Authors:Inui, T., Kumagaya, S and Myowa-Yamakoshi, M.

Title:Neurodevelopmental hypothesis about the etiology of autism spectrum disorders.

Journal(書誌情報): Frontiers in Human Neuroscience




Previous models or hypotheses of autism spectral disorder (ASD)
failed to take into full consideration the chronological and causal
developmental trajectory, leading to the emergence of diverse phenotypes
 through a complex interaction between individual etiologies and
environmental factors. Those phenotypes include persistent deficits in
social communication and social interaction (criteria A in DSM-5), and
restricted, repetitive patterns of behavior, interests, or activities
(criteria B in DSM-5). In this article, we proposed a domain-general
model that can explain criteria in DSM-5 based on the assumption that
the same etiological mechanism would trigger the various phenotypes
observed in different individuals with ASD. In the model, we assumed the
 following joint causes as the etiology of autism: (1) Hypoplasia of
the  pons in the brainstem, occurring immediately following neural tube
 closure; and (2) Deficiency in the GABA (γ-aminobutyric acid)
developmental switch during the perinatal period. Microstructural
abnormalities of the pons directly affect both the structural and
functional development of the brain areas strongly connected to it,
especially amygdala. The impairment of GABA switch could not only lead
to the deterioration of inhibitory processing in the neural network, but
 could also cause abnormal cytoarchitecture. We introduced a
perspective  that atypical development in both brain structure and
function can give  full explanation of diverse phenotypes and
pathogenetic mechanism of  ASD. Finally, we discussed about neural
mechanisms underlying the  phenotypic characteristics of ASD that are
not described in DSM-5 but  should be considered as important
foundation: sleep, global precedence,  categorical perception,
intelligence, interoception and motor control.

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