Researchers may have unlocked a new key to fighting Alzheimer's disease. A recent study suggests the root cause lies in a build-up of fat droplets within brain cells. Michael Haney at the University of Pennsylvania told New Scientist that targeting these droplets could lead to more effective treatments. "This opens up a new avenue for therapeutic development," he says.
For decades, scientists have pinned the blame for Alzheimer's on protein culprits: sticky beta-amyloid plaques and tangled tau proteins within brain cells. A heated debate has raged on - which protein is the true villain? Recent success with drugs targeting amyloid seemed to tip the scales.
However, a new player is emerging: fat droplets. But this debate ignores the fact that fat droplets can also be seen in the brains of people who have died from the disease, says Mr Haney.
Michael Haney investigated the APOE gene, a major risk factor for Alzheimer's. This gene controls how fat moves in and out of cells. Different versions (APOE2, 3, and 4) exist, with APOE4 carrying the highest Alzheimer's risk.
Mr Haney's team analyzed brain cells from dead Alzheimer's patients with either APOE4 or APOE3. They found immune cells in APOE4 brains produced more of an enzyme that boosted fat storage.
They grew immune brain cells (microglia) from people with APOE4 and APOE3. Exposing these cells to amyloid (another Alzheimer's suspect) increased fat build-up, especially in APOE4 cells.
The researchers propose that amyloid buildup triggers fat accumulation in immune cells. This, in turn, leads 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, strengthening the fat droplet theory.
