Posted July 18, 2011
Dr. Sam Gandy, a CAF Research Consortium member, and Rachel Lane, a postdoctoral researcher in Gandy’s lab, presented their findings today at the Alzheimer’s Annual International Conference in Paris. Their research identified a gene, called SorCS1, that is for a protein that can cause Type 2 diabetes and also may kill nerve cells in the brain, thus contributing to Alzheimer’s.
According to a statement released by Mount Sinai School of Medicine in New York, where Dr. Gandy is the Associate Director of the Alzheimer’s Disease Research Center:
“The researchers determined various “traffic patterns” in the cell for the amyloid precursor protein (APP) that makes Abeta and uncovered how much APP is converted into the toxic, and ultimately nerve-killing, Abeta. In some experiments Drs. Lane and Gandy altered the dose of the diabetes gene, SorCS1, and evaluated how that changed the “traffic pattern” that APP used to move around the cell and generate Abeta. In other experiments, Dr. Lane made small changes in the SorCS1 gene’s and again saw dramatic changes in the “traffic pattern” of APP around the cell.
These data suggest that SorCS1 controls the movement of APP within the cell between areas where Abeta is readily made to areas where Abeta is not so easily made. In turn, the “traffic pattern” of influences the amount of Abeta being made by cells. The implication is that people with deficiencies in SorCS1 are at higher risk of developing Alzheimer’s disease because their APP spends too much time in the region of the cell where APP is broken down to make the toxic Abeta.”
