A mechanism of virus-induced demyelination.
A mechanism of virus-induced demyelination.
复制标题
DOI：
10.1155/2010/109239
复制
发表时间：
2010-01-01
影响因子：
--
通讯作者：
Das Sarma, Jayasri
中科院分区：
文献类型：
--
作者：
Das Sarma, Jayasri
髓磷脂在中枢和外周神经系统中形成包围轴突的绝缘鞘，并且对于神经元动作电位的快速传播是必需的。脱髓鞘是一种获得性疾病，其中正常形成的髓鞘变性，使轴突暴露于细胞外环境。其结果是正常神经元之间的通讯功能障碍，在许多情况下，出现不同程度的轴突变性。存在许多中枢神经系统脱髓鞘疾病，包括多发性硬化症。虽然脱髓鞘是大多数脱髓鞘疾病的主要表现，但最近的研究清楚地记录了伴随的不同程度的轴突损失，导致长期残疾。轴突损伤可能继发于髓鞘损伤（由外向内模型）或髓鞘损伤可能继发于轴突损伤（由内向外模型）。病毒诱导的脱髓鞘模型，提供了独特的即将进入髓鞘破坏的细胞机制。它们阐明了病毒持续存在的机制，包括潜伏感染、病毒再激活和病毒诱导的组织损伤。这些研究也为研究免疫系统和中枢神经系统（CNS）之间的相互作用提供了极好的范例。在这篇综述中，我们将讨论在病毒诱导的多发性硬化小鼠模型中中枢神经系统轴突缺失和脱髓鞘的潜在细胞和分子机制。
Myelin forms an insulating sheath surrounding axons in the central and peripheral nervous systems and is essential for rapid propagation of neuronal action potentials. Demyelination is an acquired disorder in which normally formed myelin degenerates, exposing axons to the extracellular environment. The result is dysfunction of normal neuron-to-neuron communication and in many cases, varying degrees of axonal degeneration. Numerous central nervous system demyelinating disorders exist, including multiple sclerosis. Although demyelination is the major manifestation of most of the demyelinating diseases, recent studies have clearly documented concomitant axonal loss to varying degrees resulting in long-term disability. Axonal injury may occur secondary to myelin damage (outside-in model) or myelin damage may occur secondary to axonal injury (inside-out model). Viral induced demyelination models, has provided unique imminent into the cellular mechanisms of myelin destruction. They illustrate mechanisms of viral persistence, including latent infections, virus reactivation and viral-induced tissue damage. These studies have also provided excellent paradigms to study the interactions between the immune system and the central nervous system (CNS). In this review we will discuss potential cellular and molecular mechanism of central nervous system axonal loss and demyelination in a viral induced mouse model of multiple sclerosis.