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

George D Vavougios^*, Theodore Mavridis, Artemios Artemiadis, Karen A Krogfelt, Georgios Hadjigeorgiou

^*Corresponding author for this work

Department of Science and Environment

Research output: Contribution to journal › Review › peer-review

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.

Original language	English
Article number	166430
Journal	B B A - Molecular Basis of Disease
Volume	1868
Issue number	9
Pages (from-to)	166430
Number of pages	1
ISSN	0925-4439
DOIs	https://doi.org/10.1016/j.bbadis.2022.166430
Publication status	Published - 1 Sept 2022

Keywords

Alzheimer's disease
COVID-19
Drug repositioning
Innate immunity
Interferons

Link to document

10.1016/j.bbadis.2022.166430Licence: Other

Cite this

@article{713f41b045194918866e612787252677,

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

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",

author = "Vavougios, {George D} and Theodore Mavridis and Artemios Artemiadis and Krogfelt, {Karen A} and Georgios Hadjigeorgiou",

year = "2022",

month = sep,

day = "1",

doi = "10.1016/j.bbadis.2022.166430",

language = "English",

volume = "1868",

pages = "166430",

journal = "B B A - Molecular Basis of Disease",

issn = "0925-4439",

publisher = "Elsevier BV",

number = "9",

}

TY - JOUR

T1 - Trained immunity in viral infections, Alzheimer's disease and multiple sclerosis

T2 - A convergence in type I interferon signalling and IFNβ-1a

AU - Vavougios, George D

AU - Mavridis, Theodore

AU - Artemiadis, Artemios

AU - Krogfelt, Karen A

AU - Hadjigeorgiou, Georgios

PY - 2022/9/1

Y1 - 2022/9/1

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - COVID-19

KW - Drug repositioning

KW - Innate immunity

KW - Interferons

U2 - 10.1016/j.bbadis.2022.166430

DO - 10.1016/j.bbadis.2022.166430

M3 - Review

SN - 0925-4439

VL - 1868

SP - 166430

JO - B B A - Molecular Basis of Disease

JF - B B A - Molecular Basis of Disease

IS - 9

M1 - 166430

ER -