Alzheimer's Preventative On The Horizon?
One of the worst things about Alzheimer's disease has always been that there's no way to prevent it. But that may be changing.
A new study has found that a protein may inhibit the beginning of the disease.
According to newswise.com, scientists at NYU Langone Medical Center have identified a compound in animal studies that reduced by more than half the levels of amyloid (a starchlike protein that is deposited in the liver, kidneys, spleen, or other tissues in certain diseases) proteins in the brain associated with Alzheimer’s disease. The researchers hope that someday a treatment based on the molecule could be used to ward off the neuro-degenerative disease since it may be safe enough to be taken daily over many years.
Amyloid beta contributes to the plaques that develop in the Alzheimer's brain.
“What we want in an Alzheimer’s preventive is a drug that modestly lowers amyloid beta and is also safe for long-term use,” the Web site quotes Martin J. Sadowski, MD, PhD, associate professor of neurology, psychiatry, and biochemistry and molecular pharmacology. “Statin drugs that lower cholesterol appear to have those properties and have made a big impact in preventing coronary artery disease. That’s essentially what many of us envision for the future of Alzheimer’s medicine.”
Newswise reports that the prime target for Alzheimer’s prevention is amyloid beta. Decades before dementia begins, this small protein accumulates in clumps in the brain, it points out. Modestly lowering the production of amyloid beta in late middle age, and thus removing some of the burden from the brain’s natural clearance mechanisms, is believed to be a good prevention strategy.
Researchers two years ago reported that something like this happens naturally in about 0.5 percent of Icelanders, due to a mutation they carry that approximately halves amyloid beta production throughout life. These fortunate people show a slower cognitive decline in old age, live longer, and almost never get Alzheimer’s.
Prevention of Alzheimer’s dementia is now considered more feasible than stopping it after it has begun, when brain damage is already severe. Every prospective Alzheimer’s drug in clinical trials has failed even to slow the disease process at that late stage. “The key is to prevent the disease process from going that far,” Dr. Sadowski says.
So this might prove to be the miracle we've been waiting for.
A new study has found that a protein may inhibit the beginning of the disease.
According to newswise.com, scientists at NYU Langone Medical Center have identified a compound in animal studies that reduced by more than half the levels of amyloid (a starchlike protein that is deposited in the liver, kidneys, spleen, or other tissues in certain diseases) proteins in the brain associated with Alzheimer’s disease. The researchers hope that someday a treatment based on the molecule could be used to ward off the neuro-degenerative disease since it may be safe enough to be taken daily over many years.
Amyloid beta contributes to the plaques that develop in the Alzheimer's brain.
“What we want in an Alzheimer’s preventive is a drug that modestly lowers amyloid beta and is also safe for long-term use,” the Web site quotes Martin J. Sadowski, MD, PhD, associate professor of neurology, psychiatry, and biochemistry and molecular pharmacology. “Statin drugs that lower cholesterol appear to have those properties and have made a big impact in preventing coronary artery disease. That’s essentially what many of us envision for the future of Alzheimer’s medicine.”
Newswise reports that the prime target for Alzheimer’s prevention is amyloid beta. Decades before dementia begins, this small protein accumulates in clumps in the brain, it points out. Modestly lowering the production of amyloid beta in late middle age, and thus removing some of the burden from the brain’s natural clearance mechanisms, is believed to be a good prevention strategy.
Researchers two years ago reported that something like this happens naturally in about 0.5 percent of Icelanders, due to a mutation they carry that approximately halves amyloid beta production throughout life. These fortunate people show a slower cognitive decline in old age, live longer, and almost never get Alzheimer’s.
Prevention of Alzheimer’s dementia is now considered more feasible than stopping it after it has begun, when brain damage is already severe. Every prospective Alzheimer’s drug in clinical trials has failed even to slow the disease process at that late stage. “The key is to prevent the disease process from going that far,” Dr. Sadowski says.
So this might prove to be the miracle we've been waiting for.
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