Recent research suggests a new culprit in the fight against Alzheimer disease: fat droplets accumulating within brain cells. While scientists have long focused on protein abnormalities like beta-amyloid plaques and tau proteins, this study from the University of Pennsylvania highlights the role of fat droplets as a potential key factor in the disease’s progression.
Michael Haney and his team at the University of Pennsylvania explored the role of the APOE gene, a major risk factor for Alzheimer, in controlling fat movement in and out of cells. They discovered that different versions of the APOE gene, particularly APOE4, which carries the highest Alzheimer’s risk, were associated with increased fat storage in immune cells within the brain.
By analyzing brain cells from deceased Alzheimer’s patients with different APOE gene variants, the researchers observed higher levels of an enzyme responsible for fat storage in APOE4 brains. Furthermore, when immune brain cells from individuals with different APOE variants were exposed to amyloid, a hallmark of Alzheimer’s, they exhibited increased fat accumulation, particularly in APOE4 cells.
The study proposes a mechanism in which amyloid buildup triggers fat accumulation in immune cells, subsequently leading to the formation of tau tangles in neurons, ultimately resulting in cell death and memory loss.
These findings shed light on the complex interplay between genetic factors, fat metabolism, and immune responses in Alzheimer’s disease. Understanding the role of fat droplets in the disease process could pave the way for novel therapeutic approaches targeting this mechanism, potentially leading to more effective treatments for Alzheimer’s in the future.
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