A systematic evaluation of dendritic and neuronal (MAP2, SMI-311) immunolabelling within the cerebral cortex in autism

Del Valle Suarez, E.; Schmitz, C; Rezaie, P. and Gabbott, P. (2009). A systematic evaluation of dendritic and neuronal (MAP2, SMI-311) immunolabelling within the cerebral cortex in autism. In: British Neuroscience Association 20th National meeting, 19-22 Apr 2009, Liverpool.


Autism Spectrum Disorders (ASD) are pervasive eurodevelopmental disorders clinically characterised by deficits in three core behavioural parameters: social interaction, communication and repetitive behaviours. There are currently no biological markers for ASD. Diagnosis is based solely on behavioural characteristics that vary considerably in severity. Neuropathology is varied and inconsistent amongst cases. The spatial arrangement of neurons is reportedly altered within cortical areas whose functions underlie behavioural changes in ASD. The aim of this study was to investigate the extent to which the dendritic architecture of these areas may likewise be affected. Formalin-fixed blocks of brain tissue (Brodmann Areas 9,11,17,24,25,32,36,44, 45,47) from 9 ASD cases (mean age: 28.4 ± 6.4 years) and 12 neurologically ‘typical’ cases (mean age: 31.4 ± 4.9 years) matched for hemisphere, gender and age, were obtained through the Autism Tissue Program (USA), from Harvard Brain and Tissue Resource Center, and NICHD Brain and Tissue Bank for Developmental Disorders, with ethical approval. Serial sections (paraffin wax, 10μm) immunolabelled with the neuronal somato-dendritic markers MAP2 and SMI-311, were assessed against a comprehensive set of criteria defining aspects of the cellular and dendritic organisation of the cortex. Detailed screening revealed marked variability in patterns of immunolabelling amongst control and ASD cases, and within cortical areas. While laminar disorganisation and excess white matter neurons were noted in some ASD cases, there was no single morphological descriptor that could differentiate between control and ASD cases. These neuropathological findings may in part reflect the clinical diversity of ASD.

Viewing alternatives

No digital document available to download for this item

Item Actions