The neuronal migration hypothesis of dyslexia : a critical evaluation 30 years on
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The capacity for language is one of the key features underlying the complexity of human cognition and its evolution. However, little is known about the neurobiological mechanisms that mediate normal or impaired linguistic ability. For developmental dyslexia, early postmortem studies conducted in the 1980s linked the disorder to subtle defects in the migration of neurons in the developing neocortex. These early studies were reinforced by human genetic analyses that identified dyslexia susceptibility genes and subsequent evidence of their involvement in neuronal migration. In this review, we examine recent experimental evidence that does not support the link between dyslexia and neuronal migration. We critically evaluate gene function studies conducted in rodent models and draw attention to the lack of robust evidence from histopathological and imaging studies in humans. Our review suggests that the neuronal migration hypothesis of dyslexia should be reconsidered, and the neurobiological basis of dyslexia should be approached with a fresh start.
Guidi , L G , Velayos-Baeza , A , Martinez-Garay , I , Monaca , A P , Paracchini , S , Bishop , D V M & Molnár , Z 2018 , ' The neuronal migration hypothesis of dyslexia : a critical evaluation 30 years on ' , European Journal of Neuroscience , vol. 48 , no. 10 , pp. 3212-3233 . https://doi.org/10.7287/peerj.preprints.26637v1 , https://doi.org/10.1111/ejn.14149
European Journal of Neuroscience
© 2018 Guidi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ Preprints) and either DOI or URL of the article must be cited.© 2018 The Authors. European Journal of Neuroscience published by Federation of European Neuroscience Societies and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
DescriptionThis work was supported by the Wellcome Trust (092071/Z/10/Z to A.P.M., Z.M. and A.V.-B., and 082498/Z/07/Z to D.V.M.B.); L.G.G. receive a Doctoral Training Award from the Medical Research Council; S.P. is a Royal Society University Research Fellow.
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