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Determinants and Biomarkers of Progression Independent of Relapses in Multiple Sclerosis
Massimiliano Calabrese 
,
Paolo Preziosa ,
Antonio Scalfari ,
Elisa Colato,
Damiano Marastoni,
Martina Absinta,
Marco Battaglini,
Nicola De Stefano,
Massimiliano Di Filippo ,
Simon Hametner,
Owain Howell ,
Matilde Inglese,
Hans Lassmann,
Roland Martin,
Richard Nicholas ,
Richard Reynolds,
Maria A. Rocca ,
Agnese Tamanti,
Marco Vercellino,
Luisa Maria Villar ,
Massimo Filippi ,
Roberta Magliozzi
,
Paolo Preziosa ,
Antonio Scalfari ,
Elisa Colato,
Damiano Marastoni,
Martina Absinta,
Marco Battaglini,
Nicola De Stefano,
Massimiliano Di Filippo ,
Simon Hametner,
Owain Howell ,
Matilde Inglese,
Hans Lassmann,
Roland Martin,
Richard Nicholas ,
Richard Reynolds,
Maria A. Rocca ,
Agnese Tamanti,
Marco Vercellino,
Luisa Maria Villar ,
Massimo Filippi ,
Roberta Magliozzi
Annals of Neurology
Swansea University Author:
Owain Howell
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DOI (Published version): 10.1002/ana.26913
Abstract
Clinical, pathological, and imaging evidence in multiple sclerosis (MS) suggests that a smoldering inflammatory activity is present from the earliest stages of the disease and underlies the progression of disability, which proceeds relentlessly and independently of clinical and radiological relapses...
| Published in: | Annals of Neurology |
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| ISSN: | 0364-5134 1531-8249 |
| Published: |
Wiley
2024
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| Online Access: |
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| URI: | https://cronfa.swan.ac.uk/Record/cronfa66032 |
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| Abstract: |
Clinical, pathological, and imaging evidence in multiple sclerosis (MS) suggests that a smoldering inflammatory activity is present from the earliest stages of the disease and underlies the progression of disability, which proceeds relentlessly and independently of clinical and radiological relapses (PIRA). The complex system of pathological events driving “chronic” worsening is likely linked with the early accumulation of compartmentalized inflammation within the central nervous system as well as insufficient repair phenomena and mitochondrial failure. These mechanisms are partially lesion-independent and differ from those causing clinical relapses and the formation of new focal demyelinating lesions; they lead to neuroaxonal dysfunction and death, myelin loss, glia alterations, and finally, a neuronal network dysfunction outweighing central nervous system (CNS) compensatory mechanisms. This review aims to provide an overview of the state of the art of neuropathological, immunological, and imaging knowledge about the mechanisms underlying the smoldering disease activity, focusing on possible early biomarkers and their translation into clinical practice. |
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| College: |
Faculty of Medicine, Health and Life Sciences |