People with specific mutations in the gene TREM2 are three times more likely to develop Alzheimer’s disease than those who carry more common variants of the gene. But until now, scientists had no explanation for the link.
New research in mice at Washington University School of Medicine in St. Louis indicates that the high-risk mutations in TREM2 cause an energy deficit in cells that clear away debris in the brain. When such cells are running on empty, they can’t protect neurons from harmful plaques that tend to collect in the brain as people get older.
“Everybody has some plaques, but the activity of these cells affects how much damage the plaques do,” said senior author Marco Colonna, MD, the Robert Rock Belliveau, MD, Professor of Pathology. “So if you have dysfunction in these cells, you have an accelerated process of neurodegeneration. If the cells are more functional, you can delay the process.”
The findings suggest that energizing the brain’s cleanup crew – made up of a kind of immune cell known as microglia – could reduce neurological damage and forestall the memory loss and confusion experienced by people with Alzheimer’s disease.
The original and full article was published at Washington University’s School of Medicine: Alzheimer’s risk linked to energy shortage in brain’s immune cells