Abstract Although substantive understanding of brain dysfunction in autism remains meager, clinical evidence as well as animal brain research on the effects of early damage to selective brain system have now yielded enough knowledge that some provisional hypotheses concerning the etiology of autism can be generated. Basically, the underlying premise of this review is that a major dysfunction of the autistic brain resides in neural mechanisms of the structures in the medial temporal lobe, and, perhaps, more specifically the amygdaloid complex. This review begins with a summary of clinical evidence of the involvement of the medial temporal lobe structures in autism. The major behavioral disturbances seen in monkeys that had received neonatal lesions of the medial temporal lobe structures are then described. From this survey it can be seen that distinct patterns of memory losses and socioemotional abnormalities emerge as a result of extent of damage to the medial temporal lobe structures. The potential value of the experimental findings for an understanding of neural dysfunction in autism as well as directions of future research are discussed in the final section of the review.