6 - Dysfunction and hyperfunction of the hippocampus in autism?

Summary

Introduction

Autism encompasses wide disparities of memory and learning: at one extreme, some children with autism learn virtually no language and very little about the world around them; at the opposite extreme, other children with autism may show prodigious memorization and savant abilities. In family members of individuals with autism, unusual intellectual abilities are over-represented (DeLong, Ritch & Burch, 2002; Dor-Shav & Horowitz, 1984). Memory ability – but not cognitive profiles of visualization and reasoning – has been found to differentiate high- and low- functioning individuals with autism (Russo et al., 2005). This suggests that the most disabling cognitive aspects of low-functioning autism may be due to memory disability (and raises the question whether the common research focus on high-functioning autism may tend to obscure the role of memory in the cognitive deficits of autism).

The hippocampus has a unique role in memory and cognition – a role that is still being clarified, and is directly pertinent to autism. In this chapter a genetic hypothesis will be presented, focused on hippocampal function and bringing together many seemingly unrelated aspects of autism. The hypothesis relates to the role of the GABA(A) receptor subunit gene GABRA5. This gene, located in chromosome 15q11–13, has been closely associated with autism in genetic linkage studies (McCauley et al., 2004; Shao et al., 2003). The same gene has been associated independently with bipolar disorder, a fact that is relevant to the hypothesis to be proposed (Otani et al., 2005; Papadimitriou et al., 2001).