Experimental Alzheimer’s Drug Potentially Addresses Alcohol Withdrawal

An experimental drug for dementia, MW150, may help alleviate alcohol withdrawal symptoms by reducing brain inflammation associated with addiction and relapse. Researchers at the University of Kentucky explored this possibility. The drug targets the p38α MAPK brain inflammation pathway.

Though MW150 is designed for mild to moderate Alzheimer’s disease, the study suggests it might also reduce relapse risk and long-term neurological damage in individuals with alcohol use disorder. Experiments in both laboratory and animal models showed MW150 decreased certain inflammatory markers during alcohol withdrawal.

The research, published in the journal Alcohol, was conducted at the University of Kentucky’s Sanders-Brown Center on Aging. The study was led by neuroinflammation researcher Linda Van Eldik. Co-author Caleb Bailey, Ph.D., highlighted that the study provides “biological plausibility” for MW150 mitigating neuroinflammation during alcohol withdrawal.

Bailey noted the high relapse rates during withdrawal make alcohol use disorder difficult to treat. If future studies in animal models demonstrate similar results, MW150 could become a treatment for those struggling with chronic alcohol relapses.

MW150, along with a related drug Neflamapimod, is currently under investigation in clinical trials as a treatment for dementia and other neurodegenerative conditions. Bailey emphasized that since these compounds are already in development for other neurological diseases, repurposing them for alcohol-related conditions could be efficient if further studies are promising.

There are important considerations in the research. The experiments used cell cultures and animal models, which may not fully represent what occurs in humans or entire brains. Follow-up studies in living animals are needed to understand MW150’s impact on systemic health and alcohol consumption.

Dr. Amy Swift, deputy chief medical officer at Silver Hill Hospital in Connecticut, who was not part of the study, reacted to the findings. Swift noted that detoxification using tapering doses of medication is a well-established first step in treating alcohol use disorder, but does not address long-term drinking behavior. The study raises the potential for supportive medications that improve brain health during detoxification.

Swift suggested investigating whether reducing neuroinflammation could enhance a patient’s ability to engage in treatment earlier and alter their long-term relationship with alcohol. She emphasized that reducing alcohol consumption is crucial for maintaining health, as excessive alcohol has profound inflammatory effects on multiple organ systems.

Bailey stated that currently, there are no strong pharmacological treatments to mitigate damage from chronic alcohol consumption, reinforcing the importance of minimizing alcohol intake. As MW150 continues to be studied for dementia patients, understanding its interaction with alcohol will be critical for patient outcomes.