Department of Neurology, St. Josef-Hospital, Ruhr-University Bochum, Gudrunstr. 56, Bochum, Germany.
J Neural Transm (Vienna). 2013 Sep;120 Suppl 1:S49-53. doi: 10.1007/s00702-013-1037-6. Epub 2013 May 30.
Central nervous system (CNS) inflammation has been considered to be the main pathological feature of multiple sclerosis (MS). However, the complexity of this autoimmune disorder also comprises neurodegenerative processes that may occur within acute phases of inflammation, yet also temporally independent and outside of inflammatory lesions or even in so-called normal appearing white matter. Measurement strategies for neurodegeneration and neuroprotection include clinical parameters, magnetic resonance imaging and novel instruments such as diffusion tensor imaging or optical coherence tomography. Neurotrophic factors activate endogenous neuroprotective pathways. Their up-regulation by CNS-infiltrating immune cells has led to the concept of neuroprotective autoimmunity. The capacity to enhance this endogenous neuroprotection is a valuable property for therapeutic agents and has in detail been studied for glatirameracetate, laquinimod and dimethylfumarate. Multimodal measurement of neuroprotective properties of established and novel MS therapeutics and further elucidation of neuroprotective pathways within the autoimmune process will be useful to augment our insight into the complexity of the disease and to improve therapy, especially in terms of long-term disability and cognitive decline.
中枢神经系统(CNS)炎症被认为是多发性硬化症(MS)的主要病理特征。然而,这种自身免疫性疾病的复杂性还包括神经退行性过程,这些过程可能发生在炎症的急性期内,但也可能与炎症病变无关,甚至发生在所谓的正常表现的白质中。神经退行性变和神经保护的测量策略包括临床参数、磁共振成像和新型仪器,如扩散张量成像或光相干断层扫描。神经营养因子激活内源性神经保护途径。中枢神经系统浸润的免疫细胞上调其表达,导致了神经保护自身免疫的概念。增强这种内源性神经保护的能力是治疗剂的一个有价值的特性,已详细研究了用于治疗多发性硬化症的那他珠单抗、拉克替醇和富马酸二甲酯。对已建立的和新型多发性硬化症治疗药物的神经保护特性进行多模式测量,并进一步阐明自身免疫过程中的神经保护途径,将有助于我们更深入地了解疾病的复杂性,并改善治疗效果,特别是在长期残疾和认知能力下降方面。