Aguzzi, Erika A; Desai, Roshni A; Yang, Zhiyuan; Davies, Andrew L; Mahad, Don; Siow, Bernard; Yenicelik, Ayse G; ... Smith, Kenneth J; + view all Aguzzi, Erika A; Desai, Roshni A; Yang, Zhiyuan; Davies, Andrew L; Mahad, Don; Siow, Bernard; Yenicelik, Ayse G; Desai, Radha; Giama, Eleni; Almasri, AlBeshr; Colman, Miranda; Geywitz, Celine; Schirmer, Lucas; Felts, Paul A; Smith, Kenneth J; - view fewer (2025) A cause and protective treatment for acute and progressive disability and grey matter atrophy. Brain 10.1093/brain/awaf465. (In press).

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Abstract

Acutely inflamed CNS lesions can be sufficiently hypoxic to cause temporary neurological disability. A new experimental lesion reveals that brief hypoxia can also ignite a slow-burning atrophy of the grey matter, resulting in a lifetime of slowly progressive disability. The progressive disability eventually exceeds that observed acutely, indicating that acutely functioning tissue can nevertheless be destined to atrophy. Remarkably, both the temporary initial disability and the ensuing progressive disability and atrophy are significantly reduced if the acute hypoxia is avoided by four days of treatment with vasodilating nimodipine, or by simply breathing raised oxygen concentration. Thus, a lifetime of progressive disability and neurodegeneration can be the legacy of a few days of inflammatory hypoxia experienced in young adulthood, and avoided by maintaining lesion oxygenation. The findings may help to understand and treat some progressive neurological disorders, including multiple sclerosis.

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