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Scientists lay blame for Alzheimer’s on culprit proteins
Researchers may have discovered a new key to combating Alzheimer’s disease. A recent study suggests that the root cause lies in the accumulation of fat droplets inside brain cells. Michael Haney of the University of Pennsylvania said new scientist that targeting these droplets could lead to more effective treatments. “This opens a new avenue for therapeutic development,” she says.
For decades, scientists have blamed Alzheimer’s on the culprit proteins: sticky plaques of beta-amyloid and tau proteins tangled inside brain cells. A heated debate has broken out: which protein is the real villain? Recent success with drugs targeting amyloid seemed to tip the balance.
However, a new player is emerging: fat droplets. But this debate ignores the fact that fat blobs can also be seen in the brains of people who have died from the disease, Haney says.
Michael Haney investigated the APOE gene, a major risk factor for Alzheimer’s. This gene controls how fat enters and leaves cells. There are different versions (APOE2, 3 and 4), with APOE4 being the one that carries the highest risk of Alzheimer’s.
Haney’s team analyzed brain cells from dead Alzheimer’s patients with APOE4 or APOE3. They found that immune cells in APOE4 brains produced more of the enzyme that increased fat storage.
They cultured immune brain cells (microglia) from people with APOE4 and APOE3. Exposure of these cells to amyloid (another Alzheimer’s suspect) increased fat accumulation, especially in APOE4 cells.
The researchers propose that amyloid buildup triggers fat accumulation in immune cells. This, in turn, causes tau tangles in neurons, leading to cell death and memory loss.
Genes linked to a slightly increased risk of Alzheimer’s often affect fat metabolism or the immune system, strengthening the fat droplet theory.