International Meeting for Autism Research (May 7 - 9, 2009): Familial Relationship for Anti-Human Brain Antibodies in Autism Spectrum Disorders (ASD)

Familial Relationship for Anti-Human Brain Antibodies in Autism Spectrum Disorders (ASD)

Thursday, May 7, 2009
Northwest Hall (Chicago Hilton)
3:30 PM
P. E. Goines , Rheumatology, University of California, Davis, Davis, CA
D. Braunschweig , Internal Medicine, University of California at Davis, Davis, CA
R. Boyce , Internal Medicine, University of California at Davis, Davis, CA
P. Ashwood , Department of Medical Microbiology and Immunology, M.I.N.D. Institute, University of California at Davis, Sacramento, CA
J. Van de Water , Rheumatology, Allergy and Clinical Immunology, University of California at Davis, Davis, CA
Background: Autism spectrum disorders (ASD) may result from a gestational insult that alters neurodevelopment.  Mothers of children with autism have a higher incidence of circulating antibodies directed towards fetal brain proteins than mothers of typically developing (TD) children.  Some children with autism also produce brain-targeted autoantibodies in contrast to age-matched TD controls.  It is currently unknown whether mothers with antibodies toward fetal brain proteins are maternally related to ASD subjects producing brain-directed antibodies. 

Objectives:  Explore a familial relationship in autoantibody production through comparison of human brain autoantibodies in plasma from autism and control subjects whose mothers have been pre-screened for fetal brain-reactive IgG.

Methods: Subjects are children of mothers previously tested for plasma anti-fetal brain IgG.  Plasma from ASD and TD control children was analyzed using western blot for reactivity to human hypothalamus, cerebellum, fetal, and whole adult brain protein medleys.  Reactivity to brain proteins was compared with respect to familial relationships, as well as the developmental outcome of the child. 

Results: Preliminary results suggest that children of mothers with antibodies to fetal brain proteins have equal chances of developing IgG to brain proteins as children of non-reactive mothers.  Thus, it appears as though there is little to no correlation between the presence of autoantibodies in the mothers of children with autism and autoantibodies to brain proteins in their offspring. 

Conclusions: A mother-child relationship regarding anti-brain IgG may indicate a strongly heritable predisposition towards autoimmunity.  Alternatively, maternal IgG-related interference in fetal neurodevelopment may cause production of brain reactive-IgG in the child.  A lack of correlation suggests that anti-brain IgG in mothers and children may represent distinct etiologies/ manifestations of ASD.

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