The role of interferon signaling in neurodegeneration and neuropsychiatric disorders.

Front Psychiatry

Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, United States.

Published: October 2024

AI Article Synopsis

  • Recent transcriptomics studies show increased interferon (IFN) responses in various neurodegenerative diseases such as Alzheimer's and Parkinson's, highlighting these responses in both microglia and T cells.
  • The literature indicates that abnormal IFN signaling is also linked to neuropsychiatric disorders like major depression and PTSD.
  • This review aims to summarize findings about IFN responses in neurodegeneration, discuss how sex and ancestry influence these responses, and explore potential reasons for elevated antiviral IFN signaling in neurological and psychiatric conditions without viral involvement.

Article Abstract

Recent advances in transcriptomics research have uncovered heightened interferon (IFN) responses in neurodegenerative diseases including Alzheimer's disease, primary tauopathy, Parkinson's disease, TDP-43 proteinopathy, and related mouse models. Augmented IFN signaling is now relatively well established for microglia in these contexts, but emerging work has highlighted a novel role for IFN-responsive T cells in the brain and peripheral blood in some types of neurodegeneration. These findings complement a body of literature implicating dysregulated IFN signaling in neuropsychiatric disorders including major depression and post-traumatic stress disorder. In this review, we will characterize and integrate advances in our understanding of IFN responses in neurodegenerative and neuropsychiatric disease, discuss how sex and ancestry modulate the IFN response, and examine potential mechanistic explanations for the upregulation of antiviral-like IFN signaling pathways in these seemingly non-viral neurological and psychiatric disorders.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11484020PMC
http://dx.doi.org/10.3389/fpsyt.2024.1480438DOI Listing

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