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Brain atrophy in multiple sclerosis: mechanisms clinical relevance and treatment options

機譯：多發(fā)性硬化癥中的腦萎縮：機制臨床相關性和治療選擇

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Mechanisms of late axonal loss. Molecular and cellular mechanisms driving neurodegeneration and atrophy. Key elements are considered to be: (1) Mitochondria Dysfunction: Inflammation in acute demyelinating lesions lead to respiratory protein complexes inhibition, mitochondrial injury and dysfunction, release of apoptosis-inducing factors and mitochondrial DNA deletions. In chronic inactive plaques, ionic imbalance, high energy demands and clonal expansion of defective mitochondria further impair oxidative damage. These mitochondrial alterations of functional impairment and structural damage lead to histotoxic hypoxia and energy failure and consequently to neurodegeneration. [ ] Upregulation of sodium channels, acid sensing ion channels and expression of maladaptive isoforms (Nav1.6 channels), paranodal (Caspr) and juxtparanodal (Kv1.2) protein lead to high energy demands, intra-axonal calcium accumulation, and subsequent axonal degeneration. (3) Glutamate Excitotoxicity: Increased glutamate production by activated microglial cells and lymphocytes, and impaired clearance by resident cells such as astrocytes lead to higher lever of glutamate. High levels of glutamate lead to over-activation of -methyl- -aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (which are permeable for calcium and sodium ions) and subsequent calcium overload and oligodendocyte and neuron cell death. (4) Iron release: In MS lesions free iron [Fe2+] is released in the extracellular space leading to production of highly reactive hydroxyl molecules (OH ) by the Fenton reaction. Further, iron is released by activated glial cells, which become dystrophic and disintegrate, leading to a second wave of Fe release
機譯：晚期軸突丟失的機制。驅動神經變性和萎縮的分子和細胞機制。關鍵因素被認為是：（1）線粒體功能障礙：急性脫髓鞘病變中的炎癥導致呼吸蛋白復合物抑制，線粒體損傷和功能障礙，凋亡誘導因子的釋放和線粒體DNA缺失。在慢性非活性斑塊中，離子失衡，高能量需求和有缺陷的線粒體的克隆擴增進一步損害了氧化損傷。功能損傷和結構損傷的這些線粒體改變導致組織毒性缺氧和能量衰竭，并因此導致神經變性。 []鈉通道，酸感應離子通道的表達上調以及適應不良的同工型（Nav1.6通道），旁淋巴結（Caspr）和近旁淋巴結（Kv1.2）蛋白的表達導致高能量需求，軸突內鈣蓄積和隨后的軸突退化。 （3）谷氨酸興奮性毒性：活化的小膠質細胞和淋巴細胞會增加谷氨酸的產生，而星形膠質細胞等常駐細胞的清除能力受損會導致谷氨酸的杠桿作用增加。高含量的谷氨酸鹽會導致-甲基-天冬氨酸（NMDA）和α-氨基-3-羥基-5-甲基-5-甲基-4-異惡唑丙酸（AMPA）受體（鈣和鈉離子可滲透）的過度活化，并且隨后的鈣超載以及少突膠質細胞和神經元細胞死亡。 （4）鐵釋放：在MS病變中，游離鐵[Fe2 +]在細胞外空間釋放，導致通過Fenton反應產生高反應性羥基分子（OH）。此外，鐵由活化的神經膠質細胞釋放，從而變得營養(yǎng)不良并分解，導致第二波鐵釋放

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