FRIDAY, June 13 (HealthDay News) -- Boosting the level of a specific brain protein may rapidly halt excessive alcohol consumption, according to a new study done in animals.
University of California, San Francisco, researchers found that the excessive amounts of GDNF, or glial cell-derived neurotrophic factor, stopped the desire to drink alcohol in as little as 10 minutes when tested on rats. Other rodents that had been "rehabbed" to give up alcohol also did not suffer a relapse into heavy imbibing when reintroduced to alcohol and given a GDNF boost.
GDNF shows additional promise, because it does not appear to have any side effects or block other more normal "pleasure-seeking behaviors," such as craving sweets, the researchers report.
"Alcoholism is a devastating and costly psychiatric disease with enormous socioeconomic impact," senior study author Dorit Ron, the principal investigator at the UCSF-affiliated Ernest Gallo Clinic and Research Center, said in a prepared statement. "There is a tremendous need for therapies to treat alcohol abuse."
"Unfortunately, only three drugs are currently approved to treat excessive drinking, and all have serious limitations. Our findings open the door to a promising new strategy to combat alcohol abuse, addiction and especially relapse," he said.
Gallo researchers reported in 2005 that increased levels of GDNF appeared to cut the craving for alcohol, but they did not know how fast or effective it might be. GDNF is also being studied as a treatment for Parkinson's disease.
The researchers are searching to find whether any FDA-approved drugs might stimulate GDNF activity in the brain. Only one orally delivered drug, developed for experiments in the pursuit of Parkinson's treatments, has been shown to raise brain GDNF levels in rats.
The findings were published in this week's Proceedings of the National Academy of Sciences.
The U.S. National Institute on Alcohol Abuse and Alcoholism has more about alcohol abuse and alcoholism.
SOURCE: University of California, San Francisco, news release, June 9, 2008