New Research Co-Funded by Cure Alzheimer’s Fund Shows New Gene May Hold Key to Treatment
Posted: April 25, 2013 at 12:50 pm
Study shows that blocking a gene known as CD33 could enhance the brains ability to clear plaque-forming proteins linked to the development of Alzheimer's disease.
BOSTON (PRWEB) April 25, 2013
Too much CD33 appears to promote late onset Alzheimers by preventing support cells from clearing out beta-amyloid containing plaques, said Tanzi in a release issued by NIMH. The same release quotes Thomas R. Insel, M.D., Director of NIMH, as saying, These results reveal, for the first time, a potentially powerful mechanism for protecting neurons from damaging toxicity and inflammation in brain disorders.
The CD33 gene that produces the protein was one of four new AD gene candidates identified by Tanzi and colleagues in the Cure Alzheimers Fund supported Alzheimers Genome Project in 2008. The study was cited by TIME/CNN as one of that years Top Ten Medical Breakthroughs.
In the new study, Tanzi and colleagues discovered that a variant of the CD33 gene that protects against AD, lowered levels of CD33 in the brain leading to more efficient clearance of beta-amyloid. Increased CD33 levels were observed specifically on the surface of microglial cells in autopsied brains of Alzheimers patients. Microglial cells are support cells in the brain that clear away debris, including deposits of the amyloid beta protein. The study showed that higher CD33 levels in the microglial cells impaired their ability to ingest beta-amyloid and break it down. In contrast, blocking CD33 activity enhanced the ability of microglial cells to clear away beta-amyloid. When Tanzi and colleagues inactivated the CD33 gene in a mouse model of Alzheimers disease, levels of beta-amyloid and senile plaques were dramatically decreased in the brain.
Collectively, these findings suggest that CD33 is a key mediator of beta-amyloid accumulation in the brain. The results imply that blocking CD33 would enhance the brains ability to clear beta-amyloid more efficiently, reducing downstream AD pathology. Tanzis team is now trying to identify drugs that can inactivate CD33 as novel means for treating and preventing AD.
About Cure Alzheimers Fund
In seven years, with $20 million invested in research, Cure Alzheimers Fund has a strong track record in funding novel approaches to understanding the causes of Alzheimers disease and the biological processes that drive the pathology. Cure Alzheimers Fund has supported 72 projects in 51 laboratories of leading Alzheimers researchers in the US and abroad. Cure Alzheimers Fund is a 501c3 public charity and seeks no financial gain for its founders, donors or researchers. The Founders and Board members pay all expenses of the Foundation so that all contributions from others go directly to research.
Andrea Garvue Cure Alzheimer's Fund 703-276-2772 13 Email Information
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New Research Co-Funded by Cure Alzheimer’s Fund Shows New Gene May Hold Key to Treatment
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