Disrupted network interactions serve as a neural marker of dyslexia.
Journal
Communications biology
ISSN: 2399-3642
Titre abrégé: Commun Biol
Pays: England
ID NLM: 101719179
Informations de publication
Date de publication:
03 11 2023
03 11 2023
Historique:
received:
02
03
2023
accepted:
24
10
2023
medline:
6
11
2023
pubmed:
4
11
2023
entrez:
4
11
2023
Statut:
epublish
Résumé
Dyslexia, a frequent learning disorder, is characterized by severe impairments in reading and writing and hypoactivation in reading regions in the left hemisphere. Despite decades of research, it remains unclear to date if observed behavioural deficits are caused by aberrant network interactions during reading and whether differences in functional activation and connectivity are directly related to reading performance. Here we provide a comprehensive characterization of reading-related brain connectivity in adults with and without dyslexia. We find disrupted functional coupling between hypoactive reading regions, especially between the left temporo-parietal and occipito-temporal cortices, and an extensive functional disruption of the right cerebellum in adults with dyslexia. Network analyses suggest that individuals with dyslexia process written stimuli via a dorsal decoding route and show stronger reading-related interaction with the right cerebellum. Moreover, increased connectivity within networks is linked to worse reading performance in dyslexia. Collectively, our results provide strong evidence for aberrant task-related connectivity as a neural marker for dyslexia that directly impacts behavioural performance. The observed differences in activation and connectivity suggest that one effective way to alleviate reading problems in dyslexia is through modulating interactions within the reading network with neurostimulation methods.
Identifiants
pubmed: 37923809
doi: 10.1038/s42003-023-05499-2
pii: 10.1038/s42003-023-05499-2
pmc: PMC10624919
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1114Informations de copyright
© 2023. The Author(s).
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