MONDAY, April 14, 2003 (HealthDayNews) -- A protein long associated with Alzheimer's disease causes serious damage by sealing off mitochondria in affected neurons, leading to an "energy crisis" and a buildup of toxins that causes the neurons to die.
The discovery of that pathway by University of Pennsylvania scientists, which appears in the April 14 issue of the Journal of Cell Biology, offers the first specific biochemical explanation for how the brain is damaged by Alzheimer's disease.
The finding could help lead to development of medicines to counter the protein's action.
The normal function of this protein, called amyloid precursor protein (APP), remains unknown. However, in studies with mice, University of Pennsylvania scientists determined that a stretch of 50 amino acids in APP causes damage by starving mitochondria and the cells they nourish. The mitochondria are the main energy source of the cell.
"APP has an acidic, negatively charged region that causes it to jam irreversibly while traversing protein transport channels in the mitochondrial membrane. This hampers, and eventually completely blocks, mitochondria's ability to import other proteins and produce cellular energy," senior author Narayan G. Avadhani says in a news release.
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