An Alzheimer's Minibreakthrough


By: Heather J. Chin , The Bulletin

The dementia and loss of mental faculties resulting from Alzheimer's disease has long been recognized, but the exact cause has remained elusive, until perhaps now.
New research suggests that one form of beta-amyloid protein - which clumps around an afflicted brain's neurons and forms plaque that inhibits and destroys neurons needed for daily functions and memories - causes symptoms of Alzheimer's.
Previous research had been unable to determine whether the beta-amyloid plaque was a cause or a side effect of Alzheimer's disease.
In the new study, researchers caused Alzheimer's symptoms of impaired memory function in rats by injecting them with a two-molecule soluble form of beta-amyloid protein.
One-molecule and three-molecule forms of both soluble and insoluble proteins did not trigger illness in the rats, which researchers say may explain why some people with beta-amyloid plaque don't exhibit such symptoms.
Dr. Ganesh M. Shankar and Dr. Dennis J. Selkoe of Harvard Medical School published their findings in Sunday's online edition of the journal Nature Medicine. In the report, they noted that when studies were also conducted on mice, the brain cell density was reduced by 47 percent, and affected the synapses, or connections between cells that are necessary for cell communication.
Beta-amyloid extracts were taken from the brains of people who had donated their bodies to medical research.
This is the first time that research has showed the effect of a particular type of beta-amyloid in the brain, said Dr. Marcello Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging, to the Associated Press.
He added that the revelation that only one of three types of the proteins had a damaging effect on the brain is important because doctors have long wondered why they find some plaque-covered brains in autopsy that belong to a person who didn't have Alzheimer's.
"A lot of work needs to be done," stated Dr. Morrison-Bogorad, as to why one protein has a damaging effect and not others. "Nature keeps sending us down paths that look straight at the beginning, but there are a lot of curves before we get to the end."
The Harvard study was funded by the National Institute on Aging, Science Foundation Ireland, Wellcome Trust, the McKnight and Ellison foundations and the Lefler Small Grant Fund.
In a separate study out of the Feinstein Institute of Medical Research in New York, Dr. Yousef al-Abed, chief of medicinal chemistry, and his colleagues Michael Bacher and Richard Dodel of Marburg University in Germany created and tested an experimental drug that they say might neutralize or reduce the effects of the beta-amyloid plaques in the patient's brain.
Published in the Journal of Experimental Medicine, the study's results describe an experimental medicine, CNI-1493, already being tested as a medicine for the bowel affliction called Crohn's disease, that targets and transforms amyloid in the brain so that it does not clump and form plaque and also loses its toxicity.
Their results show a 70 to 85 percent reduction of amyloid buildup in the cortex and the hippocampus - the two areas of the brain most affected in Alzheimer's patients and which affect memory, attention, perceptual awareness, language, consciousness and the regulation of emotion.
Heather Chin can be reached at heather.jean.chin@gmail.com

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