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J Neuropathol Exp Neurol. 2017 Mar 1;76(3):225-237. doi: 10.1093/jnen/nlx003.

Partial Agenesis and Hypoplasia of the Corpus Callosum in Idiopathic Autism.

Author information

1
Departments of Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.
2
Research Design and Analysis Services, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.
3
Human Genetics, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.
4
Behavioral Pharmacology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York, USA.
5
Departments of Neurology, Pathology and Psychiatry, NYU Langone Medical Center, New York, New York, USA.

Abstract

To test the hypothesis that developmental anomalies of the corpus callosum (CC), contribute to the pathogenesis of autism, we characterized the type, topography, and severity of CC pathology corresponding to reduced CC areas that are detected by magnetic resonance imaging in the brains of 11 individuals with autism and 11 controls. In the brains of 3 autistic subjects, partial CC agenesis resulted in complete or partial lack of interhemispheric axonal connections in CC segments III-V. In these cases, a combination of focal agenesis and uniform axonal deficit caused reduction of CC areas by 37%, of axon numbers by 62%, and of the numerical density of axons by 39%. In the CC of 8 autistic subjects without agenesis, there was an 18% deficit of the midsagittal CC area, 48.4% deficit of axon numbers, and 37% reduction of the numerical density of axons. The significantly thinner CC, reduced CC area, and uniform axonal deficit in all autistic subjects were classified as CC hypoplasia. Thus, the byproduct of partial CC agenesis and hypoplasia is reduction of axonal connections between cortical areas known to be involved in behavioral alterations observed in people with autism.

KEYWORDS:

Agenesis; Autism; Corpus callosum; Hypoplasia; Morphometry; Neuropathology; Underconnectivity

PMID:
28395085
PMCID:
PMC5901096
DOI:
10.1093/jnen/nlx003
[Indexed for MEDLINE]
Free PMC Article

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