PGC-1 gene linked with the onset of type 2 diabetes seems to control glucose. A latest research triggered by the Mount Sinai School of Medicine claims that PGC-1 is present in lower than normal levels among patients with Alzheimer’s disease. Experts have highlighted a probable mechanism which elucidates the relationship between type 2 diabetes and the occurrence as well as progression of Alzheimer’s disease.
Investigations have suggested that healthy elderly individuals face double the risk of developing Alzheimer’s, but the mechanism behind it was unclear. Mice were genetically engineered with Alzheimer’s disease which is similar to that observed in humans. Researchers discovered that proliferator-activated receptor coactivator 1 (PGC-1) gene is a hallmark in controlling glucose. The gene may be in lower levels among Alzheimer’s patients because PGC-1 encourages degradation of the enzyme beta-secretase (BACE).
“Our research is the first to find that PGC-1 is a common denominator between Type 2 diabetes and Alzheimer’s disease. This discovery will have significant implications for the more than five million Americans affected by Alzheimer’s disease, a number that is expected to skyrocket in the next three decades as the population ages. We look forward to continuing to research this discovery and translate it into the development of novel approaches for disease prevention and treatment,” said Dr. Giulio Maria Pasinetti, MD, PhD, The Saunder Family Professor in Neurology, and Professor of Psychiatry and Geriatrics and Adult Development at Mount Sinai School of Medicine and the lead investigator.
Direct involvement of ACE in processing and ultimately generating β-amyloid appeared. Researchers assume that β-amyloid is an abnormal protein significantly associated to Alzheimer’s and brain degeneration. It is presumed that if PGC-1 can be manipulated pharmacologically to prevent BACE accumulation in the brain, new treatments and preventative strategies in Alzheimer’s disease can be laid down.
The research is published in the journal Aging Cell.