Scientists may have unlocked a new key to fighting Alzheimer’s disease, as a recent study suggests that the root cause lies in a build-up of fat droplets within brain cells. Michael Haney at the University of Pennsylvania believes that targeting these droplets could lead to more effective treatments, opening up a new avenue for therapeutic development.

For decades, the blame for Alzheimer’s has been placed on protein culprits such as sticky beta-amyloid plaques and tangled tau proteins within brain cells. However, a new study suggests that fat droplets could also play a significant role in the development of the disease. Fat droplets have been observed in the brains of individuals who have died from Alzheimer’s, indicating their potential involvement in the disease.

Michael Haney’s investigation of the APOE gene, a major risk factor for Alzheimer’s, revealed that different versions of the gene exist, with APOE4 carrying the highest risk. His team found that immune cells in APOE4 brains produced more of an enzyme that boosted fat storage. Additionally, exposing immune brain cells to amyloid, another suspect in Alzheimer’s, increased fat build-up, especially in APOE4 cells.

The researchers propose that amyloid buildup triggers fat accumulation in immune cells, leading to tau tangles in neurons, causing cell death and memory loss. Genes linked to a slightly increased Alzheimer’s risk often affect fat metabolism or the immune system, further strengthening the fat droplet theory.

This study sheds new light on the potential role of fat deposits in brain cells in causing Alzheimer’s, offering a fresh perspective for future research and treatment development.