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Alzheimer's Disease Treatment May Involve Inhibiting Mitochondria Toxins - Brain Scans May Help Predict the Degenerative Disease

May 1st 2006

Alzheimer's Disease Treatment May Involve Inhibiting Mitochondria Toxins - Brain Scans May Help Predict the Degenerative Disease


Scientists have identified the key gene locations in brain cells where significant damage occurs in patients with Alzheimer’s disease.  Researchers at the Oregon Health & Science University's Neurological Sciences Institute (NSI) believe that this could lead to a possible target for future therapies. 

The results, published in the May 1st issue of the journal Human Molecular Genetics, identify mitochondria structures inside cells as being heavily involved in the degenerative disease.  The researchers believe that toxins created by the mitochondria contribute to the disease progression.

Dr. P. Hemachandra Reddy said “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."


Dr. Reddy is a scientist and the senior author of the study.  He added “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."

The researchers studied mice that were bred with an Alzheimer’s-like neurodegenerative disease. Like human Alzheimer's patients, the brains of these mice produced elevated levels of amyloid precursor protein (APP). The mice also developed formations called beta amyloid plaques.


Reddy and his colleagues found amyloid both inside and outside of the mitochondria.  The researchers say that “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.”

Reddy said “We believe that the disease produces mutant APP and beta amyloid which in turn impacts mitochondrial function. This results in increased production of hydrogen peroxide, resulting in a progression of the disease and higher levels of beta amyloid.  In other words -- this model appears to be a vicious cycle where damage to brain cells increases and in fact feeds upon itself."


Tissue taken from the brains of Alzheimer’s patients also confirmed increased levels of beta amyloid in brain cell mitochondria.  This appears to agree with their conclusions.

"The findings are very significant in providing a greater understanding the mechanisms behind Alzheimer's," explained study co-author Joseph F. Quinn, M.D., a clinical neurologist at the Layton Center for Aging & Alzheimer's Disease Research at OHSU and an associate professor of neurology, and cell and developmental biology in the OHSU School of Medicine. "In fact, OHSU is involved in a study funded by the National Institute on Aging of antioxidant therapy for Alzheimer's including antioxidants directed at the mitochondria."

Reuters reported that scientists have identified structural and metabolic brain changes that may predict dementia or cognitive decline in normal older adults.  They found that the pattern of glucose metabolism, together with the location of brain regions that are predictive of Alzheimer's "suggests that these findings are due to the detection of presymptomatic Alzheimer's disease," the researchers conclude.  It is hoped that PET (positron emission tomography) magnetic resonance scans become predictors of the disease.  This research was conducted by Dr. William Jagust at the University of California at Berkeley. 

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