Evidence map›Paper›PMID 30218584›Full record

ReviewThe European journal of neuroscience2018

The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on.

Luiz G Guidi, Antonio Velayos-Baeza, Isabel Martinez-Garay, Anthony P Monaco, Silvia Paracchini, Dorothy V M Bishop, Zoltán Molnár

Open access · hybridAbstract readReview
In one paragraph

Review in The European journal of neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
8.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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  19. Animal models of developmental dyslexia.Frontiers in neuroscience · 2022
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Luiz G GuidiDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, UK.ORCID 0000-0001-6351-7398
Antonio Velayos-BaezaDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, UK.ORCID 0000-0002-7717-4477
Isabel Martinez-GarayDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, UK.ORCID 0000-0001-6849-7496
Anthony P MonacoOffice of the President, Tufts University, Medford, Massachusetts.ORCID 0000-0001-7480-3197
Silvia ParacchiniSchool of Medicine, University of St Andrews, St Andrews, UK.ORCID 0000-0001-9934-8602
Dorothy V M BishopDepartment of Experimental Psychology, University of Oxford, Oxford, UK.ORCID 0000-0002-2448-4033
Zoltán MolnárDepartment of Physiology, Anatomy, and Genetics, University of Oxford, Oxford, UK.ORCID 0000-0002-6852-6004
University of Oxford · GBCentre for Human Genetics · GBTufts University · USUniversity of St Andrews · GB

Funding

Medical Research Council G0900901Medical Research Council MR/N026039/1Wellcome Trust 082498/Z/07/ZWellcome Trust 092071/Z/10/Z
6 · The paper itself

Abstract

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.

Indexed as

Cell MovementDisease Models, AnimalAnimalsDyslexiaGenetic Predisposition to DiseaseHumansNeocortexNeuronsdyslexiagene functionneuronal migrationneuropathologyRNA interference

Identifiers

PMID30218584
PMCPMC6282621
OpenAlexW2790086104

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.