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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
Citation:
Chernoff, N., D. Hill, D. Diggs, B. Faison, B. Francis, J. Lang, M. Larue, T. Le, K. Loftin, J. Lugo, Judy Schmid, AND W. Winnik. 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. Taylor & Francis, Inc., Philadelphia, PA, 20(4):183-229, (2017).
Impact/Purpose:
This paper addresses Safe Sustainable Water Research on technical support for policy and guidance on cyanobacterial contaminents (SSWR 4.01B). We have reviewed the literature concerning the hypothesized role of the cyanobacterial metabolite non-essential amino acid,beta-N-methylamino-L-alanine (BMAA),in the causation of multiple neurodegenerative diseases in humans including Alzheimer's disease, Par1
Description:
The compound BMAA (β-N-methylamino-L-alanine) has been hypothesized to play a significant role in four serious neurological diseases in humans: 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 since 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 in the other neurodegenerative diseases 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 has understandably received considerable attention in the medical, scientific, and public arenas. This review examines the history of ALS/PDC and the BMAA-human disease hypothesis; the similarities and differences between ALS/PDC and the other diseases with similar symptomologies; inconsistencies and data gaps in the hypothesis; and other compounds and agents that have been suggested as the cause of ALS/PDC on Guam. The conclusion of this review is that the assumption of a causal relationship of BMAA to neurodegenerative disease is not supported by the existing data.
