the cyanobacteria derived toxin beta-n-methylamino-l-alanine and amyotrophic lateral sclerosis的蓝藻毒素beta-n-methylamino-l-alanine和肌萎缩性脊髓侧索硬化症.pdfVIP

Toxins 2010, 2, 2837-2850; doi:10.3390/toxins2122837 OPEN ACCESS Toxins ISSN 2072-6651 /journal/toxins Review The Cyanobacteria Derived Toxin Beta-N-Methylamino-L- Alanine and Amyotrophic Lateral Sclerosis Sandra Anne Banack 1,*, Tracie A. Caller 2 and Elijah W. Stommel 2 1 The Institute for Ethnomedicine/PO Box 3464, Jackson, WY 83001, USA 2 Department of Neurology, Dartmouth Hitchcock Medical Center/Lebanon, NH 03756, USA; E-Mails: Tracie.A.Caller@H (T.A.C.); Elijah.W.Stommel@H (E.W.S.) * Author to whom correspondence should be addressed; E-Mail: sandra@; Tel.: +1-801-375-6214; Fax: +1-801-373-3593. Received: 29 November 2010; in revised form: 17 December 2010; / Accepted: 17 December 2010 / Published: 20 December 2010 Abstract: There is mounting evidence to suggest that environmental factors play a major role in the development of neurodegenerative diseases like ALS (Amyotrophic Lateral Sclerosis). The non-protein amino acid beta-N-methylamino-L-alanine (BMAA) was first associated with the high incidence of Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) in Guam, and has been implicated as a potential environmental factor in ALS, Alzheimer’s disease, and other neurodegenerative diseases. BMAA has a number of toxic effects on motor neurons including direct agonist action on NMDA and AMPA receptors, induction of oxidative stress, and depletion of glutathione. As a non-protein amino acid, there is also the strong possibility that BMAA could cause