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WVU finds promising treatment for Alzheimer's
Researchers take potential first step to cure brain degeneration
By Veronica Nett
The Charleston Gazette
CHARLESTON, W.Va.-- West Virginia researchers have found a promising treatment that might reverse the debilitating effects of Alzheimer's disease, and offer the first step toward a potential cure for the more than 5 million Americans who suffer from it.
In a study published this month in the Journal of Neuroscience, researchers at the Blanchette Rockefeller Neuroscience Institute have found the potential root cause of Alzheimer's, and a way to treat the symptoms of the disease.
The degeneration of synapses -- the point of connection between two nerve cells -- in the brain plays a critical role in the development of dementia in Alzheimer's patients, said Dr. Daniel Alkon, co-author of the study and scientific director of the BRNI at the West Virginia University Robert C. Byrd Health Sciences Center.
For decades, though, the thrust of research and pharmaceutical development has not been toward synapses loss but trying to reduce the amyloid plaques and neurofibrillary tangles - twisted fibers found inside the brain's cells - that form in the brain after the loss of synapses, Alkon said.
"Alzheimer's disease is not primarily a disease of plaques and tangles, as many had previously concluded," Alkon said. "It is most importantly a disease of synapses."
Alkon and his team are the first to achieve a fundamental molecular understanding of how synapses are lost in Alzheimer's patients before the plaques and tangles develop.
"In a way, I think we have the first comprehensive picture of the cause of this disease," Alkon said. "We're virtually looking at the entire picture. We're not looking at one aspect, not the plaques or the tangles or the synapses, we're looking at all of it, and by treating the target, we treat everything at once."
By targeting synapses loss, researchers have found a potential way to stop the development of plaques and tangles in the brain that contribute to dementia and other hallmarks of Alzheimer's, "virtually eliminating all other elements of the disease," Alkon said.
Researchers found that the use of Bryostatin and similar compounds target the enzyme PKCe, which controls the creation of synapses at the molecular level, Alkon said.
The compounds promoted the growth of new synapses and preserved existing synapses in the brain, Alkon said. They also stopped the decrease of PKCe and the increase of soluble Beta amyloid, meaning that the treatments could be used to prevent formation of plaques and tangles in the brain, he said.
The neuroscience institute has received approval to begin clinical testing of Bryostatin to treat the symptoms of Alzheimer's, and will begin testing in the next several months.
Researchers at the institute also are developing a skin test to identify Alzheimer's in patients during the early stages of the disease.
"Detection early and a vaccine to stop degeneration -- it's a potential cure, Alkon said."
The synaptogenic drugs designed by researchers at the institute also have potential in the treatment of traumatic brain injury and stroke, Alkon said.
"The potential is great," Alkon said. "We need to get clinical trials going. We feel the sooner we can get this to the patients, the better."
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