By Dr. Jeffrey Walden
Researchers at the University of New South Wales have identified decreased levels of a brain protein called Neural Cell Adhesion Molecule 2 (NCAM2) in the brains of Alzheimer’s patients, particularly in regions involved in learning and memory. By identifying a potential new molecular mechanism underlying the development of these plaques, the researchers have opened the door for further study with implications for the development of new treatments for Alzheimer’s disease.
NACM2 is one of a family of proteins involved in maintaining connections between brain cells. In their research, recently published in the Journal Nature Communications, the University of New South Wales group found that the lower levels of NCAM2 corresponded with elevated levels of another group of proteins called beta-amyloids. These proteins break down NCAM2. Excessive amounts of beta-amyloid proteins are known to clump together to create plaques that interfere with normal communication between brain cells. This plaque build-up is one of the underlying biological mechanisms thought to cause Alzheimer’s symptoms.
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