A recent study conducted by a team at Purdue University sheds new light on the role of fats in the development of Alzheimer’s disease. The results, published in the journal Immunity, show that an excess of lipids in the brain’s immune cells—microglia—impairs their ability to combat pathological changes and leads to worsening neurodegeneration. 

Until now, most therapies have focused on the classic symptoms of the disease—beta-amyloid plaques and tau protein tangles. However, the team led by Professor Gaurav Chopra points out that restoring proper functioning of the brain’s immune cells by limiting fat accumulation may be key. 

Scientists demonstrated that near beta-amyloid plaques, microglia produce excessive amounts of fatty acids that are then converted into triglycerides and stored within the cells. This process is driven by the enzyme DGAT2, whose overabundance causes microglia to become “overloaded” with fat and lose their defensive functions. Blocking or degrading this enzyme in animal models reduced plaque levels, improved microglial condition, and supported neuronal health. 

The researchers suggest that this discovery opens the door to new lipid biology-based therapies that may enhance the brain’s natural defense mechanisms. 

This work is part of the One Health initiative at Purdue University, which combines research on human, animal, and plant health.