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Animal models of BMAA neurotoxicity: A critical review

机译：BMAA神经毒性的动物模型：关键评论

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摘要

Of all the molecules reported to have toxicological effects, BMAA (beta-methylamino alanine) stands out as having the most checkered past. In the late 1960's it was reported to be a toxic component of the cycad flour consumed by Chamorros on Guam which caused the high incidence of amyotrophic lateral sclerosis (ALS) in Guam, that was associated with a Parkinson's disease-like dementia complex (ALS-PDC). However, because ALS-PDC is a slow onset disease, manifesting itself as long as 30 years following exposure to the putative neurotoxin, and only acute toxic effects of BMAA were observed in animal studies, interest in BMAA waned. A seminal study by Spencer et al., in 1987 showing neurological impairments with long-term BMAA-fed monkeys revived the hypothesis that BMAA could cause ALS-PDC. However, the amounts of BMAA used in that study were viewed as being the equivalent of a person consuming their body weight of cycad flour every day. Again, the BMAA hypothesis was discarded. Recently a third iteration of the BMAA hypothesis has been proposed. It is based on the discovery of a novel dietary source of BMAA via biomagnification of BMAA in flying foxes, once consumed in great amounts by Chamorros. Also, reports that BMAA can be incorporated into plant and animal proteins, a heretofore unrecognized dietary source of BMAA, further solidified this new hypothesis. However, once again this hypothesis has its detractors and it remains controversial. This manuscript critically evaluates in vivo studies directed at establishing an animal model of BMAA-induced ALS-PDC and their implications for this hypothesis. (C) 2007 Elsevier Inc. All rights reserved.
机译：在所有报告的具有毒理作用的分子中，BMAA（β-甲基氨基丙氨酸）的格子最为突出。在1960年代后期，据报道这是Chamorros在关岛上食用的苏铁粉的有毒成分，导致关岛的肌萎缩性侧索硬化症（ALS）发生率很高，这与帕金森氏病样痴呆症（ALS- PDC）。但是，由于ALS-PDC是一种缓慢发作的疾病，在暴露于假定的神经毒素后长达30年才表现出来，并且在动物研究中仅观察到BMAA的急性毒性作用，因此对BMAA的兴趣减弱了。 Spencer等人在1987年进行的一项开创性研究显示，长期由BMAA喂养的猴子出现了神经功能障碍，这一假说重新出现了BMAA可能导致ALS-PDC的假说。但是，该研究中使用的BMAA的量被视为相当于每天消耗苏铁粉体重的人。同样，将BMAA假设丢弃。最近，提出了BMAA假设的第三次迭代。它是基于通过飞狐中的BMAA的生物放大作用发现了一种新的BMAA饮食来源，该生物曾经被Chamorros大量食用。另外，有报道称BMAA可以掺入动植物蛋白质中，而BMAA的饮食来源迄今尚未得到认可，这进一步巩固了这一新假说。但是，这一假设又有其不利之处，并且仍然存在争议。该手稿批判性地评估了旨在建立BMAA诱导的ALS-PDC动物模型的体内研究及其对这一假设的影响。 （C）2007 Elsevier Inc.保留所有权利。

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