Researchers at Purdue University have found that excess fat in the brain’s resident immune cells, called microglia, impairs their ability to combat Alzheimer's disease. The study findings were published in the journal Immunity.

Microglia clean the tissue of various types of cellular debris, including the toxic protein beta-amyloid. However, in Alzheimer's disease, these cells accumulate near amyloid plaques and begin to accumulate lipid droplets.

Aforesaid researchers have found that microglia near the plaques contain twice as much fat. Moreover, these cells remove beta-amyloid 40% less efficiently than healthy cells. The reason is the excess fatty acids, which microglia convert into triglyceride, a stored form of fat. This process worsens with age and the development of Alzheimer's disease. According to researchers, fat deposits literally paralyze microglia, preventing them from performing their protective functions.

Respective studies on mice have shown that the DGAT2 enzyme, which is responsible for the final phase of fat accumulation, plays an important role in this process. The research team found that the level of this enzyme increases in Alzheimer’s disease not due to increased production, but due to a malfunction in the mechanisms of its degradation.

In experiments, researchers suppressed DGAT2 function, or accelerated its degradation, using two different molecules. This led to a decrease in fat accumulation in microglia, restored their ability to remove amyloid plaques, and improved the health of neurons in the animals.

The aforementioned researchers note that the disruption of lipid metabolism in the brain’s immune cells is not a side effect, but an active factor in the development of the Alzheimer's disease.

This discovery could form the basis for new Alzheimer's disease therapies that aim not only to remove plaques, but also to restore the brain's internal defenses.