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1 comment   Listen   Print   article:337744:13::0
In the Media

article imagePromising development with Alzheimer's Disease research

By Tim Sandle
Nov 26, 2012 in Science
Scientists have managed to reduce the changes that occur in the body with the onset of Alzheimer's disease in mice. The research has the potential to lead to a major breakthrough in the search for a treatment for the disease.
A science group based at Charité -- Universitätsmedizin Berlin and the University of Zurich have shown that by using a chemical to block a signal in the immune system of mice that the progression of Alzheimer's disease can be slowed.
Alzheimer's disease is a form of dementia that causes gradual deterioration of the memory and thinking process and, eventually, death. Furthermore, new research, reported on the Digital Journal, has shown how the chemical changes in the brain, which can lead to Alzheimer's disease, affect spatial memory.
It is thought that the accumulation of particular abnormal proteins (including one called amyloid-ß (Aβ)) , in patients' brains, plays a central role in this disease. In many cases Aβ is the main component of deposits found in the brains of patients with Alzheimer's disease.
According to a research note, what the scientists did was to take mice with Alzheimer's disease and they then turned off particular immune system transmitters in the mice. After a period of time, this 'off-switch' showed that the mice had much lower levels of the amyloid-ß deposits.
Importantly, follow-up experiments showed substantial improvements when the mice were subjected to behavioral testing
The significance of the research is that it could not only slow down Alzheimer's disease in those who already have the condition, it could have the potential to be used as a means of preventing the disease from the outset. Currently there is neither a cure nor a treatment to stop or reverse the progression of Alzheimer’s.
The study was led by Frank L. Heppner and Burkhard Becher. The research findings have been published in Nature Medicine.
article:337744:13::0
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