Pantazou Vasiliki, Roux Thomas, Oliveira Moreira Vanessa, Lubetzki Catherine, Desmazières Anne
Paris Brain Institute (ICM), Sorbonne Université, CNRS, Inserm, GH Pitié-Salpêtrière, 47 boulevard de l'Hôpital, 75013 Paris, France.
Service de Neurologie, Centre Hospitalier Universitaire Vaudois, 46 Rue du Bugnon, 1011 Lausanne, Switzerland.
Life (Basel). 2021 Mar 11;11(3):231. doi: 10.3390/life11030231.
Multiple sclerosis (MS) is a complex central nervous system inflammatory disease leading to demyelination and associated functional deficits. Though endogenous remyelination exists, it is only partial and, with time, patients can enter a progressive phase of the disease, with neurodegeneration as a hallmark. Though major therapeutic advances have been made, with immunotherapies reducing relapse rate during the inflammatory phase of MS, there is presently no therapy available which significantly impacts disease progression. Remyelination has been shown to favor neuroprotection, and it is thus of major importance to better understand remyelination mechanisms in order to promote them and hence preserve neurons. A crucial point is how this process is regulated through the neuronal crosstalk with the oligodendroglial lineage. In this review, we present the current knowledge on neuron interaction with the oligodendroglial lineage, in physiological context as well as in MS and its experimental models. We further discuss the therapeutic possibilities resulting from this research field, which might allow to support remyelination and neuroprotection and thus limit MS progression.
多发性硬化症(MS)是一种复杂的中枢神经系统炎症性疾病,会导致脱髓鞘及相关功能缺陷。尽管存在内源性髓鞘再生,但它只是部分性的,随着时间推移,患者可能进入疾病的进展期,以神经退行性变为特征。虽然已经取得了重大治疗进展,免疫疗法降低了MS炎症期的复发率,但目前尚无能够显著影响疾病进展的疗法。髓鞘再生已被证明有利于神经保护,因此,更好地理解髓鞘再生机制以促进其发生从而保护神经元至关重要。一个关键问题是这个过程如何通过神经元与少突胶质细胞谱系的相互作用来调节。在这篇综述中,我们介绍了在生理背景以及MS及其实验模型中,关于神经元与少突胶质细胞谱系相互作用的当前知识。我们还讨论了该研究领域带来的治疗可能性,这可能有助于支持髓鞘再生和神经保护,从而限制MS的进展。