An appraisal of emerging therapeutic targets for multiple sclerosis derived from current preclinical models

被引:3
|
作者
Dixit, Aakanksha [1 ]
Savage, Hannah S. [1 ]
Greer, Judith M. [1 ]
机构
[1] Univ Queensland, UQ Ctr Clin Res, Royal Brisbane & Womens Hosp, Brisbane, Qld 4029, Australia
基金
英国医学研究理事会;
关键词
Multiple sclerosis; preclinical models; experimental autoimmune encephalomyelitis; cuprizone-induced demyelination; polarization of immune response; Regulatory T cells; CNS repair; remyelination; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; GENE-EXPRESSION; CELL-METABOLISM; ANIMAL-MODELS; T-CELL; MITOCHONDRIA; NEURONS; DISEASE; GROWTH; INJURY;
D O I
10.1080/14728222.2023.2236301
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
IntroductionMultiple sclerosis (MS) is a chronic inflammatory, demyelinating, and neurodegenerative condition affecting the central nervous system (CNS). Although therapeutic approaches have become available over the last 20 years that markedly slow the progression of disease, there is no cure for MS. Furthermore, the capacity to repair existing CNS damage caused by MS remains very limited.Areas coveredSeveral animal models are widely used in MS research to identify potential druggable targets for new treatment of MS. In this review, we look at targets identified since 2019 in studies using these models, and their potential for effecting a cure for MS.Expert opinionRefinement of therapeutic strategies targeting key molecules involved in the activation of immune cells, cytokine, and chemokine signaling, and the polarization of the immune response have dominated recent publications. While some progress has been made in identifying effective targets to combat chronic demyelination and neurodegeneration, much more work is required. Progress is largely limited by the gaps in knowledge of how the immune system and the nervous system interact in MS and its animal models, and whether the numerous targets present in both systems respond in the same way in each system to the same therapeutic manipulation.
引用
收藏
页码:553 / 574
页数:22
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