Brain Chemistry Labs, Institute for Ethnomedicine, PO Box 3464, Jackson Hole, WY, 83001, USA.
Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, PO Box 70577, Johnson City, TN, 37614, USA.
Neurotox Res. 2018 Jan;33(1):178-183. doi: 10.1007/s12640-017-9753-6. Epub 2017 May 24.
The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) now appears to be a cause of Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC). Its production by cyanobacteria throughout the world combined with multiple mechanisms of BMAA neurotoxicity, particularly to vulnerable subpopulations of motor neurons, has significantly increased interest in investigating exposure to this non-protein amino acid as a possible risk factor for other forms of neurodegenerative illness. We here provide a brief overview of BMAA studies and provide an introduction to this collection of scientific manuscripts in this special issue on BMAA.
蓝藻细菌毒素 β-N-甲基氨基-L-丙氨酸（BMAA）现在似乎是关岛肌萎缩侧索硬化/帕金森病痴呆症复合征（ALS/PDC）的病因。蓝藻细菌在世界各地产生 BMAA，加上其多种神经毒性机制，特别是对运动神经元的脆弱亚群，这极大地增加了人们对调查接触这种非蛋白氨基酸作为其他形式神经退行性疾病的可能风险因素的兴趣。我们在此简要概述了 BMAA 的研究，并在本期关于 BMAA 的科学论文集中对其进行了介绍。
