are cellular structures that use oxygen and nutrients to produce energy for a cell. In Alzheimer's disease, however, abnormalities often occur in the mitochondria of nerve cells. Such abnormalities can lead to the excessive production of free-radicals, or toxic oxygen molecules that damage the neurons. Free-radical damage, also called oxidative stress, often leads to the death of nerve cells in Alzheimer's.
George Perry, Ph.D., and colleagues have been studying the relationship between abnormal mitochondria and Alzheimer's disease. Preliminary research with autopsied brain tissue has suggested a correlation between altered mitochondrial function and amyloid precursor protein (APP) levels in the brain. APP is the parent molecule of beta-amyloid, a key suspect in Alzheimer's. When APP accumulates in the brain, it may block the ability of mitochondria to move around the neurons' axons, or "arms." Such reduced movement may help induce the mitochondrial abnormalities that, in turn, lead to the excessive release of free-radicals.
For this grant, Dr. Perry's team will conduct a more extensive study of abnormal mitochondria using autopsied brain tissue. The researchers hope to learn more about how APP and other proteins may cause mitochondrial abnormalities. In addition, they will further analyze how these abnormalities may be associated with loss of mitochondrial function. Results from the study could lead to new therapeutic avenues in the treatment of Alzheimer's disease.