The action of a small protein that is a major villian in Alzheimer's disease can be counterbalanced with another brain protein, researchers at UT Southwestern Medical Center have found in an animal study.
The findings, available online in the journal Proceedings of the National Academy of Sciences, suggest a promising new tactic against the devastating illness, the researchers said.
The harmful protein, called beta-amyloid, is found in the brain and, when functioning properly, suppresses nerve activity involved with memory and learning. Its normal function can be likened to a red traffic light, restraining nerve cells from getting overexcited when they receive stimulating signals from neighboring cells. People with Alzheimer's disease, however, accumulate too much beta-amyloid - the traffic light gets stuck on "red" and nerve cells become less responsive.
Another brain protein, called Reelin, acts as a "green light," stimulating nerve cells to respond more strongly to their neighbors' signals.
The new study shows that applying Reelin directly to brain slices from mice prevents excess beta-amyloid from completely silencing nerves.