A gene associated with the Alzheimer's disease causes immune cells in the brain to maintain inflammation in the nervous system, and this leads to the accumulation of toxic proteins in the nervous system. This is evidenced by a study of Gladstone university, which was published in the journal Cell Stem Cell.

Scientists transplanted into mice human brain cells that produced APOE4 protein. This molecule considerably increases the risk of Alzheimer's, but its exact mechanism is not known.

Then the biologists removed the immune cells (microglia) from the animals' brains. Moreover, the damage caused by the APOE4 protein was significantly mitigated. This means that Alzheimer's leads to the interaction between APOE4 and microglia.

In a healthy brain, immune cells called microglia are responsible for getting rid of protein debris and broken proteins. But in the presence of the APOE4 protein, the most important genetic risk factor for Alzheimer's, those same cells cause inflammation and the accumulation of improperly coagulated proteins—the beta-amyloid and tau.

The presence of the APOE4 variant can increase the risk of Alzheimer's by 12 times.

The new study, however, could form the basis of a therapy to prevent dementia in people with APOE4.