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.
Dan Wilson
Best Syndication
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