Women with autistic-spectrum disorder: magnetic resonance imaging study of brain anatomy

Craig, Michael C.; Zaman, Shahid; Daly, Eileen; Cutter, William; Robertson, Dene; Hallahan, Brian; Toal, Fiona; Reed, Suzie; Ambikapathy, Anita; Brammer, Mick; Murphy, Clodagh; Murphy, Declan

doi:10.1192/bjp.bp.106.034603

Cited by 70 publications

(75 citation statements)

References 33 publications

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“…For example, abnormalities in cerebellar synaptic plasticity, most notably basal LTD saturation in Nlgn3KO [136] and pat Dp/+ mice [137], have been shown to prevent subsequent LTD induction. Our current findings of cerebellar hyperplasia add to the data on ASD in humans, reporting cerebellar enlargement [127], excess cerebellar white matter [138,139], and abnormal PC number [125,140,141]. Furthermore, in addition to the impairments in social interaction and communication typical of ASD (reviewed in [141]) that are displayed by offspring after MIA, we provide experimental evidence for associated motor impairmentsanother characteristic associated with ASD (reviewed in [123]).…”

Section: Discussionsupporting

confidence: 56%

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

et al. 2015

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There have been suggestions that maternal immune activation is associated with alterations in motor behavior in offspring. To explore this further, we treated pregnant mice with polyinosinic:polycytidylic acid (poly(I:C)), a viral mimetic that activates the innate immune system, or saline on embryonic days 13-15. At postnatal day (P) 18, offspring cerebella were collected from perfused brains and immunostained as whole-mounts for zebrin II. Measurements of zebrin II+/- stripes in both sexes indicated that prenatal poly(I:C)-exposed offspring had significantly wider stripes; this difference was also seen in similarly treated offspring in adulthood (~P120). When sagittal sections of the cerebellum were immunostained for calbindin and Purkinje cell numbers were counted, we observed greater numbers of Purkinje cells in poly(I:C) offspring at both P18 and ~ P120. In adolescence (~P40), both male and female prenatal poly(I:C)-exposed offspring exhibited poorer performance on the rotarod and ladder rung tests; deficits in performance on the latter test persisted into adulthood. Offspring of both sexes from poly(I:C) dams also exhibited impaired social interaction in adolescence, but this difference was no longer apparent in adulthood. Our results suggest that maternal immune exposure at a critical time of cerebellum development can enhance neuronal survival or impair normal programmed cell death of Purkinje cells, with lasting consequences on cerebellar morphology and a variety of motor and non-motor behaviors.

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Section: Discussionsupporting

confidence: 56%

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

et al. 2015

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“…The brain regions with maximal increase in the oxidative stress marker, 3-NT, are: the orbitofrontal cortex, the Wernicke's area, the cerebellar hemispheres and vermis, putamen, and pons. The involvement of cerebellum in ASD is undisputed [21][22][23]; however, the involvement of both the putamen [24] and pons [25] in autism has only recently been recognized. While one should take caution in overinterpreting these preliminary results, the consistency regarding the cerebellar finding between the data derived from the present study and our earlier reports [11,12] is reassuring.…”

Section: Discussionmentioning

confidence: 99%

Brain Region-Specific Changes in Oxidative Stress and Neurotrophin Levels in Autism Spectrum Disorders (ASD)

Sajdel-Sulkowska

McGinnis³

et al. 2010

Cerebellum

126

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Autism spectrum disorders (ASD) are a group of neurodevelopmental disorders characterized by social and language deficits, stereotypic behavior, and abnormalities in motor functions. The particular set of behavioral impairments expressed in any given individual is variable across the spectrum. These behavioral abnormalities are consistent with our current understanding of the neuropathology of ASD which suggests abnormalities in the amygdala, temporal and frontal cortexes, hippocampus, and cerebellum. However, regions unrelated to these behavioral deficits appear largely intact. Both genetic predisposition and environmental toxins and toxicants have been implicated in the etiology of autism; the impact of these environmental triggers is associated with increases in oxidative stress, and is further exacerbated when combined with genetic susceptibility. We have previously reported increased levels of 3-nitrotyrosine (3-NT), a marker of oxidative stress, in ASD cerebella. We have also shown that this increase was associated with an elevation in neurotrophin-3 (NT-3) levels. The objectives of the current study were to determine whether the increase in oxidative stress in ASD is brain region-specific, to identify the specific brain regions affected by oxidative stress, and to compare brain region-specific NT-3 expression between ASD and control cases. The levels of 3-NT and NT-3 were measured with specific ELISAs in individual brain regions of two autistic and age- and postmortem interval (PMI)--matched control donors. In the control brain, the levels of 3-NT were uniformly low in all brain regions examined ranging from 1.6 to 12.0 pmol/g. On the other hand, there was a great variation in 3-NT levels between individual brain regions of the autistic brains ranging from 1.7 to 281.2 pmol/g. The particular brain regions with the increased 3-NT and the magnitude of the increase were both different in the two autistic cases. In the older autistic case, the brain regions with highest levels of 3-NT included the orbitofrontal cortex (214.5 pmol/g), Wernicke's area (171.7 pmol/g), cerebellar vermis (81.2 pmol/g), cerebellar hemisphere (37.2 pmol/g), and pons (13.6 pmol/g); these brain areas are associated with the speech processing, sensory and motor coordination, emotional and social behavior, and memory. Brain regions that showed 3-NT increase in both autistic cases included the cerebellar hemispheres and putamen. Consistent with our earlier report, we found an increase in NT-3 levels in the cerebellar hemisphere in both autistic cases. We also detected an increase in NT-3 level in the dorsolateral prefrontal cortex (BA46) in the older autistic case and in the Wernicke's area and cingulate gyrus in the younger case. These preliminary results reveal, for the first time, brain region-specific changes in oxidative stress marker 3-NT and neurotrophin-3 levels in ASD.

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“…Altogether, we included 15 studies describing regional grey matter volume differences. 30,32,35,38,41,[59][60][61][62][63][64][65][66][67][68] Of these, 3 studies compared both people with Asperger syndrome and autism separately with J Psychiatry Neurosci 2011;36(6) controls. 30,32,41 The final autism group comprised 9 studies (Table 1) with 151 patients (mean age 18 yr) and 190 controls (mean age 17 yr).…”

Section: Resultsmentioning

confidence: 99%

Can Asperger syndrome be distinguished from autism? An anatomic likelihood meta-analysis of MRI studies

Cheung

Chua

et al. 2011

jpn

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Women with autistic-spectrum disorder: magnetic resonance imaging study of brain anatomy

Abstract: Women with autistic-spectrum disorder have significant differences in brain anatomy from controls, in brain regions previously reported as abnormal in adult men with the disorder. Some anatomical differences may be related to clinical symptoms.

Cited by 70 publications

References 33 publications

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

Maternal Immune Activation Produces Cerebellar Hyperplasia and Alterations in Motor and Social Behaviors in Male and Female Mice

Brain Region-Specific Changes in Oxidative Stress and Neurotrophin Levels in Autism Spectrum Disorders (ASD)

Can Asperger syndrome be distinguished from autism? An anatomic likelihood meta-analysis of MRI studies

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