Autism spectrum disorders (ASD) are a group of neuro-developmental disabilities, which, in many cases, is characterized by severe impairments in communication skills, social interaction, psychomotor coordination, behavioral control and emotional stability often accompanied by deficits in cognition, attention and sensory processing. According to a recent study conducted by Dr. Fouad Alshaban (Shafallah Medical Genetics Center, Doha, Qatar), the accurate prevalence rate of autism-spectrum disorders in Qatar is still uncertain. However, there is a general concern that it might be increasing in the last few years. The symptoms of ASDs are typically present before age 3 years, but frequently a formal diagnosis take longer to be established, which may compromises the efficacy of developmental and life-quality improving strategies. In most countries of the world the scenario is not much different. It has been shown that autism-associated neuroligin-3 mutations disrupt tonic endocannabinoid signaling in animals. Endocaanabinoids are neuromodulators produced by the brain, which act upon the same receptors and neuronal circuits affected by exogenous cannabinoids from the plant Cannabis sativa. This system is central for brain homeostatic activity control, learning, social interaction, memory formation and emotional modulation, among several neuronal and physiological functions. Here we present our proposal to use primates and valproate-treated rodents (an animal model for autism) in order to deepen our knowledge about the involvement of defects in endocannabinoid system as etiological factors capable of generating behavioral and cognitive aspects related to human autism. The reasoning behind the use of two species is to facilitate the conceptual bridge between the findings obtained in valproate-treated rodents and the understanding of the importance of the endocannabinoid system for social interaction and emotional behavior in primates. At first, this combination has the potential to point out possible pharmacological treatments based on modulation of the endocannabinoid system and in the identification of biomarkers in rodents. Secondly, this knowledge can help to develop, and to ethically justify, the creation of primate models for the study of pharmacologically treatable aspects related to human behavior that cannot be studied in rodents. In Brazil we have the privilege to work with non-human primates in a high-standard, naturalistic facility, the Primatology Center of the University of Brasilia (in the capital of Brazil). Therefore, we are taking advantage of this capability to test new hypotheses relating endocannabinoid signaling defects with autism symptoms and eventually generate a non-human primate animal model that, in one hand, may help on the discovery of molecular markers for early diagnosis and, on the other hand, may help the development of pharmacological tools to treat important symptoms of ASD. We want to share and discuss our ongoing project in this meeting as part of an effort to foster found raising and potential collaborations between our group and research groups from Qatar.


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