Papapetropoulos Spiridon
Department of Neurology, University of Miami, Miller School of Medicine, Room 4004, 1501 NW 9th Avenue, Miami, FL 33136, USA.
Neurochem Int. 2007 Jun;50(7-8):998-1003. doi: 10.1016/j.neuint.2006.12.011. Epub 2007 Jan 14.
The naturally occurring, non-essential amino acid beta-N-methylamino-L-alanine (BMAA) has been recently found in high concentrations in brain tissues of patients with tauopathies such as the Amyotrophic Lateral Sclerosis-Parkinsonism-Dementia Complex (ALS/PDC) in the South Pacific island of Guam and in a small number of Caucasian, North American patients with sporadic Alzheimer's disease. BMAA is produced by cyanobacteria that are present in all conceivable aquatic and/or terrestrial ecosystems and may be accumulated in living tissues in free and protein-bound forms through the process of biomagnification. Although its role in human degenerative disease is highly debated, there is mounting evidence in support of the neurotoxic properties of BMAA that may be mediated via mechanisms involving among others the regulation of glutamate. Glutamate-related excitotoxicity is among the most prominent factors in the etiopathogenesis of human neurodegenerative diseases. Due to the wide geographical distribution of cyanobacteria and the possible implications of BMAA neurotoxic properties in public health more research towards this direction is warranted.
天然存在的非必需氨基酸β-N-甲基氨基-L-丙氨酸（BMAA），最近在患有tau蛋白病的患者脑组织中被发现高浓度存在，比如在南太平洋关岛的肌萎缩侧索硬化症-帕金森病-痴呆综合征（ALS/PDC）患者中，以及少数患有散发性阿尔茨海默病的白种北美患者中。BMAA由蓝藻细菌产生，这些蓝藻细菌存在于所有可以想象到的水生和/或陆地生态系统中，并且可能通过生物放大作用以游离和蛋白质结合的形式在生物组织中积累。尽管其在人类退行性疾病中的作用备受争议，但越来越多的证据支持BMAA的神经毒性特性，这可能通过包括调节谷氨酸等机制介导。谷氨酸相关的兴奋性毒性是人类神经退行性疾病发病机制中最突出的因素之一。由于蓝藻细菌的广泛地理分布以及BMAA神经毒性特性对公共卫生可能产生的影响，有必要朝这个方向开展更多研究。
