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dc.contributor.authorThomas, Michael S. C.en
dc.contributor.authorDavis, Rachaelen
dc.contributor.authorKarmiloff-Smith, Annetteen
dc.contributor.authorKnowland, Victoria C. P.en
dc.contributor.authorCharman, Tonyen
dc.date.accessioned2021-09-23T15:25:01Z
dc.date.available2021-09-23T15:25:01Z
dc.date.issued2015-04-06
dc.identifier.citationThomas, M., Davis, R., Karmiloff-Smith, A., Knowland, V. and Charman, T. (2016) 'The over-pruning hypothesis of autism', Developmental Science, 19(2), pp. 284-305.en
dc.identifier.issn1467-7687en
dc.identifier.urihttps://doi.org/10.1111/desc.12303
dc.identifier.urihttps://eresearch.qmu.ac.uk/handle/20.500.12289/11497
dc.descriptionRachael Davis - ORCID: 0000-0002-3887-6003 https://orcid.org/0000-0002-3887-6003en
dc.descriptionPreviously deposited in BIROn - Birkbeck Institutional Research Online on 13 Apr 2015 at: https://eprints.bbk.ac.uk/id/eprint/11590/
dc.descriptionItem not available in this repository.
dc.description.abstractThis article outlines the over-pruning hypothesis of autism. The hypothesis originates in a neurocomputational model of the regressive sub-type (Thomas, Knowland & Karmiloff-Smith, 2011a, 2011b). Here we develop a more general version of the over-pruning hypothesis to address heterogeneity in the timing of manifestation of ASD, including new computer simulations which reconcile the different observed developmental trajectories (early onset, late onset, regression) via a single underlying atypical mechanism; and which show how unaffected siblings of individuals with ASD may differ from controls either by inheriting a milder version of the pathological mechanism or by co-inheriting the risk factors without the pathological mechanism. The proposed atypical mechanism involves overly aggressive synaptic pruning in infancy and early childhood, an exaggeration of a normal phase of brain development. We show how the hypothesis generates novel predictions that differ from existing theories of ASD including that (1) the first few months of development in ASD will be indistinguishable from typical, and (2) the earliest atypicalities in ASD will be sensory and motor rather than social. Both predictions gain cautious support from emerging longitudinal studies of infants at-risk of ASD. We review evidence consistent with the over-pruning hypothesis, its relation to other current theories (including C. Frith's under-pruning proposal; C. Frith, 2003, 2004), as well as inconsistent data and current limitations. The hypothesis situates causal accounts of ASD within a framework of protective and risk factors (Newschaffer et al., 2012); clarifies different versions of the broader autism phenotype (i.e. the implication of observed similarities between individuals with autism and their family members); and integrates data from multiple disciplines, including behavioural studies, neuroscience studies, genetics, and intervention studies.en
dc.description.sponsorshipMRC Career Establishment. Grant Number: G0300188 ESRC. Grant Number: RES-062-23-2721 Leverhulme Study Abroad Fellowship held at the University of Chicago Bloomsbury Studentship Awarden
dc.description.urihttps://doi.org/10.1111/desc.12303en
dc.format.extent284-305en
dc.language.isoenen
dc.publisherWileyen
dc.relation.ispartofDevelopmental Scienceen
dc.titleThe over-pruning hypothesis of autismen
dc.typeArticleen
dcterms.accessRightsnone
dcterms.dateAccepted2015-02-06
dc.description.volume19en
dc.description.ispublishedpub
rioxxterms.typeJournal Article/Reviewen
rioxxterms.publicationdate2015-04-06
refterms.depositExceptionNAen
refterms.accessExceptionNAen
refterms.technicalExceptionNAen
refterms.panelUnspecifieden
qmu.authorDavis, Rachaelen
dc.description.statuspub
dc.description.number2en
refterms.versionNAen


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