From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition

Adam M H Young; Bhismadev Chakrabarti; David Roberts; Meng-Chuan Lai; John Suckling; Simon Baron-Cohen

doi:10.1186/s13229-016-0068-x

From molecules to neural morphology: understanding neuroinflammation in autism spectrum condition

Mol Autism. 2016 Jan 20:7:9. doi: 10.1186/s13229-016-0068-x. eCollection 2016.

Authors

Adam M H Young¹, Bhismadev Chakrabarti², David Roberts³, Meng-Chuan Lai⁴, John Suckling⁵, Simon Baron-Cohen⁶

Affiliations

¹ Autism Research Centre, Department of Psychiatry, University of Cambridge, Douglas House, 18B Trumpington Road, Cambridge, UK ; School of Clinical Medicine, Addenbrookes Hospital, University of Cambridge, Cambridge, UK.
² Autism Research Centre, Department of Psychiatry, University of Cambridge, Douglas House, 18B Trumpington Road, Cambridge, UK ; Centre for Integrative Neuroscience and Neurodynamics, School of Psychology and Clinical Language Science, University of Reading, Reading, UK.
³ School of Clinical Medicine, Addenbrookes Hospital, University of Cambridge, Cambridge, UK.
⁴ Autism Research Centre, Department of Psychiatry, University of Cambridge, Douglas House, 18B Trumpington Road, Cambridge, UK ; Centre for Addiction and Mental Health and Department of Psychiatry, University of Toronto, Toronto, Canada ; Department of Psychiatry, National Taiwan University Hospital and College of Medicine, Taipei, Taiwan.
⁵ Brain Mapping Unit, Department of Psychiatry, University of Cambridge, Cambridge, UK ; Behavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.
⁶ Autism Research Centre, Department of Psychiatry, University of Cambridge, Douglas House, 18B Trumpington Road, Cambridge, UK ; CLASS Clinic, Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK.

Abstract

Growing evidence points toward a critical role for early (prenatal) atypical neurodevelopmental processes in the aetiology of autism spectrum condition (ASC). One such process that could impact early neural development is inflammation. We review the evidence for atypical expression of molecular markers in the amniotic fluid, serum, cerebrospinal fluid (CSF), and the brain parenchyma that suggest a role for inflammation in the emergence of ASC. This is complemented with a number of neuroimaging and neuropathological studies describing microglial activation. Implications for treatment are discussed.

Keywords: Autism; Brain; Inflammation; NF-κB.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Amniotic Fluid / chemistry
Animals
Antigens, Surface / immunology
Autism Spectrum Disorder / genetics
Autism Spectrum Disorder / immunology
Autism Spectrum Disorder / pathology*
Autoantibodies / analysis
Body Fluids / chemistry*
Brain / embryology
Brain / immunology
Brain / pathology
Brain Chemistry*
Chemokines / analysis
Cytokines / analysis*
Female
Glutamic Acid / metabolism
HLA Antigens / immunology
Haplorhini
Humans
Immunity, Maternally-Acquired
Inflammation
Inflammation Mediators / analysis*
Lipopolysaccharides / blood
Maternal-Fetal Exchange
Mice
Nerve Tissue Proteins / immunology
Neuroglia / physiology
Neuroimaging
Pregnancy
Pregnancy Complications, Infectious / blood
Prenatal Exposure Delayed Effects
Signal Transduction

Substances

Antigens, Surface
Autoantibodies
Chemokines
Cytokines
HLA Antigens
Inflammation Mediators
Lipopolysaccharides
Nerve Tissue Proteins
Glutamic Acid

Grants and funding

G0600977/MRC_/Medical Research Council/United Kingdom