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A surprising role for myelin in Williams syndrome

A new study reveals an unexpected mechanism underlying behavioral abnormalities in the neurodevelopmental disorder Williams syndrome. A deficit in myelination, resulting from the deletion of a Williams syndrome-associated gene in forebrain excitatory neurons, causes hypersociability by impairing action potential conduction. Accordingly, rescuing myelination or conduction normalizes this behavior.

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Fig. 1: A new model of Williams syndrome.


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This work was supported by the NSERC (PGSD3-487560), the National Institutes of Health/National Institute of Neurological Disorders and Stroke (R01NS062796, R01NS097428, R01NS095889, R01NS088155), The Adelson Medical Research Foundation: ANDP (A130141), and the Rachleff Family Endowment.

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Correspondence to Jonah R. Chan.

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Osso, L.A., Chan, J.R. A surprising role for myelin in Williams syndrome. Nat Neurosci 22, 681–683 (2019).

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  • Williams syndrome

    • Beth A. Kozel
    • Boaz Barak
    • Barbara R. Pober

    Nature Reviews Disease Primers (2021)


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