Biologists at the University of California-Irvine have trained their sights on the inflammatory aspects of Alzheimer's disease as way to possibly derail the pathology of the brain disease.
In a paper recently published in Proceedings of the National Academy of Sciences, researchers at the university’s School of Biological Sciences say the role of a protein called TOM-1 may help rebalance Alzheimer's research toward the inflammatory processes that underlie the disease. Their findings come from a rodent model of the Alzheimer's, so they must be viewed as preliminary.
“Scientists have known for a long time that inflammation is a driver of Alzheimer’s disease,” said Frank M. LaFerla, Ph.D., the school’s dean and whose laboratory conducted the research. “But inflammation is complex and involved many factors. That’s why we decided to look at TOM-1.”
TOM-1 helps regulate a key component of the inflammatory response, but its role in the Alzheimer’s has largely been unexplored, explained Alessandra C. Martini, Ph.D., the paper’s first author and post-doctoral researchers in the lab.
“We were interested in TOM-1 because its levels are low in the Alzheimer’s brain and in the brains of Alzheimer’s rodent models,” Martini said.
The scientists found that reducing the amount of TOM-1 in Alzheimer’s rodent models increased pathology and inflammation and exacerbated cognitive problems associated with the disease. When TOM-1 levels were restored, the effects were reversed.
“You can think of TOM-1 as being like the brakes of a car and the brakes aren’t working for people with Alzheimer’s,” LaFerla said. “This research shows that fixing the brakes at the molecular level could provide an entirely new therapeutic avenue.”
Source: UCI News, September 30