Spencer P S, Ludolph A C, Kisby G E
Center for Research on Occupational and Environmental Toxicology, Oregon Health Sciences University, Portland 97201.
Ann N Y Acad Sci. 1992 May 11;648:154-60. doi: 10.1111/j.1749-6632.1992.tb24533.x.
At the present time, it seems unlikely that progressive neurodegenerative diseases, such as ALS, Parkinson's disease, and dementia of the Alzheimer type, are triggered by environmental agents with excitotoxic potential. These include excitotoxic agents that behave as glutamate agonists or disrupt energy metabolism: both types elicit permanent but self-limiting neuronal diseases with patterns of neuronal deficit that reflect selective chemical exposure (MPP+ and parkinsonism), differential susceptibility to energy dysmetabolism (NPA and dystonia), or the distribution of glutamate-receptors (domoic acid and memory loss). If environmental agents play an etiologic role in progressive neurodegenerative diseases, they are likely to target a critical, irreplaceable neuronal molecule that is required to maintain long-term neuronal integrity.
目前，诸如肌萎缩侧索硬化症、帕金森病和阿尔茨海默型痴呆等进行性神经退行性疾病似乎不太可能由具有兴奋性毒性潜力的环境因素引发。这些因素包括表现为谷氨酸激动剂或破坏能量代谢的兴奋性毒性剂：这两种类型都会引发永久性但自限性的神经元疾病，其神经元缺陷模式反映了选择性化学暴露（MPP+与帕金森症）、对能量代谢异常的不同易感性（NPA与肌张力障碍）或谷氨酸受体的分布（软骨藻酸与记忆丧失）。如果环境因素在进行性神经退行性疾病中起病因学作用，它们很可能靶向维持长期神经元完整性所需的关键、不可替代的神经元分子。
