Ectopias and dysplastic changes were reported in the brains of autistic subjects, by several groups [4, 62–64, 91]. Bailey et al. [4] detected olivary dysplasia in the brain of three of the five autistic subjects, and ectopic neurons related to the olivary complex in two cases. Moreover, in the brains of four autistic subjects, cortical dysgenesis was found. In the brains of the autistic subjects, a strikingly consistent finding was cingulate cortex disordered lamination [62–64, 100]. A recent study of the cingulate cortex of nine autistic subjects revealed a developmental malformation with irregular lamination in three cases, and an increased number of neurons within the subcortical white matter in two [100]. Simms et al. [100] suggest that the excessive number of neurons in the subcortical white matter reflects the lack of proper resolution of the transient zone in the developing brain of autistic subjects. Studies by Fatemi et al. [37, 38] link the migration and lamination defects to a striking reduction of reelin (by 40%) and Bcl-2 (by 34–51%) in the brains of autistic subjects. Our studies along with others’
