Potential Alzheimer's Drug Target Identified
( CD36 membrane protein )
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As much as they devastate neurons, the pathologic amyloid-beta particles linked to Alzheimer's disease also severely disturb brain blood flow, contributing to dementia, researchers at Weill Cornell Medical College have found.
But there may be some good news, the scientists report in the March 7 early edition of the Proceedings of the National Academy of Sciences (PNAS). They have found a single receptor, CD36, inside affected blood vessels they say is key to the vascular damage, which suggests it could become a beneficial drug target.
The findings have "broad biological and clinical implications," says the study's lead investigator, Dr. Costantino Iadecola, the George C. Cotzias Distinguished Professor of Neurology and Neuroscience at Weill Cornell Medical College and a neurologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
Evidence has been building that Alzheimer's affects brain blood flow, contributing to dementia, and there has been growing interest in trying to understand how this happens and to develop countermeasures, he says.
"Now we know that when amyloid-beta particles -- the presumed culprit in Alzheimer's disease -- build up in the blood and brain, CD36 sets off a response that than ends up damaging the vessels, which reduces blood flow," Dr. Iadecola says. "This is like what happens in an ischemic stroke in that the brain does not receive sufficient nourishment, except that in Alzheimer's disease brain vessels are not blocked. In Alzheimer's disease there is sufficient blood flow to maintain a low level of brain activity, but not enough to provide the extra energy that brain needs when it becomes more active."
As proof of their discovery, the researchers found that when they disabled CD36 in experimental animals, the brain blood vessels worked just fine, supplying nutrition to neurons affected by Alzheimer's -- which helped them function better. "Our study is the first to identify CD36's role in Alzheimer's vascular troubles and to suggest that it could be a target for preventing some of the neuronal dysfunction that is observed in Alzheimer's disease," Dr. Iadecola says. Read more: medilexicon.com
But there may be some good news, the scientists report in the March 7 early edition of the Proceedings of the National Academy of Sciences (PNAS). They have found a single receptor, CD36, inside affected blood vessels they say is key to the vascular damage, which suggests it could become a beneficial drug target.
The findings have "broad biological and clinical implications," says the study's lead investigator, Dr. Costantino Iadecola, the George C. Cotzias Distinguished Professor of Neurology and Neuroscience at Weill Cornell Medical College and a neurologist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center.
Evidence has been building that Alzheimer's affects brain blood flow, contributing to dementia, and there has been growing interest in trying to understand how this happens and to develop countermeasures, he says.
"Now we know that when amyloid-beta particles -- the presumed culprit in Alzheimer's disease -- build up in the blood and brain, CD36 sets off a response that than ends up damaging the vessels, which reduces blood flow," Dr. Iadecola says. "This is like what happens in an ischemic stroke in that the brain does not receive sufficient nourishment, except that in Alzheimer's disease brain vessels are not blocked. In Alzheimer's disease there is sufficient blood flow to maintain a low level of brain activity, but not enough to provide the extra energy that brain needs when it becomes more active."
As proof of their discovery, the researchers found that when they disabled CD36 in experimental animals, the brain blood vessels worked just fine, supplying nutrition to neurons affected by Alzheimer's -- which helped them function better. "Our study is the first to identify CD36's role in Alzheimer's vascular troubles and to suggest that it could be a target for preventing some of the neuronal dysfunction that is observed in Alzheimer's disease," Dr. Iadecola says. Read more: medilexicon.com
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