Autism Studies and Related Medical Conditions, January 2009 - TACA

mentally healthy women. Such results allow to consider elevated level of aAB to
NGF as a risk factor of mental pathology.
Zerrate, M. C., M. Pletnikov, et al. (2007). "Neuroinflammation and behavioral
abnormalities after neonatal terbutaline treatment in rats: implications for autism." J
Pharmacol Exp Ther 322(1): 16-22.
Autism is a neurodevelopmental disorder presenting before 3 years of age with
deficits in communication and social skills and repetitive behaviors. In addition to
genetic influences, recent studies suggest that prenatal drug or chemical
exposures are risk factors for autism. Terbutaline, a beta2-adrenoceptor agonist
used to arrest preterm labor, has been associated with increased concordance
for autism in dizygotic twins. We studied the effects of terbutaline on microglial
activation in different brain regions and behavioral outcomes in developing rats.
Newborn rats were given terbutaline (10 mg/kg) daily on postnatal days (PN) 2
to 5 or PN 11 to 14 and examined 24 h after the last dose and at PN 30.
Immunohistochemical studies showed that administration of terbutaline on PN 2
to 5 produced a robust increase in microglial activation on PN 30 in the cerebral
cortex, as well as in cerebellar and cerebrocortical white matter. None of these
effects occurred in animals given terbutaline on PN 11 to 14. In behavioral tests,
animals treated with terbutaline on PN 2 to 5 showed consistent patterns of
hyper-reactivity to novelty and aversive stimuli when assessed in a novel open
field, as well as in the acoustic startle response test. Our findings indicate that
beta2-adrenoceptor overstimulation during an early critical period results in
microglial activation associated with innate neuroinflammatory pathways and
behavioral abnormalities, similar to those described in autism. This study
provides a useful animal model for understanding the neuropathological
processes underlying autism spectrum disorders.
Zimmerman, A. W., S. L. Connors, et al. (2007). "Maternal antibrain antibodies in
autism." Brain Behav Immun 21(3): 351-7.
Autism is a neurodevelopmental disorder of prenatal onset that is behaviorally
defined. There is increasing evidence for systemic and neuroimmune
mechanisms in children with autism. Although genetic factors are important,
atypical prenatal maternal immune responses may also be linked to the
pathogenesis of autism. We tested serum reactivity in 11 mothers and their
autistic children, maternal controls, and several groups of control children, to
prenatal, postnatal, and adult rat brain proteins, by immunoblotting. Similar
patterns of reactivity to prenatal (gestational day 18), but not postnatal (day 8)
or adult rat brain proteins were identified in autistic children, their mothers, and
children with other neurodevelopmental disorders, and differed from mothers of
normal children, normal siblings of children with autism and normal child
controls. Specific patterns of antibody reactivity were present in sera from the
autism mothers, from 2 to 18 years after the birth of their affected children and
were unrelated to birth order. Immunoblotting using specific antigens for myelin
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