Familial abnormalities of endocannabinoid signaling in schizophrenia |
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| Authors: | Dagmar Koethe Franziska Pahlisch Martin Hellmich Cathrin Rohleder Juliane K. Mueller Andreas Meyer-Lindenberg |
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| Affiliation: | 1. Brain and Mind Centre, The University of Sydney, Sydney, Australia;2. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany;3. Department of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany;4. Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA;5. Institute for Medical Statistics and Computational Biology, University of Cologne, Cologne, Germany |
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| Abstract: | ![]()
Objectives: Epidemiological and experimental evidence suggests that the endocannabinoid system plays a pathophysiological role in schizophrenia. This is reflected by elevated cerebrospinal levels of the endocannabinoid anandamide in schizophrenia and its initial prodromal states.Methods: We analyzed plasma concentrations of anandamide, 2-arachidonoyl-sn-glycerol, palmitoylethanolamide and oleoylethanolamide from 25 twin pairs discordant for schizophrenia, six discordant for bipolar disorder and eight healthy twin pairs to determine hereditary traits.Results: Twin pairs discordant for schizophrenia or bipolar disorder had significantly higher levels of anandamide and palmitoylethanolamide compared to healthy twins (both P?P?=?0.042) and 2-arachidonoyl-sn-glycerol levels (P?=?0.049) than twins who remained healthy.Conclusions: We suggest that the protective upregulation of endocannabinoid signalling reflects either a hereditary trait or mirrors a modulating response to genetically influenced cerebral function involving, e.g., other neurotransmitters or energy metabolism. |
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| Keywords: | Psychosis monozygotic twins genetic risk anandamide (AEA) endocannabinoids |
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