Trained immunity in viral infections, Alzheimer's disease and multiple sclerosis: A convergence in type I interferon signalling and IFNβ-1a

George D Vavougios; Theodore Mavridis; Artemios Artemiadis; Karen A Krogfelt; Georgios Hadjigeorgiou

doi:10.1016/j.bbadis.2022.166430

Trained immunity in viral infections, Alzheimer's disease and multiple sclerosis: A convergence in type I interferon signalling and IFNβ-1a

Biochim Biophys Acta Mol Basis Dis. 2022 Sep 1;1868(9):166430. doi: 10.1016/j.bbadis.2022.166430. Epub 2022 May 10.

Authors

George D Vavougios¹, Theodore Mavridis², Artemios Artemiadis³, Karen A Krogfelt⁴, Georgios Hadjigeorgiou⁵

Affiliations

¹ Department Neurology, University of Cyprus, Lefkosia, Cyprus; Department of Respiratory Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa 41500, Greece. Electronic address: [email protected].
² 1st Neurology Department, Eginition Hospital, Medical School, National & Kapodistrian University of Athens, Greece.
³ Department Neurology, University of Cyprus, Lefkosia, Cyprus.
⁴ Molecular Virology Laboratory, Hellenic Pasteur Institute, Athens, Greece; Department of Molecular and Medical Biology, Centre for Mathematical Modeling - Human Health and Disease, PandemiX Center, Universitetsvej 1, 28A.1, DK-4000 Roskilde, Denmark.
⁵ Department Neurology, University of Cyprus, Lefkosia, Cyprus. Electronic address: [email protected].

PMID: 35550850
DOI: 10.1016/j.bbadis.2022.166430

Abstract

Type I interferon (IFN-I) signalling represents a major target for modulation in a virus' bid for latency. IFN-I perturbations are also present in such as Alzheimer's disease (AD) and multiple sclerosis (MS), where viral infections are known to increase symptomatic burden. IFN-I modulation such as via IFNβ-1a, an established MS treatment, has been researched to a limited extent to both AD and COVID-19. In this mini review, we present emerging research on trained immunity as a pathogenetic basis for Alzheimer's disease and the emerging context for IFNβ-1a repositioning, via mechanisms shared with multiple sclerosis and induced by viral infections.

Keywords: Alzheimer's disease; COVID-19; Drug repositioning; Innate immunity; Interferons.

Publication types

Review

MeSH terms

Alzheimer Disease*
COVID-19*
Humans
Interferon-beta
Multiple Sclerosis*
Virus Diseases*

Substances

Interferon-beta