A gene variant triples the risk of getting Alzheimer's disease — fat buildup in brain cells may be to blame, study finds

A gene variant called APOE4 dramatically increases the risk of late-onset Alzheimer's disease, the most common form of dementia.

Now, emerging research is revealing APOE4's true role in the condition, and a new study pinpoints a possible way to treat it.

Historically, scientists studying Alzheimer's disease have focused on two proteins that accumulate in patients' brains: amyloid-beta and tau.

However, there's a "third thing that people didn't pay attention to, until recently," said study co-author Li-Huei Tsai , a neuroscientist at MIT.

That third thing is the accumulation of droplets of fat, or lipids, in the brain, she told Live Science.

The APOE gene makes proteins responsible for transporting fat around cells throughout the body and brain.

A version of the gene called APOE4, which increases the risk of late-onset Alzheimer's three- to 12-fold, makes proteins that are less efficient at this function, Tsai said.

But how APOE4 affects different brain cells was not clearly understood.

Tsai's team has been working to close that gap for about a decade.

"APOE4 can influence many different cell types," she emphasized.

"It's not just one cell type." Zeroing in on the clues In past laboratory research, Tsai's team found that APOE4 causes a buildup of cholesterol in astrocytes, star-shaped brain cells that support the function of neurons.

Genetic analyses suggested that the gene variant may mess with how these cells process fat.

Another study zoomed in on oligodendrocytes, cells that help insulate neurons' outgoing wires with a fatty material called myelin.

This material helps neurons send messages more efficiently.