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Cellular and Molecular Aspects of the β-N-Methylamino-l-alanine (BMAA) Mode of Action within the Neurodegenerative Pathway: Facts and Controversy

1
Toulouse NeuroImaging Centre (ToNIC), INSERM 1214, Poison Control Centre, Toulouse-Purpan University Hospital, 31059 Toulouse, France
2
UR AFPA—INRA USC 340, EA 3998, Équipe Qualité de l’Alimentation et Vieillissement (QUALIVIE), Université de Lorraine, 54500 Vandoeuvre-les-Nancy, France
3
ANSES—French Agency for Food, Environmental and Occupational Health & Safety, Direction de l’Evaluation des Risques, 14 Rue Pierre et Marie Curie, 94701 Maisons-Alfort, France
4
UMR CNRS 6214, INSERM U1083, Mitovasc Institute, Angers University, 49045 Angers, France
*
Author to whom correspondence should be addressed.
Received: 30 November 2017 / Revised: 19 December 2017 / Accepted: 20 December 2017 / Published: 22 December 2017
(This article belongs to the Special Issue The Cyanobacterial Neurotoxin BMAA)
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Abstract

The implication of the cyanotoxin β-N-methylamino-l-alanine (BMAA) in long-lasting neurodegenerative disorders is still a matter of controversy. It has been alleged that chronic ingestion of BMAA through the food chain could be a causative agent of amyotrophic lateral sclerosis (ALS) and several related pathologies including Parkinson syndrome. Both in vitro and in vivo studies of the BMAA mode of action have focused on different molecular targets, demonstrating its toxicity to neuronal cells, especially motoneurons, and linking it to human neurodegenerative diseases. Historically, the hypothesis of BMAA-induced excitotoxicity following the stimulation of glutamate receptors has been established. However, in this paradigm, most studies have shown acute, rather than chronic effects of BMAA. More recently, the interaction of this toxin with neuromelanin, a pigment present in the nervous system, has opened a new research perspective. The issues raised by this toxin are related to its kinetics of action, and its possible incorporation into cellular proteins. It appears that BMAA neurotoxic activity involves different targets through several mechanisms known to favour the development of neurodegenerative processes. View Full-Text
Keywords: BMAA; neuromelanin; glutamate receptor; excitotoxicity; neurodegenerative disorders; intracellular calcium BMAA; neuromelanin; glutamate receptor; excitotoxicity; neurodegenerative disorders; intracellular calcium
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Delcourt, N.; Claudepierre, T.; Maignien, T.; Arnich, N.; Mattei, C. Cellular and Molecular Aspects of the β-N-Methylamino-l-alanine (BMAA) Mode of Action within the Neurodegenerative Pathway: Facts and Controversy. Toxins 2018, 10, 6.

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