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Exploring the role of Type I Interferons in Neurological Diseases

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Type I Interferons (IFNs), including interferon-alpha (IFN-α) and interferon-beta (IFN-β), are pivotal components of the body's antiviral defense mechanism. Beyond their well-established roles in combating viral infections, these cytokines have become increasingly significant in the context of neurological diseases. Type I IFNs are integral to the immune response within the central nervous system (CNS), where they help regulate inflammation, maintain neural homeostasis, and protect against neurodegenerative processes.IFN-beta

 

In neurological research, type I IFNs have been most extensively studied in the context of multiple sclerosis (MS), an autoimmune disease characterized by chronic inflammation and demyelination of CNS tissues. IFN-β is a cornerstone of MS therapy, known for its ability to modulate immune activity, reduce relapse rates, and slow disease progression. Beyond MS, type I IFNs are being investigated for their roles in other neurological disorders, including viral encephalitis, neuromyelitis optics spectrum disorder, and more recently found to impact neurodegenerative diseases like Alzheimer's and Parkinson's.

 

Understanding the dual nature of type I IFNs--both protective and potentially pathogenic--is crucial. While they can initiate protective antiviral responses and modulate autoimmunity, dysregulation of type I IFN signaling is also implicated in exacerbating neuroinflammation and contributing to neuropathology. this complexity underscores the importance of precise regulation of type I IFNs in the CNS to harness their therapeutic potential while minimizing adverse effects.

 

The exploration of type I IFNs in neurological diseases is a dynamic and rapidly evolving field, offering insights that could lead to innovative treatments and improved outcomes for patients with a variety of CNS disorders. This research not only deepens our understanding of the immune-neural interface but also opens new avenues for therapeutic intervention.

 

Selected Publications for Additional Readings:

  • Viengkhou, B et al., (2024), "The brain microvasculature is a primary mediator of interferon-α neurotoxicity in human cerebral interferonopathies", Immunity, DOI: 10.1016/j.immuni.2024.05.017 
  • Vavougious, GD. et al., (2024), "Type I interferon signaling, cognition and neurodegeneration following COVID-19: update on a mechanistic pathogenetic model with implications for Alzheimer's disease", Front. Hum. Neurosci. 18:1352118, DOI: 10.3389/fnhum.2024.1352118
  • Viengkhou, B. et al., (2024), "Interferon-α receptor antisense oligonucleotides reduce neuroinflammation and neuropathology in a mouse model of cerebral interferonopathy", J.Clin Invest. 134(4):e169562, DOI: 10.1172/JCI169562
  • Crow, Y, and Stetson, D. (2022), "The Type I Interferonopathies: 10 years on", Nat rev Immunol. 22(8):471,, DOI: 10.1038/s41577-021-00633-9
  • Raftopoulou, R. et al., (2022), "The role of type I IFN in autoimmune and autoinflammatory diseases with CNS involvement", Front. Neurol., 13:1026449, DOI: 10.3389/fneur.2022.1026449

 

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