Researchers at Oregon Health & Science University's Neurological Sciences Institute (NSI) have located a possible target for future therapies aimed at delaying or stopping Alzheimer's disease. Specifically, the therapy would target a structure in brain cells previously identified as being heavily involved in the degenerative disease.
The research was led by P. Hemachandra Reddy, Ph.D., NSI scientist and senior author of the study. The results are published in the May 1 issue of the journal Human Molecular Genetics.
"This latest research more clearly demonstrates how structures, called mitochondria, in brain cells are a key part of the disease process in Alzheimer's. In fact, mitochondria appear to be a site where significant disease progression takes place," explained Reddy. "Research published by our lab in 2004 highlighted genes tied to this process. We also believe that toxins produced by the mitochondria contribute to Alzheimer's disease progression. In other words, the entire system may be one big feedback loop. Therefore, it is possible that therapies which encourage normal mitochondrial function may in fact delay or stop the disease in its early stages by breaking the loop."
To conduct the research, Reddy and his colleagues studied mice that are bred to have an Alzheimer's-like neurodegenerative disease. Like human Alzheimer's patients, the brains of these mice produce elevated levels of amyloid precursor protein (APP). They also develop formations called beta amyloid plaques. By observing mitochondrial function in brain cells of these mice, Reddy and his colleagues determined that beta amyloid could be found both inside and outside of the mitochondria. Because mitochondrial oxidative damage is a hallmark of Alzheimer's, the scientists believe the higher accumulations of these substances may be responsible. In addition, the scientists found increased levels of hydrogen peroxide in the Alzheimer's mice, likely produced by the mitochondria due to the oxidative damage.