Maiworm Michelle
Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.
Front Neurol. 2024 Aug 1;15:1385042. doi: 10.3389/fneur.2024.1385042. eCollection 2024.
Neuroplasticity as a mechanism to overcome central nervous system injury resulting from different neurological diseases has gained increasing attention in recent years. However, deficiency of these repair mechanisms leads to the accumulation of neuronal damage and therefore long-term disability. To date, the mechanisms by which remyelination occurs and why the extent of remyelination differs interindividually between multiple sclerosis patients regardless of the disease course are unclear. A member of the neurotrophins family, the brain-derived neurotrophic factor (BDNF) has received particular attention in this context as it is thought to play a central role in remyelination and thus neuroplasticity, neuroprotection, and memory.
To analyse the current literature regarding BDNF in different areas of multiple sclerosis and to provide an overview of the current state of knowledge in this field.
To date, studies assessing the role of BDNF in patients with multiple sclerosis remain inconclusive. However, there is emerging evidence for a beneficial effect of BDNF in multiple sclerosis, as studies reporting positive effects on clinical as well as MRI characteristics outweighed studies assuming detrimental effects of BDNF. Furthermore, studies regarding the Val66Met polymorphism have not conclusively determined whether this is a protective or harmful factor in multiple sclerosis, but again most studies hypothesized a protective effect through modulation of BDNF secretion and anti-inflammatory effects with different effects in healthy controls and patients with multiple sclerosis, possibly due to the pro-inflammatory milieu in patients with multiple sclerosis. Further studies with larger cohorts and longitudinal follow-ups are needed to improve our understanding of the effects of BDNF in the central nervous system, especially in the context of multiple sclerosis.
近年来,神经可塑性作为克服不同神经系统疾病所致中枢神经系统损伤的一种机制,受到了越来越多的关注。然而,这些修复机制的缺陷会导致神经元损伤的积累,进而导致长期残疾。迄今为止,髓鞘再生发生的机制以及为何多发性硬化症患者之间的髓鞘再生程度存在个体差异(无论病程如何)尚不清楚。作为神经营养因子家族的一员,脑源性神经营养因子(BDNF)在这方面受到了特别关注,因为它被认为在髓鞘再生以及神经可塑性、神经保护和记忆中起核心作用。
分析当前关于BDNF在多发性硬化症不同方面的文献,并概述该领域的现有知识状态。
迄今为止,评估BDNF在多发性硬化症患者中作用的研究尚无定论。然而,有新证据表明BDNF对多发性硬化症有有益作用,因为报告对临床和MRI特征有积极影响的研究超过了认为BDNF有有害影响的研究。此外,关于Val66Met多态性的研究尚未最终确定这在多发性硬化症中是一个保护因素还是有害因素,但同样,大多数研究假设通过调节BDNF分泌和抗炎作用有保护作用,在健康对照和多发性硬化症患者中有不同影响,这可能是由于多发性硬化症患者的促炎环境所致。需要进行更大样本队列和纵向随访的进一步研究,以增进我们对BDNF在中枢神经系统中的作用的理解,特别是在多发性硬化症的背景下。