Both acute and smoldering neuroinflammation may occur from disease onset. Addressing both processes early on could help prevent disease progression and impact long-term disability outcomes in patients with MS.1,3,4

Illustration showing concurrent pathways of acute and smoldering neuroinflammation and the effects of these pathways in the brain with images of microglia, b-cells, t-cells, lesions and the blood brain barrier.

Occurring exclusively in the CNS, smoldering neuroinflammation has been largely inaccessible due to the lack of treatments that directly target disease-associated microglia and cross the blood-brain barrier.1,7,8

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Cross the blood-brain barrier

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Target disease-associated microglia

One way to impact smoldering neuroinflammation is to cross the blood-brain barrier and act directly on microglia to reduce neuroinflammatory and neurodegenerative processes.8

Illustration of a walker

Given the significant unmet need to effectively address disability accumulation, the next generation of DMTs should impact the main driver of disability: smoldering neuroinflammation.1,9,10

Hear from the experts

Celia Oreja-Guevara, MD, PhD, discusses the underlying biology of acute and smoldering neuroinflammation at EAN 2023 

Headshot of Celia Oreja-Guevara, MD PHD
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Smoldering Stories

Hear how smoldering neuroinflammation impacted the lives of patients with MS

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   References:

  1. Giovannoni G, Popescu V, Wuerfel J, et al. Smouldering multiple sclerosis: the ‘real MS’. Ther Adv Neurol Disord. 2022;15:17562864211066751. doi:10.1177/17562864211066751
  2. Cree BAC, Hollenbach JA, Bove R, et al; University of California, San Francisco MS-Epic Team. Silent progression in disease activity-free relapsing multiple sclerosis. Ann Neurol. 2019;85(5):653-666.
  3. Simpson A, Mowry EM, Newsome SD. Early aggressive treatment approaches for multiple sclerosis. Curr Treat Options Neurol. 2021;23:19. doi:10.1007/s11940-021-00677-1
  4. Scalfari A. MS can be considered a primary progressive disease in all cases, but some patients have superimposed relapses - Yes. Mult Scler. 2021;27(7):1002-1004.
  5. Yong VW. Microglia in multiple sclerosis: protectors turn destroyers. Neuron. 2022;110(21):3534-3548.
  6. Kuhlmann T, Moccia M, Coetzee T, et al. Multiple sclerosis progression: time for a new mechanism-driven framework. Lancet Neurol. 2023;22(1):78-88.
  7. Häusser-Kinzel S, Weber MS. The role of B cells and antibodies in multiple sclerosis, neuromyelitis optica, and related disorders. Front Immunol. 2019;10:201. doi:10.3389/fimmu.2019.00201
  8. Correale J, Halfon MJ, Jack D, Rubstein A, Villa A. Acting centrally or peripherally: a renewed interest in the central nervous system penetration of disease-modifying drugs in multiple sclerosis. Mult Scler Relat Disord. 2021;56:103264. doi:10.1016/j.msard.2021.103264
  9. Geladaris A, Torke S, Weber MS. Bruton’s Tyrosine Kinase inhibitors in multiple sclerosis: pioneering the path towards treatment of progression? CNS Drugs. 2022;36(10):1019-1030.
  10. Absinta M, Lassmann H, Trapp BD. Mechanisms underlying progression in multiple sclerosis. Curr Opin Neurol. 2020;33(3):277-285.