Hypothesis: A motor neuron toxin produced by a clostridial species residing in gut causes ALS
Hypothesis: A motor neuron toxin produced by a clostridial species residing in gut causes ALS
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DOI：
10.1016/j.mehy.2004.07.041
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发表时间：
2005-01-01
影响因子：
4.7
通讯作者：
Koepsell, TD
中科院分区：
文献类型：
--
作者：
Longstreth, WT;Meschke, JS;Koepsell, TD
我们推测，一种尚未被确定的运动神经元毒素产生的梭菌引起易感个体散发性肌萎缩侧索硬化症（ALS）。这种梭菌会在肠道中不被发现，并长期产生针对运动系统的毒素，如破伤风和肉毒杆菌毒素。在进入下运动神经元后，毒素将被转运回细胞体，就像破伤风毒素一样，并破坏下运动神经元-ALS的基本特征。和破伤风毒素一样，一些毒素会穿过邻近的细胞，到达上运动神经元，并以同样的方式破坏这些运动神经元。虚弱会无情地发展，直到没有足够的运动神经元维持生命。如果这一假设是正确的，用适当的抗生素或抗毒素治疗可能会减缓或阻止疾病的进展，免疫接种可能会预防疾病。(c)2004爱思唯尔有限公司保留所有权利。
We hypothesize that a yet-to-be-identified motor neuron toxin produced by a clostridial species causes sporadic amyotrophic lateral sclerosis (ALS) in susceptible individuals. This clostridial species would reside undetected in the gut and chronically produce a toxin that targets the motor system, like the tetanus and botulinum toxins. After gaining access to the lower motor neuron, the toxin would be transported back to the cell body, as occurs with the tetanus toxin, and destroy the lower motor neuron - the essential feature of ALS. Again like the tetanus toxin, some of the toxin would cross to neighboring cells and to the upper motor neuron and similarly destroy these motor neurons. Weakness would relentlessly progress until not enough motor neurons remained to sustain life. If this hypothesis were correct, treatment with appropriate antibiotics or antitoxins might slow or halt progression of disease, and immunization might prevent disease. (c) 2004 Elsevier Ltd. All rights reserved.