Unraveling Alzheimer’s: Investigating the Role of Brain Cell Fat Accumulation

A collaborative team comprising neurologists, stem cell specialists, and molecular biologists from various U.S. institutions, spearheaded by researchers at Stanford University School of Medicine, has unearthed compelling evidence suggesting that the fundamental cause of Alzheimer’s disease could be the accumulation of fat within brain cells. Their findings have been published in the esteemed journal Nature.
While previous studies have predominantly linked Alzheimer’s to the buildup of beta-amyloid plaques and the aggregation of tau protein within brain cells, this latest research sheds light on an alternative underlying mechanism. Alois Alzheimer, upon first identifying the disease, observed the presence of fat droplets accumulating within brain cells alongside the well-documented plaques and tau buildup. Surprisingly, subsequent investigations have largely overlooked the potential role of these fat deposits in disease progression.
Focusing their efforts on the APOE gene—a gene known to encode a protein crucial for transporting fat droplets into nerve cells—the research team delved into its implications for Alzheimer’s risk. Previous studies have identified four APOE variants, labeled APOE1 through APOE4, with APOE4 known for its heightened capacity to transport fat into brain cells compared to APOE2, which exhibits the least efficiency.
In their quest to discern the relationship between APOE variants and Alzheimer’s risk, the team conducted a series of experiments. Employing single-cell RNA sequencing, they analyzed the protein composition within nerve cells and applied their findings to tissue samples from deceased Alzheimer’s patients possessing dual copies of either APOE4 or APOE3.
Their investigations revealed that individuals harboring the APOE4 gene exhibited an increased presence of immune cells containing an enzyme that facilitates the transportation of fat droplets into brain cells. Furthermore, when amyloid was introduced to brain cells carrying either APOE4 or APOE3 variants, these cells demonstrated heightened fat accumulation.
In light of these findings, the researchers posit that the accumulation of amyloid in the brain initiates a cascade effect, prompting the influx of fat into brain cells, ultimately culminating in the development of Alzheimer’s disease.

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