Years before people begin to show symptoms characteristic of Alzheimer's disease, the so-called amyloid plaques begin to form in their brains, damaging nearby cells.
For decades, doctors have looked for ways to remove these plaques as a way to prevent or treat the disease. Now it seems to have been discovered how, although at the moment the test has been done in mice.
APOE
Amyloid plaques are composed mainly of a brain protein called beta amyloid. But nested within the plates are small amounts of another protein: APOE. APOE gene variants are the major risk factor for Alzheimer's disease.
Now, researchers at the University of Washington School of Medicine have shown that an antibody not only targets APOE to eliminate it, but also removes plaques.
The findings, available from March 26 in the Journal of Clinical Investigation, could lead to a way to stop brain damage caused by amyloid plaques while the disease is still in its early stages, perhaps before the symptoms appear. .
Apparently, once the antibodies bind to their APOE target, they attract the attention of the roving immune cells, which carry the antibody and the target to destroy them. The researchers tested several antibodies that recognize human APOE in mice genetically predisposed to develop amyloid plaques. The APOE genes of the mice had been replaced with a human APOE gene. The antibodies were developed in collaboration with Denali Therapeutics.
There is no treatment to prevent or delay the onset of Alzheimer's disease. However, some antibodies that eliminate amyloid plaques are being evaluated in clinical trials. While such antibodies are promising, they sometimes carry the side effect of inflammation and swelling in the brain. However, antibodies that target APOE may be successful in removing plaques in people and are less likely to trigger a destructive immune response.