SouthernWorldwide.com – An experimental drug intended for dementia treatment is showing potential in easing alcohol withdrawal symptoms by addressing brain inflammation linked to addiction and relapse.
Researchers at the University of Kentucky have been studying an experimental medication, code-named MW150. This drug targets a specific brain inflammation pathway known as p38α MAPK.
MW150 is currently designed to treat mild to moderate Alzheimer’s disease and has not yet received approval.
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Scientists hypothesize that neuroinflammation plays a role in the risk of relapse and long-term neurological damage experienced by individuals with alcohol use disorder.
Initial laboratory and animal-model experiments indicated that MW150 was effective in reducing certain inflammatory markers during alcohol withdrawal phases.
This research, published in the journal Alcohol, originated from the University of Kentucky’s Sanders-Brown Center on Aging and was spearheaded by neuroinflammation researcher Linda Van Eldik.
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Caleb Bailey, Ph.D., a co-author of the study and researcher within Van Eldik’s lab, stated that the findings offer “biological plausibility” for MW150’s ability to mitigate neuroinflammation associated with alcohol withdrawal.
Bailey highlighted that alcohol use disorder is challenging to treat due to high relapse rates, particularly during the withdrawal period.
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The researchers noted that MW150, along with a similar drug called Neflamapimod, is already undergoing clinical trials as a potential therapy for dementia and other neurodegenerative conditions.
“This adds significant weight to our current work,” Bailey commented. “Given that these compounds are further along in development for other neurological diseases, it raises the possibility of a more efficient repurposing for alcohol-related conditions in the future, should subsequent studies continue to yield promising results.”
The research does have some limitations, as it was conducted using cell cultures and animal models.
“These ‘dish’-based models offer limited insight into what occurs within a complete organism, or even a whole brain, for that matter,” Bailey explained.
“A series of follow-up studies in living animals is necessary to fully comprehend how future MW150 treatment for alcohol use and withdrawal impacts systemic health and/or alcohol consumption.”
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Dr. Amy Swift, deputy chief medical officer at Silver Hill Hospital in Connecticut, who was not involved in the study, shared her perspective on the findings.
“Simply put, detoxification addresses the immediate dangers of alcohol withdrawal but does not treat alcohol use disorder itself. Its primary function is to prevent potentially fatal complications.”
Swift suggested that incorporating supportive medications, especially those aimed at enhancing overall brain health, could fill a critical gap in the early stages of detoxification treatment.
“Considering the significant inflammatory effects alcohol has across various organ systems, it is valuable to investigate whether reducing neuroinflammation could improve a patient’s capacity to engage in treatment earlier in their recovery journey. This, in turn, could meaningfully alter their long-term relationship with alcohol,” she added.
Bailey reiterated that from a physical health perspective, no level of alcohol consumption is beneficial.
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“Currently, we lack robust pharmacological treatments to mitigate the damage caused by chronic alcohol consumption,” he stated. “Therefore, minimizing alcohol intake remains the most effective strategy for maintaining health.”
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As studies on the MW150 compound for dementia patients progress, Bailey indicated that “information regarding the interaction between these drugs and alcohol—whether positive or negative—will be crucial for patient outcomes.”
