Alzheimer's Drug May Curb Binge Eating

Deborah Brauser

November 20, 2014

The Alzheimer's disease (AD) drug memantine (Namenda, Forest Laboratories, Inc), a medication that blocks N-methyl-D-aspartate (NMDA) receptors, may also decrease binge eating behaviors, preliminary research suggests.

The study showed that after receiving memantine, a group of rats displayed significantly decreased food seeking behavior and compulsive eating. In addition, memantine administered into the brain's nucleus accumbens, a region responsible for addictive behaviors, decreased bingeing behaviors.

"We found that memantine...blocks binge eating of junk food, blocks the strength of cues associated with junk food, and blocks the compulsivity associated with binge eating," senior author Pietro Cottone, PhD, associate professor of pharmacology and psychiatry at Boston University School of Medicine (BUSM), Massachusetts, and codirector of the Laboratory of Addictive Disorders, said in a release.

The investigators note that because the medication is already approved for indications other than AD, these findings plus future research could potentially lead to the use of memantine as an effective treatment for patients with binge eating disorder (BED).

"Our study gives a better understanding of the underpinning neurobiological mechanisms of the disorder," said coinvestigator Valentina Sabino, PhD, also from BUSM, in the same release.

The study was published online November 1 in Neuropsychopharmacology.

Multiple Indications

Memantine is often used to treat AD because of its neuroprotective properties, note the researchers.

However, as reported by Medscape Medical News, previous research has suggested that memantine may also do the following:

"Addiction-related behaviors have been linked to impairments in the glutamatergic system in the nucleus accumbens and the [NMDA] receptor has been proposed as a promising target for the treatment of a variety of addictive disorders," the investigators write.

"A large body of evidence shows that memantine reduces the reinforcing and rewarding effects of drugs of abuse," they add.

They report that 10 million individuals in the United States have been affected by BED, a disorder that is now listed in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5).

"The aim of this study was...to systematically characterize the neuropharmacological effect of memantine using a battery of tasks developed to evaluate different features of maladaptive feeding behavior induced by limiting access to highly palatable food," the investigators explain.

In addition, they wanted to assess which brain area might mediate effects of the medication on excessive food intake.

Male rats were acclimated to a "regular chow diet" of food pellets and then habituated to 1 hour a day of either a highly palatable diet, consisting of a sugary and chocolate-flavored food, or the chow only. After the rats' food-responive behaviors had been stabilized, all were injected with memantine.

A "second-order schedule of reinforcement" was used to assess memantine's effects on food seeking behavior. Food intake in a "bright compartment of a light/dark conflict test" after receiving memantine was also measured.

Finally, a set of rats had memantine directly microinfused into the shell and core of the nucleus accumbens to evaluate response to food and bingelike eating.

Controls Food Seeking

Results showed significantly decreased bingelike eating after rats in the palatable diet group received 2.5 mg/kg, 5 mg/kg, or 10 mg/kg doses of memantine (all, P ≤ .05).

"When administered at the highest dose, memantine treatment reduced binge-like eating...by 39.0% (P = .0001)," report the investigators. Although that dosage also reduced binge eating of the chow diet by 25.6%, the reduction was not statistically significant.

After receiving memantine, food-restricted rats in the palatable diet group also showed significant curbing of both food seeking behavior and compulsive eating.

Memantine did not have any significant effects on the group receiving the chow diet.

The rats that received microfusions of memantine into the nucleus accumbens shell had significantly decreased bingelike eating behaviors (P ≤ .05). However, there were no significant differences when the microfusion was administered into the nucleus accumbens core.

"Together, these findings substantiate a role of memantine as a potential pharmacological treatment for BED," write the investigators, adding that the medication appears to block the "incentive mechanisms controlling food seeking."

They note that the results also suggest that brain chemistry changes reflecting the addictive nature of BED may mirror those found in drug and alcohol addiction.

The study authors have reported no relevant financial relationships

Neuropsychopharmacology. Published online November 10, 2014. Abstract

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