Drugs already in development to treat Alzheimer's disease may eventually be tapped for a different purpose altogether: re-growing the ends of injured nerves to relieve pain and paralysis. According to a new Johns Hopkins study, experimental compounds originally designed to combat a protein that builds up in Alzheimer's-addled brains appear to make crushed or cut nerve endings grow back significantly faster, a potential boon for those who suffer from neuropathies or traumatic injuries.
The new drugs target a protein known as "-Site amyloid precursor protein cleaving enzyme 1," or BACE1, which plays a key role in generating the amyloid protein plaques that are thought to gum up normal nerve signaling in the brain. Previous laboratory research showed that BACE1 also is involved in creating the insulation material known as myelin, which coats the projections that nerve cells extend to connect with each other, as well as generating a molecular cascade that causes these projections to degenerate when they're injured.
Based on these earlier findings, assistant professor of neurology Mohamed Farah, Ph.D., professor of neurology John Griffin, M.D., and their colleagues tried blocking the action of BACE1 to analyze the effect on injured axon projections. The researchers started their experiments with mice whose ability to make BACE1 had been genetically knocked out. After these animals' sciatic nerves were cut or crushed, the scientists closely watched what happened as the axons regenerated.
Compared to normal mice that make BACE1, the animals lacking this protein cleaned up the debris around the injury site significantly faster. Since this debris can inhibit regeneration, Farah and his colleagues expected that the axons would re-grow faster. Sure enough, the cut ends of the animals' nerve cells generated more new sprouts, which grew into extensions that reached their targets muscles or other nerve cells days faster than the mice that
|Contact: Christen Brownlee|
Johns Hopkins Medical Institutions