• Yanick J Crow.
• Medical Research Council Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh, UK; Laboratory of Neurogenetics and Neuroinflammation, Imagine Institute, INSERM UMR1163, Paris, France. Electronic address: yanick.crow@ed.ac.uk.
• Lancet Neurol. 2024 Nov 1; 23 (11): 115811681158-1168.

AbstractThe ability to mount an interferon-mediated innate immune response is essential in protection against neurotropic viruses, but antiviral type I interferons also have neurotoxic potential. The production of type I interferons can be triggered by self-derived nucleic acids, and the brain can be susceptible to inappropriate upregulation of type I interferon signalling. Homoeostatic dysregulation of type I interferons has been implicated in rare inborn errors of immunity (referred to as type I interferonopathies) and more common neurodegenerative disorders (eg, Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis). Recent developments include new insights into the pathogenesis of these disorders that involve dysregulated type I interferon signalling, as well as advances in their diagnosis and management. The role of type I interferons in brain cellular health suggests the future therapeutic potential of approaches that target these interferons and their signalling.Copyright © 2024 Elsevier Ltd. All rights reserved.

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