Regular ArticleIs autism due to cerebral–cerebellum disconnection?
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Cited by (18)
From molecules to behavior: An integrative theory of autism spectrum disorder
2016, Medical HypothesesCitation Excerpt :Crucially for our hypothesis, these aspects are also reported as abnormal in autistic individuals [40]. Skoyles [41] hypothesized that cognitive disorders, such as ASD, arise from an impaired interaction between the cerebellum and the PFC. This idea is not new in the field of cognitive disorders, as Andreasen et al. [42] reported dysfunctional patterns of blood flow in the cerebellar-thalamic-prefrontal circuit in schizophrenic subjects, suggesting a dysfunctional interaction. Moreover, motor and cognitive deficits seem to relate to each other in ASD [35], as better motor skills predict better daily living skills [43] and motor control deficits relate to the severity of ASD symptoms [44].
Dynamic screening of autistic children in various mental states using pattern of connectivity between brain regions
2015, Applied Soft Computing JournalCitation Excerpt :Recent studies have indicated that autistic patients mostly have thinner calcium channels in their neural systems [21]. This fact can reduce functional connections within the local neural architectures and changes the global patterns as well [17,22,23]. Such alterations of the brain functional and structural connectome in ASD subjects have been indicated in neuroimaging studies [20,24–28].
Embryological exposure to valproic acid disrupts morphology of the deep cerebellar nuclei in a sexually dimorphic way
2015, International Journal of Developmental NeuroscienceCitation Excerpt :It is important to underscore just how early in development VPA induced ASD is occurring. In both humans, and rodents the critical window of exposure happens prior to cortical development at a time when brainstem and cranial motor nerve nuclei are forming (Skoyles, 2002). This suggests that (at least for this teratogen) cortical deficits occur secondary to the initial teratogenic mechanism of action.
A proposed mechanism for autism: An aberrant neuroimmune response manifested as a psychiatric disorder
2011, Medical HypothesesCitation Excerpt :These reasons demonstrate that the overall prevalence rate for the disorder might not actually be increasing, but that increased awareness of the disorder might be allowing for more accurate assessment and diagnosis of those with the disorder. There have been numerous proposed causes and causal hypotheses regarding autism, including Fragile-X syndrome, childhood vaccines (particularly concerning the mercury-based preservative thimerosal previously used in these vaccines), teratogenic agents such as thalidomide [9], xenobiotics, immune cell imbalance, Western cleanliness and the eradication of disease (the “hygiene hypothesis”) [10], neurotransmitter imbalances, and autoimmunity. Brudnak (2001) suggests that gut-associated lymphoid tissue (GALT) activation by bacterial infection during early fetal gestation causes the release of pro-inflammatory cytokines that in-turn act as a neuroimmune “switch” for autism development, and that the relative levels of IL-2 (a pro-inflammatory cytokine) and IL-10 (an anti-inflammatory cytokine) can be analyzed for switch activation [11].
A model of attentional impairments in autism: First steps toward a computational theory
2005, Cognitive Systems Research
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Correspondence to: John R. Skoyles PhD, Centre for Philosophy of Natural and Social Science, London School of Economics, Houghton Street, London WC2A 2AE UK. Phone: +4402077943052; E-mail:[email protected]