Neuroaxonal Regeneration is More Pronounced in Early Multiple Sclerosis than in Traumatic Brain Injury Lesions
Neuroaxonal Regeneration is More Pronounced in Early Multiple Sclerosis than in Traumatic Brain Injury Lesions
复制标题
早期多发性硬化症的神经轴突再生比创伤性脑损伤病变更明显
作者：
Lucas Schirmer;D. Merkler;F. König;W. Brück;C. Stadelmann
不可逆的神经轴索损伤的程度是中枢神经系统（CNS）创伤性和炎症性病症造成永久性残疾的关键决定因素。然而，结构性损伤在一定程度上可以通过神经塑性事件得到补偿。然而，尚不清楚神经轴突去和再生的相同动力学和机制是否在炎症和创伤条件下发生。我们分析了早期多发性硬化症 (MS) 病变和创伤性脑损伤 (TBI) 中的神经轴突变性和可塑性。通过 SMI31+ 溶色神经元和 SMI32+ 轴突轮廓的存在来识别的神经轴突变性是白皮质 TBI 损伤的特征。由淀粉样前体蛋白 (APP)+ 球体确定的轴突运输干扰在 TBI 和 MS 病变中都存在类似程度。在两种病理条件下都发现表达生长相关蛋白 43 (GAP43) 和突触素 (Syn) 的神经元。然而，GAP43 和 Syn 免疫阳性的轴突肿胀在皮层下 MS 病变中明显普遍，表明 MS 具有更高的再生潜力。在这种情况下，GAP43+/APP+轴突球体比率与TBI和MS病变中的巨噬细胞浸润相关，支持吞噬细胞激活可能促进神经可塑性事件的观点。此外，轴突 GAP43+ 和 Syn+ 肿胀与 TBI 后生存期延长相关，表明持续的再生反应。
The extent of irreversible neuroaxonal damage is the key determinant of permanent disability in traumatic and inflammatory conditions of the central nervous system (CNS). Structural damage is nevertheless in part compensated by neuroplastic events. However, it is unknown whether the same kinetics and mechanisms of neuroaxonal de‐ and regeneration take place in inflammatory and traumatic conditions. We analyzed neuroaxonal degeneration and plasticity in early multiple sclerosis (MS) lesions and traumatic brain injury (TBI). Neuroaxonal degeneration identified by the presence of SMI31+ chromatolytic neurons and SMI32+ axonal profiles were characteristic features of leukocortical TBI lesions. Axonal transport disturbances as determined by amyloid precursor protein (APP)+ spheroids were present in both TBI and MS lesions to a similar degree. Neurons expressing growth‐associated protein 43 (GAP43) and synaptophysin (Syn) were found under both pathological conditions. However, axonal swellings immunopositive for GAP43 and Syn clearly prevailed in subcortical MS lesions, suggesting a higher regenerative potential in MS. In this context, GAP43+/APP+ axonal spheroid ratios correlated with macrophage infiltration in TBI and MS lesions, supporting the idea that phagocyte activation might promote neuroplastic events. Furthermore, axonal GAP43+ and Syn+ swellings correlated with prolonged survival after TBI, indicating a sustained regenerative response.
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DOI：
10.1073/pnas.87.4.1561
发表时间：
1990-02-01
影响因子：
11.1
作者：
KOO, EH;SISODIA, SS;PRICE, DL
通讯作者：
PRICE, DL
影响因子：
158.5
作者：
Trapp, BD;Peterson, J;Bö, L
通讯作者：
Bö, L
DOI：
10.1056/nejmoa1100648
发表时间：
2011-12-08
期刊：
The New England journal of medicine
影响因子：
--
作者：
Lucchinetti CF;Popescu BF;Bunyan RF;Moll NM;Roemer SF;Lassmann H;Brück W;Parisi JE;Scheithauer BW;Giannini C;Weigand SD;Mandrekar J;Ransohoff RM
通讯作者：
Ransohoff RM
影响因子：
8.3
作者：
Li, Y;Jiang, N;Chopp, M
通讯作者：
Chopp, M
影响因子：
82.9
作者：
Nikic, Ivana;Merkler, Doron;Kerschensteiner, Martin
通讯作者：
Kerschensteiner, Martin