Linking neocortical, cognitive, and genetic variability in autism with alterations of brain plasticity: The Trigger-Threshold-Target model

NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS

卷:47

Review

Mottron, Laurent^1,2,3,4  Belleville, Sylvie^4,5  Rouleau, Guy A.⁶  Collignon, Olivier⁷ 

[1] Univ Montreal CETEDUM, Ctr Excellence Troubles Envahissants Dev, Montreal, PQ, Canada

[2] Hop Riviere des Prairies, Dept Psychiat, Montreal, PQ, Canada

[3] Univ Montreal, Inst Univ Psychiat, Ctr Rech, Montreal, PQ, Canada

[4] Univ Montreal, Montreal, PQ, Canada

[5] Inst Univ Geriat Montreal, Ctr Rech, Montreal, PQ, Canada

[6] McGill Univ, Montreal Neurol Inst, Montreal, PQ, Canada

[7] Univ Trento, Ctr Mind Brain Sci, Trento, Italy

关键词: Autism;    Asperger;    Perception;    Language;    Speech;    Intellectual disability;    Cross-modal plasticity;    Synaptic plasticity;    Cortical reallocation;    Double-hit mechanism;    Syndromic autism;    Enhanced perceptual functioning;    Veridical mapping;   

DOI  :  10.1016/j.neubiorev.2014.07.012

来源: Elsevier

【 摘 要 】

The phenotype of autism involves heterogeneous adaptive traits (strengths vs. disabilities), different domains of alterations (social vs. non-social), and various associated genetic conditions (syndromic vs. nonsyndromic autism). Three observations suggest that alterations in experience-dependent plasticity are an etiological factor in autism: (1) the main cognitive domains enhanced in autism are controlled by the most plastic cortical brain regions, the multimodal association cortices; (2) autism and sensory deprivation share several features of cortical and functional reorganization; and (3) genetic mutations and/or environmental insults involved in autism all appear to affect developmental synaptic plasticity, and mostly lead to its upregulation. We present the Trigger-Threshold-Target (TTT) model of autism to organize these findings. In this model, genetic mutations trigger brain reorganization in individuals with a low plasticity threshold, mostly within regions sensitive to cortical reallocations. These changes account for the cognitive enhancements and reduced social expertise associated with autism. Enhanced but normal plasticity may underlie non-syndromic autism, whereas syndromic autism may occur when a triggering mutation or event produces an altered plastic reaction, also resulting in intellectual disability and dysmorphism in addition to autism. Differences in the target of brain reorganization (perceptual vs. language regions) account for the main autistic subgroups. In light of this model, future research should investigate how individual and sex-related differences in synaptic/regional brain plasticity influence the occurrence of autism. (C) 2014 The Authors. Published by Elsevier Ltd.

【 授权许可】

Free