**5. Evidence from monogenic forms of ASD**

The clinical and genetic heterogeneity present in ASD has made the study of the pathophysiology of the disease challenging. The study of genetically defined autism, as in the case of monogenic forms of ASD, which show a relatively homogeneous and well-characterized clinical manifestation, allows us to understand cellular and molecular mechanisms relevant to the disease. Although monogenic causes of ASD are often syndromic and not all patients with the syndrome show autistic features, by studying patients with and without ASD, we can start deciphering the pathomechanisms that lead to the disorder. As shown below, human postmortem and brain imaging studies of syndromic forms of ASD support the role of

*The Cerebellum and Autism: More than Motor Control DOI: http://dx.doi.org/10.5772/intechopen.85897*

the cerebellum in the pathophysiology of the disease. Animal models of monogenic autism are easily generated and provide opportunities for direct manipulation of these brain regions and circuits to test their precise functions in social behavior paradigms. We will describe below the main syndromes with reported cerebellar dysfunction and supporting data from animal models (**Table 1**). In all, human and animal data point out a role for the cerebellum in social deficits in ASD.
