Scientists blame proteins for Alzheimer’s disease
Researchers may have uncovered a new key to fighting Alzheimer’s disease. Recent research suggests that the underlying cause lies in the accumulation of lipid droplets within brain cells. Michael Haney of the University of Pennsylvania said: new scientist It is thought that targeting these droplets may lead to more effective treatments. “This opens up new avenues for treatment development,” he says.
For decades, scientists have pinpointed the cause of Alzheimer’s disease in protein sources: sticky beta-amyloid plaques and the tangled protein tau in brain cells. There is a heated debate about which protein is the real villain. Recent successes with drugs targeting amyloid seem to have tipped the scales.
But new players are emerging. It’s a fat droplet. But this argument ignores the fact that lipid droplets are also found in the brains of people who die from the disease, Haney said.
Michael Haney studied the APOE gene, a major risk factor for Alzheimer’s disease. This gene controls how fat moves in and out of cells. Different versions exist (APOE2, 3, and 4), with APOE4 having the highest risk for Alzheimer’s disease.
Haney’s team analyzed brain cells from deceased Alzheimer’s patients who had either APOE4 or APOE3. They found that APOE4 brain immune cells produced more of an enzyme that promotes fat storage.
They expanded immune brain cells (microglia) from people with APOE4 and APOE3. Exposure of these cells to amyloid, another Alzheimer’s disease suspect, increased fat accumulation, especially in APOE4 cells.
Researchers propose that amyloid accumulation causes fat accumulation in immune cells. This causes tau tangles within neurons, leading to cell death and memory loss.
Genes associated with small increases in Alzheimer’s disease risk often influence fat metabolism and the immune system, reinforcing the lipid droplet theory.
