Sun Junjun, Zhou Hong, Bai Feng, Zhang Zhijun, Ren Qingguo
J Alzheimers Dis. 2017;58(3):597-612. doi: 10.3233/JAD-170036.
Myelin is a lipid-rich multilamellar membrane that wraps around long segments of neuronal axons and it increases the conduction of action potentials, transports the necessary trophic support to the neuronal axons, and reduces the energy consumed by the neuronal axons. Together with axons, myelin is a prerequisite for the higher functions of the central nervous system and complex forms of network integration. Myelin impairments have been suggested to lead to neuronal dysfunction and cognitive decline. Accumulating evidence, including brain imaging and postmortem and genetic association studies, has implicated myelin impairments in Alzheimer's disease (AD). Increasing data link myelin impairments with amyloid-β (Aβ) plaques and tau hyperphosphorylation, which are both present in patients with AD. Moreover, aging and apolipoprotein E (ApoE) may be involved in the myelin impairments observed in patients with AD. Decreased neuronal activity, increased Aβ levels, and inflammation further damage myelin in patients with AD. Furthermore, treatments that promote myelination contribute to the recovery of neuronal function and improve cognition. Therefore, strategies targeting myelin impairment may provide therapeutic opportunities for patients with AD.
髓磷脂是一种富含脂质的多层膜，包裹着神经元轴突的长段，它能增加动作电位的传导，将必要的营养支持输送到神经元轴突，并减少神经元轴突消耗的能量。与轴突一起，髓磷脂是中枢神经系统高级功能和复杂网络整合形式的先决条件。有人认为髓磷脂损伤会导致神经元功能障碍和认知能力下降。越来越多的证据，包括脑成像、尸检和基因关联研究，表明髓磷脂损伤与阿尔茨海默病（AD）有关。越来越多的数据将髓磷脂损伤与淀粉样β蛋白（Aβ）斑块和tau蛋白过度磷酸化联系起来，这两者在AD患者中都存在。此外，衰老和载脂蛋白E（ApoE）可能与AD患者中观察到的髓磷脂损伤有关。神经元活动减少、Aβ水平升高和炎症会进一步损害AD患者的髓磷脂。此外，促进髓鞘形成的治疗有助于神经元功能的恢复并改善认知。因此，针对髓磷脂损伤的策略可能为AD患者提供治疗机会。
