Autism Studies and Related Medical Conditions, January 2009 - TACA

eceptors and glutamate transporters in the cerebellum. These abnormalities
may be directly involved in the pathogenesis of the disorder.
Silva, S. C., C. Correia, et al. (2004). "Autoantibody repertoires to brain tissue in autism
nuclear families." J Neuroimmunol 152(1-2): 176-82.
The hypothesis of an immune dysfunction in autism spectrum disorders has
previously been put forward without, however, compelling evidence of a direct
relation to its etiology or pathogenesis. To further understand if autoimmunity
could play a significant role in autism, we analyzed autoantibody repertoires to
brain tissue extract in the plasma of 171 autism children, their parents, and 54
controls, by quantitative immunoblotting. Multiparametric analysis revealed
significant differences between patients and controls, and showed that one single
reactivity in Section 32 of the blot had the most power to discriminate between
these samples. Family correlation coefficients and heritability estimates did not
provide any evidence that this reactivity was genetically determined. While the
molecular weight of the target protein suggested that it might be an isoform of
Myelin Basic Protein (MBP), inhibition assays with human MBP argued against
this hypothesis. The study evidences the widespread occurrence of
autoreactivities to brain tissue in autism patients, which may represent the
immune system's neuroprotective response to a previous brain injury occurred
during neurodevelopment. The molecular identification of the target protein in
Section 32 will contribute to the understanding of the role of immune responses
against brain antigens in autistic patients.
Singer, H. S., C. M. Morris, et al. (2007). "Antibodies against fetal brain in sera of
mothers with autistic children." J Neuroimmunol.
Serum antibodies in 100 mothers of children with autistic disorder (MCAD) were
compared to 100 age-matched mothers with unaffected children (MUC) using as
antigenic substrates human and rodent fetal and adult brain tissues, GFAP, and
MBP. MCAD had significantly more individuals with Western immunoblot bands at
36 kDa in human fetal and rodent embryonic brain tissue. The density of bands
was greater in fetal brain at 61 kDa. MCAD plus developmental regression had
greater reactivity against human fetal brain at 36 and 39 kDa. Data support a
possible complex association between genetic/metabolic/environmental factors
and the placental transfer of maternal antibodies in autism.
Singer, H. S., C. M. Morris, et al. (2006). "Antibrain antibodies in children with autism
and their unaffected siblings." J Neuroimmunol 178(1-2): 149-55.
Serum autoantibodies to human brain, identified by ELISA and Western
immunoblotting, were evaluated in 29 children with autism spectrum disorder
(22 with autistic disorder), 9 non-autistic siblings and 13 controls. More autistic
subjects than controls had bands at 100 kDa in caudate, putamen and prefrontal
cortex (p