2005 - Memantine and Binge Eating
First from April 2005
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A new anti-obesity drug treatment: First clinical evidence that, antagonising glutamate-gated Ca2+ ion channels with memantine normalises binge-eating disorders
M. Hermanussena, , and J.A.F. Tresguerresb
aAschauhof 3, 24340 Altenhof, Germany
bDepartment of Physiology, Medical School, Universidad Complutense, Madrid, Spain
Received 5 April 2005; accepted 5 April 2005. Available online 10 May 2005.
Abstract
The regulation of appetite relies on complex hypothalamic neurocircuitry of which the arcuate nucleus, and the hormone leptin play important roles.
Arcuate nucleus neurones are essential for the regulation of eating behaviour, but they can be intoxicated by elevated serum levels of the amino acid glutamate (GLU).
Neurotoxic effects of GLU are mediated by the N-methyl-d-aspartate receptor (NMDA-R). But the neurotoxic effects of GLU can be prevented.
Concurrent administration of dizocilpine maleate (MK-801), a selective and highly potent non-competitive NMDA-R antagonist, antagonises GLU-gated Ca2+ ion channels and completely prevents the adverse effects of GLU.
Also the non-competitive NMDA-R antagonist memantine displays neuroprotective properties.
In view of a previously published hypothesis that human obesity results from chronic over-consumption of GLU, we performed a therapeutic trial in five obese, but otherwise healthy women.
Memantine treatment markedly decreased appetite within few hours and complete suppressed the binge-eating disorder within 24 h.
Body weight decreased markedly within a few days. The findings strongly support the hypothesis that elevated levels of nutritional GLU play an important role in the pathomechanism of human obesity.
We suggest to treat human obesity by protecting the hypothalamic signalling cascade of leptin action with low to moderate affinity, non-competitive NMDA-R antagonists that selectively block the GLU-gated Ca2+ ion channels.
Keywords: Obesity; Glutamate; Arcuate nucleus; NMDA receptor; Binge-eating disorder
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sciencedirect.com
And Second from Nov 2005
Glücksburger Auxologie-Tage
Second German Congress of Auxology, November 17–20, 2005
Blocking the NMDA-receptor in the treatment of obesity.
Hermanussen M, Tresguerres JAF. Aschauhof, Germany; Madrid, Spain.
The arcuate nucleus is a major site of the hypothalamic signalling cascade of leptin action, and plays a key role in the regulation of appetite.
But its neurones are sensitive, and can be intoxicated by elevated serum levels of the amino acid glutamate (GLU).
Neurotoxic effects of GLU are mediated by the N-methyl-D-aspartate receptor (NMDA-R). NMDA-R are GLU-gated Ca2+ ion channels. Antagonising these Ca2+ ion channels completely prevents the adverse effects of GLU.
Previously we hypothesised that human obesity results from chronic over-consumption of GLU. Recent therapeutic trial in obese, but otherwise healthy probands, further supported this hypothesis.
Memantine is a clinical well-tolerated, non-competitive NMDA-R antagonist that displays neuroprotective properties. Memantine treatment markedly decreases appetite within few hours and complete suppresses binge-eating disorders.
Memantine treatment decreases body weight in obese persons at a rate of 1 to 1.5 kg per week.
These findings strongly support the view that elevated levels of nutritional GLU play an important role in the pathomechanism of human obesity.
We suggest to treat human obesity by protecting the hypothalamic signalling cascade of leptin action with low to moderate affinity, non-competitive NMDA-R antagonists that selectively block the GLU-gated Ca2+ ion channels.
auxologie.de
And there is this - but I do not know if this is
(chemically-wise) related to the conditions above
Am J Psychiatry 162:2191-a-2192, November 2005
doi: 10.1176/appi.ajp.162.11.2191-a
Memantine for Treatment-Resistant OCD
MICHAEL POYUROVSKY, M.D., RONIT WEIZMAN, M.D., ABRAHAM WEIZMAN, M.D., and LORRIN KORAN, M.D.
Tirat Carmel, Israel
ajp.psychiatryonline.org |
