WASHINGTON – Scientists have a new lead on a possible treatment to slow Alzheimer’s disease by targeting a protein involved in limiting flexibility in the aging brain, according to a study released Thursday.
Researchers led by Stanford University neurobiologist Carla Shatz discovered that eliminating a certain protein from mice brains stopped the disease’s symptoms from manifesting.
The researchers focused on a mouse protein called PirB, and its human homologue, LilrB2, which can be found on the surface of nerve cells in the brain. The protein appears to bind with beta-amyloid, a protein remnant that weakens the connections between neurons. Experiments showed that when PirB partners with beta-amyloid, it can “trigger a cascade of harmful reactions” that breaks down those connections, the researchers said. One of the hallmarks of Alzheimer’s is large buildups of beta-amyloids called “plaques.”
Scientists say a drug targeting this protein could help slow the onset of Alzheimer’s.
The findings were based on experiments in mice bred to develop Alzheimer’s disease. In mice without the PirB gene, the synapses were more resistant to the beta-amyloid effects.