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Editorial commentary
Hyperexcitability and ALS
  1. Yu-ichi Noto1,
  2. Matthew C Kiernan2,3
  1. 1 Neurology, Kyoto Prefectural University of Medicine, Kyoto, Japan
  2. 2 Bushell Chair of Neurology, Brain and Mind Centre, University of Sydney, Sydney, New South Wales, Australia
  3. 3 Neurology, Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia
  1. Correspondence to Dr Yu-ichi Noto, Neurology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan; y-noto{at}koto.kpu-m.ac.jp

http://dx.doi.org/10.1136/jnnp-2021-328756

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    The development of hyperexcitability involving the central and peripheral nervous system has emerged as a pathophysiological process linked to the development of amyotrophic lateral sclerosis (ALS).1 In terms of causation, from a cortical perspective, hyperexcitability may evolve due to a range of factors, including dysfunction of glutamate transport mechanisms, defective RNA editing resulting in abnormal activation of specific glutamate receptors, and alteration of inhibitory signalling through pathological changes involving interneurons. Evidence supporting the role of cortical hyperexcitability has accumulated predominantly through neurophysiological …

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    Footnotes

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    • Contributors All authors contributed to the final version of the manuscript.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Provenance and peer review Commissioned; internally peer reviewed.

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