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A critical review of the postulated role of the non-essential amino acid, β-N-methylamino-L-alanine, in neurodegenerative disease in humans.
Journal of Toxicology and Environmental Health, Part B: Critical Reviews ( IF 7.2 ) Pub Date : 2017-06-10 , DOI: 10.1080/10937404.2017.1297592
N Chernoff 1 , D J Hill 1 , D L Diggs 2 , B D Faison 3 , B M Francis 4 , J R Lang 2 , M M Larue 2 , T-T Le 2 , K A Loftin 5 , J N Lugo 6 , J E Schmid 1 , W M Winnik 1
Affiliation  

The compound BMAA (β-N-methylamino-L-alanine) has been postulated to play a significant role in four serious neurological human diseases: Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) found on Guam, and ALS, Parkinsonism, and dementia that occur globally. ALS/PDC with symptoms of all three diseases first came to the attention of the scientific community during and after World War II. It was initially associated with cycad flour used for food because BMAA is a product of symbiotic cycad root-dwelling cyanobacteria. Human consumption of flying foxes that fed on cycad seeds was later suggested as a source of BMAA on Guam and a cause of ALS/PDC. Subsequently, the hypothesis was expanded to include a causative role for BMAA in other neurodegenerative diseases including Alzheimer's disease (AD) through exposures attributed to proximity to freshwaters and/or consumption of seafood due to its purported production by most species of cyanobacteria. The hypothesis that BMAA is the critical factor in the genesis of these neurodegenerative diseases received considerable attention in the medical, scientific, and public arenas. This review examines the history of ALS/PDC and the BMAA-human disease hypotheses; similarities and differences between ALS/PDC and the other diseases with similar symptomologies; the relationship of ALS/PDC to other similar diseases, studies of BMAA-mediated effects in lab animals, inconsistencies and data gaps in the hypothesis; and other compounds and agents that were suggested as the cause of ALS/PDC on Guam. The review concludes that the hypothesis of a causal BMAA neurodegenerative disease relationship is not supported by existing data.

中文翻译:

对非必需氨基酸,β-N-甲基氨基-L-丙氨酸,在人类神经退行性疾病中的假定作用的严格评论。

据推测,化合物BMAA(β-N-甲基氨基-L-丙氨酸)在四种严重的神经系统人类疾病中起重要作用:关岛发现的肌萎缩性侧索硬化/帕金森病痴呆复合物(ALS / PDC),以及ALS,帕金森病,和全球性的痴呆症。在第二次世界大战期间和之后,具有所有三种疾病症状的ALS / PDC首先引起了科学界的注意。它最初与用于食品的苏铁粉有关,因为BMAA是共生苏铁根居蓝细菌的产物。后来有人建议人类食用苏铁种的果蝠作为关岛上BMAA的来源,并引起ALS / PDC。随后,该假说被扩展到包括BMAA在其他神经退行性疾病(包括阿尔茨海默氏病)中的致病作用 致病性疾病(AD)的原因是由于大多数蓝藻物种声称其接近淡水和/或食用海鲜而引起的接触。BMAA是导致这些神经退行性疾病发生的关键因素的假说在医学,科学和公共领域受到了广泛关注。这篇综述检查了ALS / PDC的历史以及BMAA-人类疾病假说;ALS / PDC与其他症状相似的疾病之间的异同;ALS / PDC与其他类似疾病的关系,对BMAA介导的实验动物作用的研究,假设的不一致和数据缺口;以及被认为是关岛ALS / PDC病因的其他化合物和药物。
更新日期:2019-11-01
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