Microdysgenesis within the entorhinal cortex of the 23- and the 60-year-old autistic subjects in the examined cohort is unique because the selective deficit of neurons was limited almost exclusively to the stellate neurons in the second layer. It is possible that the observed dysgenesis is a result of defective migration of neurons to their intended destinations. The presence of a thicker molecular layer and the deeper location of islands in the entorhinal cortex of subjects with schizophrenia were previously interpreted as evidence that the stellate neurons do not reach their destinations during development, probably due to abnormal migration [36, 57]. Studies indicating the involvement of reelin and Bcl2 genes in the pathogenesis of schizophrenia [37, 47, 60] and the reduced expression of reelin and Bcl2 in people with autism suggest that these two genes play a role in abnormal brain development and contribute to the structural and functional anomalies seen in autism and schizophrenia [37].
