Protein may help detect Alzheimer's
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CHICAGO, July 10 (Reuters) - Sampling spinal fluid for a protein that makes up the plaques that clog the brains of Alzheimer's disease patients may help diagnose the mind-wasting disease, researchers said on Monday.
As plaques build up in the brain, levels of the protein -- A beta 42 -- are thought to decline elsewhere in the body, including the spinal fluid, according to the study appearing in the Archives of Neurology.
Other than giving suspected Alzheimer's patients mental tests, a diagnosis can only be confirmed after death from the tell-tale plaques found in the brain.
One hundred eight-four adults averaging 50 years old and free of Alzheimer's at the start of the study had their spinal fluid tested for the protein found in brain plaques.
In subjects with a genetic predisposition to Alzheimer's disease, protein levels in the spinal fluid declined slightly through adulthood and then dropped sharply between age 50 and 60 -- presumably as plaque formation in their brains accelerated.
In people without the genetic predisposition, protein levels in the spinal fluid rose until age 50, then began declining slowly.
No direct connection was found between levels of the protein and Alzheimer's symptoms, but the mental decline from Alzheimer's is thought to progress only after years of plaque buildup and usually becomes evident in old age, the study said.
"These findings have implications for the preclinical diagnosis of Alzheimer's disease, as well as for treatment," said study author Elaine Peskind of VA Puget Sound Health Care System and University of Washington School of Medicine, Seattle.
"Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid (plaque) deposition," she added.
As plaques build up in the brain, levels of the protein -- A beta 42 -- are thought to decline elsewhere in the body, including the spinal fluid, according to the study appearing in the Archives of Neurology.
Other than giving suspected Alzheimer's patients mental tests, a diagnosis can only be confirmed after death from the tell-tale plaques found in the brain.
One hundred eight-four adults averaging 50 years old and free of Alzheimer's at the start of the study had their spinal fluid tested for the protein found in brain plaques.
In subjects with a genetic predisposition to Alzheimer's disease, protein levels in the spinal fluid declined slightly through adulthood and then dropped sharply between age 50 and 60 -- presumably as plaque formation in their brains accelerated.
In people without the genetic predisposition, protein levels in the spinal fluid rose until age 50, then began declining slowly.
No direct connection was found between levels of the protein and Alzheimer's symptoms, but the mental decline from Alzheimer's is thought to progress only after years of plaque buildup and usually becomes evident in old age, the study said.
"These findings have implications for the preclinical diagnosis of Alzheimer's disease, as well as for treatment," said study author Elaine Peskind of VA Puget Sound Health Care System and University of Washington School of Medicine, Seattle.
"Therapeutic strategies aimed at prevention of Alzheimer's disease may need to be applied in early midlife or even younger ages to have maximal effect on amyloid (plaque) deposition," she added.
A recent study directed by Mount Sinai School of Medicine identifies a faulty molecule in the brain found in cases of mild cognitive impairment (MCI). Researchers say this faulty molecule may be responsible for the progression of MCI to mild Alzheimer's disease (AD) dementia. http://www.medicalnewstoday.com/medicalnews.php?newsid=46754&nfid=al
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