| プレナリーレクチャー3 |
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| PL3
The Trigger-Threshold-Target-Neglect Model for Autism：from genetic to cognitive neuroscience
Mottron Laurent
Research Chair in Autism Cognitive Neuroscience and Professor, University of Montréal, Canada
The recent discovery that genetic mutations involved in autism mostly upregulate early synaptic development supports a new conceptualization of autism, the Trigger-Threshold-Target-Neglect（TTTN）model. According to the TTTN model, autism results from a plastic reaction triggered by heterogeneous alterations, largely genetic in nature, but occasionally environmental, as those following exposure of the embryo to Valproic Acid during pregnancy. These genetic mutations underlie a lower threshold of brain reorganization targeting"sensitive"cerebral territories. This model is supported by the observation that a）the main cognitive domains enhanced in autism are subserved by the most plastic cortical brain region, the multimodal associative cortex；b）autistic cognitive enhancements are overlapping with those involved in cross modal plasticity following sensory impairment；c）autism is associated with an enhanced topographical variability of task-related activation in associative regions, indicative of an enhanced regional plasticity in functional allocation. The plastic reaction would be the only consequence of the genetic alteration in non-syndromic（or primary）autism, whereas syndromic（or secondary）autism would occur when the mutation alters typical plasticity mechanisms, resulting in intellectual disability and dysmorphism, in addition to autism. Differences in the regional target（perceptual vs. linguistic）of brain reorganization would account for the main subgroups of autistic spectrum phenotype. Neglect in the functions not targeted by this reorganization would be responsible for autistic deficits or lack of expertise, as in the social domain.
The TTTN model accounts for pairs of specific strengths and deficits is the ASD phenotype, like the coupling between speech delay and perceptual strengths in classical autism, and the coupling between precocious speech strengths and motor clumsiness in Asperger syndrome. At the neurobiological level, one consequence of this model is to question the validity of animal models of autism as they are currently conceived, as well as the justification of transposing to humans the pharmacological reversal of enhanced plasticity in these animal models. At the cognitive-neuroscience level, this model casts doubt on the definition of autism as a primary disorder of social cognition. Finally, at the early intervention level, the TTTN model orients toward the exposition of autistic toddlers to complex visual and auditory structures, thereby strongly modifying the current premises of early intensive behavioral intervention. | | | |
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