(Boston) - The Alzheimer's drug memantine may perform double-duty helping binge eaters control their compulsion. Researchers have demonstrated that memantine, a neuroprotective drug, may reduce the addictive and impulsive behavior associated with binge eating.
The Boston University School of Medicine (BUSM) study, which appears online in Neuopsychopharmacology, also found that a specific area in the brain, the nucleus accumbens, which is responsible for addictive behaviors, facilitates the effects of memantine.
Binge-eating disorder is a prevalent illness in America, affecting more than 10 million people. It is characterized by periods of excessive uncontrolled consumption of food, followed by uncomfortable fullness and feelings of self-disgust. New evidence indicates that changes in brain chemistry reflecting the addictive nature of binge eating may parallel drug and alcohol addiction.
Using an experimental model to simulate binge-eating behavior, researchers were able to identify the area of the brain associated with binge-eating and then suppress the behavior by applying memantine directly into that area.
"We found that memantine, which blocks glutamate NMDA receptors, blocks binge eating of junk food, blocks the strength of cues associated with junk food and blocks the compulsivity associated with binge eating," explained senior author Pietro Cottone, PhD, an associate professor of pharmacology and psychiatry at BUSM and co-director of the Laboratory of Addictive Disorders.
This research opens new avenues for binge eating treatment especially since memantine is a drug already approved for other indications. "Individuals with binge eating disorder have a very poor quality of life and decreased lifespan. Our study gives a better understanding of the underpinning neurobiological mechanisms of the disorder," added coauthor Valentina Sabino, PhD, assistant professor of pharmacology and psychiatry at BUSM and co-director of the Laboratory of Addictive Disorders.
Other researchers participating in this study included: Karen Smith, PhD (BUSM), Rahul Rao, MA (BUSM), Clara Velázquez-Sánchez, PhD (BUSM), Marta Valenza, PhD (BUSM), Chiara Giuliano, PhD (University of Cambridge, UK) and Barry Everitt, ScD (University of Cambridge, UK).
This work was supported by grant numbers DA030425, MH091945, and MH093650A1 from the National Institute on Drug Abuse (NIDA) and the National Institute of Mental Health (NIMH), by the Peter Paul Career Development Professorship (to P.C.), the McManus Charitable Trust (to V.S.) and by Boston University's Undergraduate Research Opportunities Program (UROP).
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