Bokulic Panichi Leona, Stanca Stefano, Dolciotti Cristina, Bongioanni Paolo
Neuroscience Department, Azienda Ospedaliero-Universitaria Pisana, 56126 Pisa, Italy.
NeuroCare Onlus, 56124 Pisa, Italy.
Int J Mol Sci. 2025 May 12;26(10):4623. doi: 10.3390/ijms26104623.
Neurodegenerative diseases (NDs), including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis/motor neuron disease, and multiple sclerosis, are characterized by progressive loss of neuronal structure and function, leading to severe cognitive, motor, and behavioral impairments. They pose a significant and growing challenge due to their rising prevalence and impact on global health systems. The societal and emotional toll on patients, caregivers, and healthcare infrastructures is considerable. While significant progress has been made in elucidating the pathological hallmarks of these disorders, the underlying cellular and molecular mechanisms remain incompletely understood. Increasing evidence implicates oligodendrocytes and their progenitors-oligodendrocyte progenitor cells (OPCs)-in the pathogenesis of several NDs, beyond their traditionally recognized role in demyelinating conditions such as MS. Oligodendrocytes are essential for axonal myelination, metabolic support, and neural circuit modulation in the central nervous system. Disruptions in oligodendrocyte function and myelin integrity-manifesting as demyelination, hypomyelination, or dysmyelination-have been associated with disease progression in various neurodegenerative contexts. This review consolidates recent findings on the role of OPCs in NDs, explores the concept of myelin plasticity, and discusses therapeutic strategies targeting oligodendrocyte dysfunction. By highlighting emerging research in oligodendrocyte biology, this review aims to provide a short overview of its relevance to neurodegenerative disease progression and potential therapeutic advances.
神经退行性疾病(NDs),包括阿尔茨海默病、帕金森病、肌萎缩侧索硬化症/运动神经元病和多发性硬化症,其特征是神经元结构和功能逐渐丧失,导致严重的认知、运动和行为障碍。由于其患病率不断上升以及对全球卫生系统的影响,它们构成了重大且日益严峻的挑战。对患者、护理人员和医疗保健基础设施造成的社会和情感负担相当大。尽管在阐明这些疾病的病理特征方面取得了重大进展,但潜在的细胞和分子机制仍未完全了解。越来越多的证据表明,少突胶质细胞及其前体细胞——少突胶质前体细胞(OPCs)——在几种神经退行性疾病的发病机制中发挥作用,这超出了它们在诸如多发性硬化症等脱髓鞘疾病中传统上被认可的作用。少突胶质细胞对于中枢神经系统中的轴突髓鞘形成、代谢支持和神经回路调节至关重要。少突胶质细胞功能和髓鞘完整性的破坏——表现为脱髓鞘、髓鞘形成不足或髓鞘形成异常——已与各种神经退行性疾病背景下的疾病进展相关联。本综述整合了关于少突胶质前体细胞在神经退行性疾病中作用的最新发现,探讨了髓鞘可塑性的概念,并讨论了针对少突胶质细胞功能障碍的治疗策略。通过强调少突胶质细胞生物学方面的新兴研究,本综述旨在简要概述其与神经退行性疾病进展的相关性以及潜在的治疗进展。