Familial abnormalities of endocannabinoid signaling in schizophrenia. (7th February 2019)

• Record Type: Journal Article
• Authors: Koethe, Dagmar; Pahlisch, Franziska; Hellmich, Martin; Rohleder, Cathrin; Mueller, Juliane K.; Meyer-Lindenberg, Andreas; Torrey, E. Fuller; Piomelli, Daniele; Leweke, F. Markus
• Is Part Of: World journal of biological psychiatry. Volume 20:Number 2(2019)
• Page Start: 117
• Page End: 125
• Publication Date: 2019-02-07
• Subjects: Psychosis -- monozygotic twins -- genetic risk -- anandamide (AEA) -- endocannabinoids; Biological psychiatry -- Periodicals; Biological Psychiatry -- Periodicals; 616.89
• DOI: 10.1080/15622975.2018.1449966
• Languages: English
• ISSNs: 1562-2975

Abstract

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 < 0.002). Non-affected twins discordant for schizophrenia, who developed a psychotic disorder within 5 years follow-up showed lower anandamide ( 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.