Department of Neuroscience, Central Clinical School, Monash University, Melborune, VIC 3004, Australia.
Laboratory of Experimental Neurology and Neuroimmunology, Department of Neurology, AHEPA University Hospital, Stilponos Kiriakides Str. 1, 54636 Thessaloniki, Greece.
Int J Mol Sci. 2023 Jul 5;24(13):11112. doi: 10.3390/ijms241311112.
Multiple sclerosis (MS) is a heterogeneous disease of the central nervous system that is governed by neural tissue loss and dystrophy during its progressive phase, with complex reactive pathological cellular changes. The immune-mediated mechanisms that promulgate the demyelinating lesions during relapses of acute episodes are not characteristic of chronic lesions during progressive MS. This has limited our capacity to target the disease effectively as it evolves within the central nervous system white and gray matter, thereby leaving neurologists without effective options to manage individuals as they transition to a secondary progressive phase. The current review highlights the molecular and cellular sequelae that have been identified as cooperating with and/or contributing to neurodegeneration that characterizes individuals with progressive forms of MS. We emphasize the need for appropriate monitoring via known and novel molecular and imaging biomarkers that can accurately detect and predict progression for the purposes of newly designed clinical trials that can demonstrate the efficacy of neuroprotection and potentially neurorepair. To achieve neurorepair, we focus on the modifications required in the reactive cellular and extracellular milieu in order to enable endogenous cell growth as well as transplanted cells that can integrate and/or renew the degenerative MS plaque.
多发性硬化症(MS)是一种中枢神经系统的异质性疾病,在其进行性阶段受神经组织损失和营养不良的支配,伴有复杂的反应性病理细胞变化。在急性发作复发期间促使脱髓鞘病变的免疫介导机制与进行性 MS 慢性病变期间的特征不同。这限制了我们针对疾病的有效靶向能力,因为它在中枢神经系统白质和灰质内演变,从而使神经科医生在个体过渡到继发性进行性阶段时没有有效的治疗选择。本综述强调了已经确定的分子和细胞后果,这些后果与进行性 MS 个体的神经退行性变特征合作和/或促成了神经退行性变。我们强调需要通过已知和新的分子和成像生物标志物进行适当监测,这些标志物可以准确检测和预测进展,以便进行新设计的临床试验,证明神经保护和潜在神经修复的疗效。为了实现神经修复,我们专注于反应性细胞和细胞外环境所需的修饰,以使内源性细胞生长以及可以整合和/或更新退行性 MS 斑块的移植细胞成为可能。