Presence of the Neurotoxin BMAA in Aquatic Ecosystems: What Do We Really Know?

Elisabeth Faassen

doi:10.3390/toxins6031109

Abstract

The neurotoxin β-N-methylamino-l-alanine (BMAA) is suspected to play a role in the neurological diseases amyotrophic lateral sclerosis, Alzheimer’s disease, and Parkinson’s disease. BMAA production by cyanobacteria has been reported and contact with cyanobacteria infested waters or consumption of aquatic organisms are possible pathways to human exposure. However, there is little consensus regarding whether BMAA is present in cyanobacteria or not, and if so, at what concentrations. The aim of this review is to indicate the current state of knowledge on the presence of BMAA in aquatic ecosystems. Some studies have convincingly shown that BMAA can be present in aquatic samples at the µg/g dry weight level, which is around the detection limit of some equally credible studies in which no BMAA was detected. However, for the majority of the reviewed articles, it was unclear whether BMAA was correctly identified, either because inadequate analytical methods were used, or because poor reporting of analyses made it impossible to verify the results. Poor analysis, reporting and prolific errors have shaken the foundations of BMAA research. First steps towards estimation of human BMAA exposure are to develop and use selective, inter-laboratory validated methods and to correctly report the analytical work.

Highlights

Introduction β-N-Methylamino-L-alanine (BMAA) is a neurotoxin that has been linked to the progressive neurological diseases amyotrophic lateral sclerosis (ALS), Alzheimer’s disease and Parkinson’s disease [1,2,3,4]
There is evidence that BMAA can be present in cyanobacteria dominated samples [23,27,48,68,74], while in some credible studies, BMAA has not been detected in cyanobacteria [31,43,47,49,71,75]
The evidence for presence of BMAA is generated by studies that have used LC-MS/MS, which is at present regarded as one of the most suitable techniques for BMAA analysis due to its high selectivity and sensitivity [43,52]

Summary

Introduction

Introduction βN-Methylamino-L-alanine (BMAA) is a neurotoxin that has been linked to the progressive neurological diseases amyotrophic lateral sclerosis (ALS), Alzheimer’s disease and Parkinson’s disease [1,2,3,4]. As BMAA was shown to be neurotoxic [5], exposure to BMAA was considered as a possible cause of the high incidence of ALS/Parkinsonism-dementia complex (ALS/PDC) on this island [2]. The role of BMAA in the aetiology of ALS/PDC on Guam was heavily debated (e.g., [7,8,9]) and BMAA exposure is at present regarded as one of the possible causes of Western Pacific ALS-PDC [10]. The possibility of a global presence of BMAA, and, of widespread human exposure to this neurotoxin led to the hypothesis that BMAA might be related to the global presence of neurodegenerative diseases [14]. But not all, of the differences between these studies might be tracked down to the analytical procedures applied [22]

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Conclusion