A new study suggests that fat accumulation inside brain immune cells may play a critical role in Alzheimer’s disease. Purdue University researchers found that microglia, the brain’s protective cells, lose their ability to clear toxic proteins when overloaded with fat. This buildup stems from excessive conversion of fatty acids into stored fat, a process driven by the enzyme DGAT2. Instead of providing energy, these fat deposits paralyze microglia, leaving them unable to remove amyloid beta plaques.
The team discovered that reducing DGAT2 levels or blocking its activity restored microglial function, enhanced the clearance of amyloid beta, and improved brain health in animal models. These findings highlight a new “lipid model” of neurodegeneration, shifting attention from traditional protein targets to fat metabolism in brain cells. By linking lipid buildup to immune dysfunction, the research opens the door to novel therapies aimed at restoring the brain’s own defenses against Alzheimer’s.
26-09-2025