Autism spectrum disorder (ASD) is a developmental disability that can cause significant social, communication and behavioral challenges. The learning, thinking, and problem-solving abilities of people with ASD can range from gifted to severely challenged. A diagnosis of ASD now includes several conditions that used to be diagnosed separately: autistic disorder, pervasive developmental disorder not otherwise specified (PDD-NOS), and Asperger syndrome. These conditions are now all called autism spectrum disorder.
Epidemiologically speaking, according to the Center for Disease Control, the United States is number one in the incidence of autism i.e., 168 in 10,000 American children have the disorder, which equates to 1 in 59 children!
Since there is no medical test to diagnose the disorders, the provider must listen to the parent/caretaker and look at the child’s behavior and development to make a diagnosis. The American Academy of Pediatrics (AAP) recommends that all children be screened for ASD at ages 18 and 24 months, along with regular developmental surveillance. Unfortunately, many children do not receive a final diagnosis until much older.
A number of lines of evidence suggest that altered eCB signaling may underlie some of the behavioral impairments in ASD. For example, it has been shown that eCBs play a role in controlling emotional responses , behavioral reactivity to context and social interaction. Here, we provide an overview of the current evidence of changes to eCB signaling in experimental models of autism, specifically pertaining to the neuregulin 3 (Nlgn3) and Fragile X (FXS) mouse models. Collectively, these studies shed light on the link between alterations in eCB signaling in mediating ASD-related phenotypes and offer an alternative approach to therapeutic intervention and treatment.
Autism is neurodevelopmental in nature and atypical development of circuit connectivity has been suggested to underlie its key phenotypic features. Studies examining idiopathic forms of autism have revealed a set of genes involved in neurodevelopmental processes that mediate the formation, stabilization and pruning of synapses that consistently associate with autism-related phenotypes in animal models. Specifically, several members of the neuroligin (NLGN) family of genes, postsynaptic cell adhesion molecules that interact with presynaptic neurexins (NRXNs) to control synapse development and function, have been identified in mouse models of ASDs. Animal models have shown that NLGNs enhance synapse formation in vitro , but are not required for synapse formation in vivo. In addition, NLGNs and NRXNs are important organizing molecules for excitatory glutamatergic and inhibitory GABAergic synapses in the mammalian brain. Studies that suggest altered neurotransmission resulting from mutations or full gene deletion of NLGNs, particularly NLGN3, have prompted the investigation of the role of eCB signaling in mediating neurotransmitter release in the hippocampus and cortex.
A comprehensive systematic review of the evidence, conducted by a group of Stanford University researchers in 2016, provides convincing evidence about the broader role of endocannabinoid signaling in social functioning. Recognizing the growing body of evidence that cannabinoid signaling may be involved in social functioning, the researchers used a well-established systematic research construct to integrate and analyze the role of endocannabinoid signaling social functioning across multiple diagnostic categories, including autism. They found that the majority of the evidence supports the hypothesis that primary receptors and effectors in the cannabinoid system—including delta-9-tetrahydrocannabinol, cannabidiol, anandamide, and 2-arachidonoylglycerol—all have relevant effects on measures of social functioning, such as anxiety, chronic stress, attachment, affiliation, and communication. It is important to note that the authors drew data from studies on autism, as well as other psychological and psychiatric disorders (like major depressive disorder, PTSD, and bipolar disorder), but their conclusion regarding the role of endocannabinoids on social functioning in general has promising implications for patients with autism who are specifically interested in therapeutics that target symptoms of social anxiety.
the endocannabinoid system (ECS) is often placed at the center of the symptoms children with CBD exhibit. The ECS plays a central role in helping regulate emotions, motor control and manages many other cognitive processes. The interaction of CBD with the ECS shows much promise in helping control autism and significantly curtailing its symptoms.
This interaction is also responsible for the treatment of neurodegenerative conditions like Tourette’s and epilepsy. For this reason, many are hopeful that CBD may also help improve the plight of autistic children.