A study suggested that diametric shifts in the levels of two proteins involved in folding, moving and cutting other proteins enables accumulation of the destructive brain plaque found in Alzheimer’s disease.
VPS35 is a protein that folds others into specific positions to unleash their functions.
According to Georgia Health Sciences University researchers, when levels are reduced as they are in aging, it unleashes the normally dormant BACE1, a protein responsible for beta amyloid plaque production.
Developmental neurobiologist and Weiss Research Professor at GHSU and the study’s corresponding author Dr. Wen-Cheng Xiong said that when researchers modified a mouse model of Alzheimer’s so that VPS35 production was essentially cut in half, BACE1 activity was increased, accelerating aging and development of related problems such as memory deficits and poor communication between brain cells as well as beta amyloid accumulation.
Xiong said that it was known that expression of VPS35 was down and BACE1 was up in Alzheimer’s but the direct relationship was unknown.
“We believe impaired function of VPS35 could be a risk factor for Alzheimer’s and Parkinson’s diseases,” Xiong said.
Discovering the relationship makes VPS35 a potential biomarker for the diseases as well as a target for new therapies to keep VPS35 elevated.
The accelerated aging model Xiong developed and patented will enable these future drug studies.
The study was published in a report in The Journal of Cell Biology.