Authors: Nicolas Langer, Barbara Peysakhovich, Jennifer Zuk, Marie Drottar, Danielle D Sliva, Sara Smith, Bryce L C Becker, P Ellen Grant, Nadine Gaab.

Article: White Matter Alterations in Infants at Risk for Developmental Dyslexia.

Publication: Cerebral Cortex (Oxford University Press). Volume 27, Issue 2, Pages 1027–1036, 2017 | DOI: 10.1093/cercor/bhv281

[Full Text]


Developmental dyslexia (DD) is a heritable condition characterized by persistent difficulties in learning to read. White matter alterations in left-lateralized language areas, particularly in the arcuate fasciculus (AF), have been observed in DD, and diffusion properties within the AF correlate with (pre-)reading skills as early as kindergarten. However, it is unclear how early these alterations can be observed. We investigated white matter structure in 14 infants with (FHD+; ages 6.6-17.6 months) and 18 without (FHD-; ages 5.1-17.6 months) familial risk for DD. Diffusion scans were acquired during natural sleep, and early language skills were assessed. Tractography for bilateral AF was reconstructed using manual and automated methods, allowing for independent validation of results. Fractional anisotropy (FA) was calculated at multiple nodes along the tracts for more precise localization of group differences. The analyses revealed significantly lower FA in the left AF for FHD+ compared with FHD- infants, particularly in the central portion of the tract. Moreover, expressive language positively correlated with FA across groups. Our results demonstrate that atypical brain development associated with DD is already present within the first 18 months of life, suggesting that the deficits associated with DD may result from altered structural connectivity in left-hemispheric regions.

Tagged as: infants and neural connectivity


Langer N, Peysakhovich B, Zuk J, Drottar M, Sliva DD, Smith S, Becker BL, Grant PE, Gaab N. White Matter Alterations in Infants at Risk for Developmental Dyslexia. Cereb Cortex. 2017 Feb 1;27(2):1027-1036. doi: 10.1093/cercor/bhv281. PMID: 26643353; PMCID: PMC6074795.

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