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TNF alpha in MS and Its Animal Models: Implications for Chronic Pain in the Disease
Journal article   Open access   Peer reviewed

TNF alpha in MS and Its Animal Models: Implications for Chronic Pain in the Disease

Aislinn D. Maguire, John R. Bethea and Bradley J. Kerr
Frontiers in neurology, v 12, pp 780876-780876
06 Dec 2021
PMID: 34938263
url
https://doi.org/10.3389/fneur.2021.780876View
Published, Version of Record (VoR)CC BY V4.0 Open

Abstract

Clinical Neurology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology
Multiple Sclerosis (MS) is a debilitating autoimmune disease often accompanied by severe chronic pain. The most common type of pain in MS, called neuropathic pain, arises from disease processes affecting the peripheral and central nervous systems. It is incredibly difficult to study these processes in patients, so animal models such as experimental autoimmune encephalomyelitis (EAE) mice are used to dissect the complex mechanisms of neuropathic pain in MS. The pleiotropic cytokine tumor necrosis factor alpha (TNF alpha) is a critical factor mediating neuropathic pain identified by these animal studies. The TNF signaling pathway is complex, and can lead to cell death, inflammation, or survival. In complex diseases such as MS, signaling through the TNFR1 receptor tends to be pro-inflammation and death, whereas signaling through the TNFR2 receptor is pro-homeostatic. However, most TNF alpha-targeted therapies indiscriminately block both arms of the pathway, and thus are not therapeutic in MS. This review explores pain in MS, inflammatory TNF signaling, the link between the two, and how it could be exploited to develop more effective TNF alpha-targeting pain therapies.

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16 citations in Scopus

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Clinical Neurology
Neurosciences
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