Download full-text

Full-text

Available from: Richard Bruggeman, Apr 01, 2015
0 Followers
 · 
165 Views
  • Source
    • "Delta-9-tetrahydrocannabinol (D 9 THC), the main 72 psychoactive substance in Cannabis sativa, acts as an exogenous 73 (GABA) terminations (Devane et al., 1992; Chevaleyre et al., 2006), 82 but they are also present in the periphery of the nervous system 83 (Pertwee, 1999). CB2-Rs have a similar structure and are predom- 84 inantly expressed in the spleen and immune cells (Graham et al., 85 2009). Although the proportion of CB2-Rs in the CNS is lower than 86 that of CB1-Rs, their presence in brain cells has been demonstrated 87 (Onaivi et al., 2012). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Endocannabinoid system is involved in the regulation of the brain-immune axis. Cannabis consumption is related with the development, course, and severity of psychosis. The epidemiological evidence for increased occurrence of immunological alterations in patients with psychosis has not been sufficiently addressed. The aim of this review is to establish whether there is any scientific evidence of the influence of cannabinoids on aspects of immunity that affect susceptibility to psychotic disorder induction. Methods A comprehensive search of PubMed /MEDLINE, EMBASE and ISI Web of Knowledge was performed using combinations of key terms distributed into three blocks: “immune”, “cannabinoid”, and “endocannabinoid receptor”. Studies were considered to be eligible for the review if they were original articles, they reported a quantitative or qualitative relation between cannabinoid ligands, their receptors, and immune system, and they were carried out in vitro or in mammals, included humans. All the information was systematically extracted and evaluated. Results We identified 122 articles from 446 references. Overall, endocannabinoids enhanced immune response, whereas exogenous cannabinoids had immunosuppressant effects. A general change in the immune response from Th1 to Th2 was also demonstrated for cannabinoid action. Endogenous and synthetic cannabinoids also modulated microglia function and neurotransmitter secretion. Conclusion The actions of cannabinoids through the immune system are quite regular and predictable in the peripheral but remain fuzzy in the central nervous system. Despite this uncertainty, it may be hypothesized that exposure to exocannabinoids, in particular during adolescence might prompt immunological dysfunctions that potentially cause a latent vulnerability to psychosis. Further investigations are warranted to clarify the relationship between the immunological effects of cannabis and psychosis.
    Brain Behavior and Immunity 08/2014; DOI:10.1016/j.bbi.2014.01.018 · 6.13 Impact Factor
  • Source
    • "Patients with autism or schizophrenia often show explicit memory dysfunction, which can be particularly severe for episodic memory (Ben Shalom 2003; Barch and Ceaser 2012). An inflammatory trigger has been proposed for these disorders (e.g., Patterson 2009), and genome-wide association studies (GWAS) have identified links between the relative risk of autism or schizophrenia and genetic variation in the MHC class I region (HLA in humans) (Torres et al. 2001; Purcell et al. 2009; Shi et al. 2009; Stefansson et al. 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Memory impairment is a common feature of conditions that involve changes in inflammatory signaling in the brain, including traumatic brain injury, infection, neurodegenerative disorders, and normal aging. However, the causal importance of inflammatory mediators in cognitive impairments in these conditions remains unclear. Here we show that specific immune proteins, members of the major histocompatibility complex class I (MHC class I), are essential for normal hippocampus-dependent memory, and are specifically required for NMDAR-dependent forms of long-term depression (LTD) in the healthy adult hippocampus. In β2m(-/-)TAP(-/-)mice, which lack stable cell-surface expression of most MHC class I proteins, NMDAR-dependent LTD in area CA1 of adult hippocampus is abolished, while NMDAR-independent forms of potentiation, facilitation, and depression are unaffected. Altered NMDAR-dependent synaptic plasticity in the hippocampus of β2m(-/-)TAP(-/-)mice is accompanied by pervasive deficits in hippocampus-dependent memory, including contextual fear memory, object recognition memory, and social recognition memory. Thus normal MHC class I expression is essential for NMDAR-dependent hippocampal synaptic depression and hippocampus-dependent memory. These results suggest that changes in MHC class I expression could be an unexpected cause of disrupted synaptic plasticity and cognitive deficits in the aging, damaged, and diseased brain.
    Learning & memory (Cold Spring Harbor, N.Y.) 08/2013; 20(9):505-17. DOI:10.1101/lm.031351.113 · 4.38 Impact Factor
  • Source
    • "Genotyping of Utrecht and Leiden cases and controls was carried out by mass spectrometry (the homogeneous MassARRAY system; Sequenom, San Diego, California, USA) under standard conditions, except for the control group B, which was genotyped on an Illumina HumanHap 550k platform (Stefansson et al., 2009). "
    [Show abstract] [Hide abstract]
    ABSTRACT: This study aimed to test the association between the Val158Met polymorphism (rs4680) of the catechol-O-methyl transferase gene and anorexia nervosa (AN). First, an association study on two cohorts (306 cases and 1009 controls from Utrecht, and 174 cases and 466 controls from Leiden/NTR) was performed. Subsequently, the results were integrated into a meta-analysis, together with all the case-control and family-based studies, which were testing the same hypothesis and were available in the literature. Altogether, eight studies (11 datasets) were included in this meta-analysis, with a total of 2021 cases, 2848 controls, and 89 informative (heterozygous) trios. The present association studies found no association between AN and rs4680 when testing the allelic contrast [Utrecht odds ratio (OR)=1.14, P=0.14; Leiden OR=1.02, P=0.85]. There was an indication of an association under the dominant model of genetic effect in the Utrecht cohort (for the Met allele, OR=1.42, P=0.03). Nevertheless, the meta-analyses of both the allelic contrast and the dominant effect were nonsignificant (the allelic pooled OR=1.03, P=0.42 and the dominant pooled OR=1.1, P=0.18). The meta-analyses were performed under the fixed-effect model and there was no significant heterogeneity among the effect sizes. Meta-analytically combined evidence from the present genotypings and the literature search shows that the effect sizes are homogeneous across studies and that rs4680 is not associated with AN.
    Psychiatric genetics 02/2012; 22(3):130-6. DOI:10.1097/YPG.0b013e328351859e · 2.27 Impact Factor