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Review
. 2019 Apr 11;16(1):80.
doi: 10.1186/s12974-019-1477-5.

TNFα inhibitors as targets for protective therapies in MSA: a viewpoint

Affiliations
Review

TNFα inhibitors as targets for protective therapies in MSA: a viewpoint

Alain Ndayisaba et al. J Neuroinflammation. .

Abstract

Multiple system atrophy (MSA) is a unique and fatal α-synucleinopathy associated with oligodendroglial inclusions and secondary neurodegeneration affecting striatum, substantia nigra, pons, and cerebellum. The pathogenesis remains elusive; however, there is emerging evidence suggesting a prominent role of neuroinflammation. Here, we critically review the relationship between αS and microglial activation depending on its aggregation state and its role in neuroinflammation to explore the potential of TNFα inhibitors as a treatment strategy for MSA and other neurodegenerative diseases.

Keywords: Disease-modifying treatment; Multiple system atrophy; Neurodegeneration; Neuroinflammation; TNFα; TNFα inhibitors.

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Conflict of interest statement

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable as no patients/participants are involved in this review.

Competing interests

The authors declare that they have no competing interests.

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Figures

Fig. 1
Fig. 1
TNFα in MSA pathogenesis. Misfolded αS leads to microglial activation and subsequent microglial release of pro-inflammatory cytokines. High levels of TNFα in vulnerable brain areas in MSA contribute to αS aggregation and establish a pro-apoptotic environment in chronic disease

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