A gene related to Alzheimer’s Disease has been isolated by researchers at Tel Aviv University in Israel. This could be a major step in finding a cure for this disease.
It has been known for some time now that there is a genetic predisposition involved in the development of Alzheimer’s Disease. It is not a communicable illness, nor is it caused by environmental factors. But some external factors may hasten its onset.
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But sufferers and the people who love them are not really concerned with the how or why, they just want a cure already. So how does isolating such a gene help?
Well it could lead to testing to see who is at risk for getting Alzheimer’s and as gene therapies advance, the gene itself could be integral to a future cure.
The gene, called RGS2 (Regulator of Protein Signaling 2), has never before been implicated in AD.
The research was led by Dr. David Gurwitz of the Department of Human Molecular Genetics and Biochemistry at TAU’s Sackler School of Medicine and Prof. Illana Gozes, the incumbent of the Lily and Avraham Gildor Chair for the Investigation of Growth Factors; Head of the Elton Laboratory for Molecular Neuroendocrinology at TAU’s Sackler School of Medicine; and a member of TAU’s Adams Super Center for Brain Studies and TAU’s Sagol School of Neuroscience.
“Alzheimer’s researchers have until now zeroed in on two specific pathological hallmarks of the chronic neurodegenerative disease: deposits of misfolded amyloid-β (Aβ) peptide plaques, and phosphorylated tau protein neurofibrillary tangles found in diseased brains, ” Dr. Gurwitz said. “But recent studies suggest amyloid-β plaques are also a common feature of healthy older brains. This raises questions about the central role of Aβ peptides in Alzheimer’s disease pathology.”
“Several genes and their protein products are already known to be implicated in Alzheimer’s disease pathology, but RGS2 has never been studied in this context, ” Dr. Gurwitz said. “We now propose that whether or not Aβ is a primary culprit in Alzheimer’s disease, neuroprotective mechanisms activated during early disease phases lead to reduced RGS2 expression.”
