Progression Independent of Relapse Activity in Multiple Sclerosis: Closer to Solving the Pathologic Puzzle

Carmen Tur1, Maria A Rocca1

  • 1From the Multiple Sclerosis Centre of Catalonia (Cemcat) (C.T.), Department of Neurology, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Spain; NMR Unit, Queen Square MS Centre (C.T.), Department of Neuroinflammation, UCL Queen Square Institute of Neurology, University College London, United Kingdom; Neuroimaging Research Unit (M.A.R.), Institute of Experimental Neurology, Division of Neuroscience, and Neurology Unit, IRCCS San Raffaele Scientific Institute; and Vita-Salute San Raffaele University (M.A.R.), Milan, Italy.

Neurology
|January 2, 2024
PubMed

Insights

Progression independent of relapse activity (PIRA) is a key driver of disability in multiple sclerosis (MS), even in relapsing-remitting forms. Understanding PIRA

Area of Science:

  • Neuroimmunology
  • Neurodegeneration
  • Multiple Sclerosis Pathophysiology

Background:

  • Progression independent of relapse activity (PIRA) contributes significantly to disability accumulation in multiple sclerosis (MS).
  • PIRA affects individuals with relapsing-remitting MS (RRMS) and can occur at any disease stage.
  • Early PIRA onset is linked to poorer long-term prognoses in MS patients.

Discussion:

  • The precise pathological mechanisms underlying PIRA remain incompletely understood.
  • Emerging evidence suggests PIRA predominantly involves neurodegenerative processes.
  • PIRA may also be influenced by concurrent acute inflammatory activity in some MS cases.

Key Insights:

  • PIRA is a critical factor in MS disability accrual, distinct from relapse activity.
  • Neurodegeneration is increasingly recognized as a primary driver of PIRA.
  • Understanding PIRA's pathology is essential for developing effective MS treatments.

Outlook:

  • Further research into PIRA's pathological substrates is crucial.
  • Identifying PIRA mechanisms may lead to strategies to prevent irreversible disability in MS.
  • Targeting neurodegenerative pathways could offer new therapeutic avenues for MS management.

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