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Alzheimer’s Disease: Landmark Gene Discoveries Open Up New Therapeutic Opportunities
Date:9/23/2013

Boston, MA (PRWEB) September 23, 2013

In a paper recently published in the prestigious journal Neuron, Harvard Medical School/Mass General Hospital Geneticist Dr. Rudy Tanzi, together with lead author, Dr. Jaehong Suh and their team, identified two rare mutations in the human gene called "ADAM10" that lead to the most common, late-onset variant of Alzheimer's. Tanzi's research suggests that the ADAM10 gene makes an enzyme called alpha-secretase, which cleaves the Amyloid Precursor Protein (APP) to prevent the formation of beta-amyloid, the toxic protein that triggers brain pathology in Alzheimer's disease.

This landmark genetic discovery by Tanzi, who is also Research Consortium Chair at Cure Alzheimer' Fund, further supports the widely-held "Amyloid Hypothesis" and suggests specific new therapeutic approaches to stopping Alzheimer's disease.

In their study, Tanzi and Suh first identified two new human gene mutations in ADAM10 and then inserted them into Alzheimer's mouse models to track their effects in the brain. Subsequently, the team was able to demonstrate how the mutant genes diminish alpha-secretase activity leading to increased levels of beta-amyloid, the main component of senile plaques in Alzheimer’s disease.

These findings are the first to document novel Alzheimer's gene mutations in animal models since the mutations in the original four Alzheimer's genes -- APP, PSEN1, PSEN2, and APOE -- were discovered in the 1990’s.

Furthermore, the effects in mouse brains strongly suggest that diminished alpha-secretase activity owing to the ADAM10 gene mutations causes Alzheimer's and therefore supports ADAM10 as a promising therapeutic target for the treatment and prevention of the disease. "If we can find or de
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