Researchers have assumed for quite some time that amyloid brain plaques in autopsies for Alzheimer’s patients are said to be quite injurious and cause the disease. But in a shocking revelation, a research from Washington University in St. Louis disclosed that brain plaques were apparently found in the autopsies of people with no indications of mental impairment.
This research claimed to exhibit for the first time that brain plaques in apparently healthy people seemed to be linked to augmented threat of diagnosis with Alzheimer’s disease years later. The researchers account that volunteers with brain plaques appear to have more chances for declining scores on yearly cognitive tests, to display indications of reduction in a major brain region affected by Alzheimer’s and to finally be detected with the disease.
“We don’t have enough data yet to definitively say that people who scan positive for these brain plaques have presymptomatic Alzheimer’s disease, but something is clearly going on that does not bode well for the health of their aging brains,” commented John C. Morris, M.D., the Harvey A. and Dorismae Hacker Friedman Distinguished Professor of Neurology and director of Washington University’s Alzheimer’s Disease Research Center (ADRC) and the Friedman Center for Aging,
Morris and others at the ADRC seemed to have earlier discovered the confirmation that Alzheimer’s disease damages the brain for years before the usual diagnosis. They appear to be insisting for earlier identification as a necessary step to effective treatment of Alzheimer’s disease. But to do that they primarily ought to look for initial pointers of disease and then wait years to observe if people with the signal could develop symptomatic Alzheimer’s in the future.
The new researches could be feasible due to the growth of an imaging agent, Pittsburgh Compound B (PiB) that enabled researchers to use positron emission tomography scans to diagnose amyloid plaques in living brains for the first time.
Magnetic resonance imaging scans supposedly examined by Denise Head, Ph.D., assistant professor of psychology, exposed that brain regions hit hard by Alzheimer’s disease like the parahippocampal gyrus, seemed to be smaller in subjects with plaques.
In the second research which was headed by Morris, the scientists apparently followed a group of around 159 volunteers. These subjects’ ages ranged from 51 to 88 who were scanned using PiB between 2004 and 2008. When they were scanned, nobody appeared to display any signs of mental impairment. Around Twenty-three of the volunteers later contracted mild impairment, and around nine members of that group were detected with Alzheimer’s disease.
Those who supposedly remained mentally healthy did not scan positive for plaques, but volunteers later apparently detected with problems did. Comparisons of the volumes of major brain structures is said to have disclosed the same differences observed in the other research. Subjects who developed mental impairment appear to have had considerable decrease in their parahippocampal gyrus and other structures affected by Alzheimer’s.
Morris is of the opinion that premature identification and examining of new treatments could be feasible in the subsequent 10 years.
The findings were published in the Archives of Neurology.