Energy Shortage in Brain’s Immune Cells Might Explain Alzheimer’s Risk with TREM2 Mutations

Energy Shortage in Brain’s Immune Cells Might Explain Alzheimer’s Risk with TREM2 Mutations
A lack of energy in brain cells called microglia might explain why people with mutations in the TREM2 gene are more likely to develop Alzheimer's disease, according to a mouse study that showed exhausted microglia lacked the capacity to confine amyloid plaques. By restoring the energy levels in these cells, it might be possible to treat people with this specific genetic makeup. But researchers say their findings might have even wider implications. If it is also possible to make microglia more energized in people with normal brain function, it might turn out to benefit all Alzheimer's patients, the team at Washington University School of Medicine (WUSC) suggested. “Everybody has some plaques, but the activity of these cells affects how much damage the plaques do,” Marco Colonna, MD, the Robert Rock Belliveau, MD, Professor of Pathology and the study's senior author, said in a press release. “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,” he said. The study, “TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease,” is the first to explain why mutations in the TREM2 gene increase the risk for Alzheimer's. Microglia — which are also the main immune cell of the brain — play a crucial role in keeping the brain litter-free. With their ability to engulf debris and dead cells, they play a similar role in the brain as macrophage immune cells do in the rest of the body. In their report, publi
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