Alteration of brain volume in IL-6 overexpressing mice related to autism

Hongen Wei, Susumu Mori, Kegang Hua, Xiaohong Li

Research output: Contribution to journalArticle

Abstract

Abnormal neuroimmune responses have been reported to be associated with autism and could be appropriate targets for pharmacologic intervention. Our previous studies showed that neuroimmune factor, interleukin (IL)-6, was significantly elevated in the fontal cortex and cerebellum of autistic subjects. The IL-6 overexpressing mice displayed several autism-like features as well as an abnormal dendritic spine morphology and synaptic function. The purpose of this study was to examine the volumetric differences in the brain of IL-6 overexpressing mice and compare with corresponding control mice using magnetic resonance imaging. Here we show that IL-6 overexpressing mice display an increase in the total brain volume. In addition, the lateral ventricle is also enlarged in the IL-6 overexpressing mice. The brain structures surrounding the lateral ventricle were squeezed and deformed from the normal location. These results indicate that IL-6 elevation in the brain could mediate neuroanatomical abnormalities. Taking together with our previous findings, a mechanism by which IL-6 may be involved in the pathogenesis of autism is proposed.

Original languageEnglish (US)
Pages (from-to)554-559
Number of pages6
JournalInternational Journal of Developmental Neuroscience
Volume30
Issue number7
DOIs
StatePublished - Nov 2012

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Autistic Disorder
Interleukin-6
Lateral Ventricles
Brain
Dendritic Spines
Cerebellum
Magnetic Resonance Imaging
mouse interleukin-6

Keywords

  • Autism
  • Brain
  • Interleukin-6
  • Magnetic resonance imaging
  • Volume measurement

ASJC Scopus subject areas

  • Developmental Biology
  • Developmental Neuroscience

Cite this

Alteration of brain volume in IL-6 overexpressing mice related to autism. / Wei, Hongen; Mori, Susumu; Hua, Kegang; Li, Xiaohong.

In: International Journal of Developmental Neuroscience, Vol. 30, No. 7, 11.2012, p. 554-559.

Research output: Contribution to journalArticle

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