Endocannabinoid Signaling in Autism
Mutations found in individuals with autism block the action of molecules made by the brain that act on the same receptors that marijuana's active chemical acts on, according to new research. The findings implicate specific molecules, called endocannabinoids, in the development of some autism cases and point to potential treatment strategies.
Cannabinoid receptor type 2, but not type 1, is up-regulated in peripheral blood mononuclear cells of children affected by autistic disorders.
Autistic disorders (ADs) are heterogeneous neurodevelopmental disorders arised by the interaction of genes and environmental factors. Dysfunctions in social interaction and communication skills, repetitive and stereotypic verbal and non-verbal behaviours are common features of ADs. In this study, we investigated the involvement of cannabinoid system in PBMCs from autistic children compared to age-matched normal healthy developing controls in autistic children and healthy subjects, respectively.
A Novel Approach to the Symptomatic Treatment of Autism
Parents of some autistic children report that cannabis eases behavioral problems more effectively than conventional pharmaceuticals. Their anecdotal evidence should be taken seriously by medical researchers.
Consequences of cannabinoid and monoaminergic system disruption in a mouse model of autism spectrum disorders.
Autism spectrum disorders (ASDs) are heterogenous neurodevelopmental disorders characterized by impairment in social, communication skills and stereotype behaviors. While autism may be uniquely human, there are behavioral characteristics in ASDs that can be mimicked using animal models.
Targeting the endocannabinoid system in the treatment of fragile X syndrome.
Fragile X syndrome, the most common monogenic cause of inherited intellectual disability and autism, is caused by the silencing of the FMR1 gene, leading to the loss of fragile X mental retardation protein, a synaptically expressed RNA-binding protein regulating translation...We found that CB1R blockade through pharmacological and genetic approaches normalized cognitive impairment, nociceptive desensitization, susceptibility to audiogenic seizures, over-activated mTOR signaling and altered spine morphology, whereas pharmacological blockade of CB2R normalized anxiolytic-like behavior.
Deficient adolescent social behavior following early-life inflammation is ameliorated by augmentation of anandamide signaling.
Early-life inflammation has been shown to exert profound effects on brain development and behavior, including altered emotional behavior, stress responsivity and neurochemical/neuropeptide receptor expression and function...We investigated the role that the endocannabinoid (eCB) system plays in sociability after early-life LPS.