Animal models of BMAA neurotoxicity: A critical review

Karamyan, Vardan T.; Speth, Robert C.

doi:10.1016/j.lfs.2007.11.020

Cited by 150 publications

(94 citation statements)

References 83 publications

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“…This biomagnification hypothesis was challenged by the fact that exposing animals to a BMAA-enriched diet did not produce toxic effects or produced symptoms of acute toxicity, which was inconsistent with the model of a progressive neurodegenerative disease (Karamyan and Speth 2008). However, while an animal model for BMAAinduced ALS was lacking, the hypothesis was not discarded due to the verified in vitro neurotoxicity of BMAA (Liu et al 2009;Lobner et al 2007;Rao et al 2006).…”

Section: Introductionmentioning

confidence: 99%

The non-protein amino acid β-N-methylamino-l-alanine in Portuguese cyanobacterial isolates

et al. 2011

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The tailor made amino acid β-N-methyl-amino-L-alanine (BMAA) is a neurotoxin produced by cyanobacteria. It has been associated with certain forms of progressive neurodegenerative disease, including sporadic Amyotrophic Lateral Sclerosis and Alzheimer's disease. Some different reports of BMAA in cyanobacterial blooms from lakes, reservoirs, and other water resources have been made by different investigators. We here report the detection of BMAA of both free and protein-bound produced by cyanobacteria, belonging to the Chroococcales, Oscillatoriales and Nostocales ordered. We use a rapid and sensitive HPLC-FD method that utilizes methanol elution and the Waters AQC Tag chemistry. On other hand, we have used three different assay procedures for BMAA extraction from cyanobacteria: Trichloroacetic acid (TCA), Methanol/Acetone and hydrochloric acid (HCl). All assays let successfully detect BMAA in all cyanobacteria samples analyzed. Nevertheless, with TCA and HCl extraction procedures the highest BMAA values, for free as well as protein-bound BMAA were detected. BMAA content could not be related to the taxonomy of the isolates or to their geographical origin, and no correlation between free and protein-bound BMAA concentrations were observed within or between taxonomic groups. These data offer confirmation of the taxonomic and geographic ubiquity of BMAA from naturally occurring populations of cyanobacteria, for the first time reported for estuaries.

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Section: Introductionmentioning

confidence: 99%

The non-protein amino acid β-N-methylamino-l-alanine in Portuguese cyanobacterial isolates

et al. 2011

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“…Humans are therefore not only exposed to phycotoxins through direct contact with toxic algal blooms, but ingestion of contaminated food can be a major exposure route as well [13,24]. Yearly, phycotoxins are responsible for over 60.000 human intoxications worldwide [25]. Moreover, phycotoxins can kill wildlife (e.g.…”

Section: Phycotoxinsmentioning

confidence: 99%

“…Possible human exposure routes to BMAA include exposure to BMAA-containing phytoplankton, or through ingestion of higher aquatic organisms that have been in contact with such blooms [58]. The neurotoxicity of BMAA has been recognized both in vitro and in vivo [59,60], and BMAA-mediated excitotoxicity and oxidative stress have been experimentally demonstrated (e.g. [61][62][63][64]).…”

Section: The Role Of Bmaa In the Aetiology Of Neurodegenerative Diseasesmentioning

confidence: 99%

“…Furthermore, there is some indication that BMAA incorporation leads to protein misfolding in vitro [65], but this area needs further research. But even though it is established that BMAA is a neurotoxin, an animal model for BMAA-induced neurodegenerative diseases is still lacking [60,66]. Recently, some progress has been made with a rat [67] and an primate model [68], but further work in this field is still required.…”

Section: The Role Of Bmaa In the Aetiology Of Neurodegenerative Diseasesmentioning

confidence: 99%

“…The possibility of a global presence of BMAA, and thus of widespread human exposure to this neurotoxin led to the hypothesis that BMAA might be related to the global presence of neurodegenerative diseases [34]. The current state of knowledge recognizes the neurotoxicity of BMAA on cellular and in vivo level [59,60] but an animal model for BMAA induced ALS is still lacking [60,66]. Recently, additional toxicity mechanisms have been proposed that might better explain the relation between BMAA exposure and the chronic nature of ALS/PDC [45,141].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The neurotoxin BMAA in aquatic systems : analysis, occurrence and effects

Faassen

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Evolution of Neurotoxins: From Research Modalities to Clinical Realities

Kostrzewa

2009

CP Neuroscience

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In the 1950s, the discovery of anti-nerve growth factor, an immunotoxin stunting sympathetic neural development, signaled the advent of neurotoxins as research modalities. Other selective neurotoxins were discovered in rapid succession. In the 1960s, 6-hydroxydopamine and 6-hydroxydopa were shown to destroy noradrenergic and dopaminergic nerves. Excitotoxins (glutamate, aspartate, and analogs) were discovered in the 1970s. DSP-4 [N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine] proved to be selective for noradrenergic destruction, while 5,6- and 5,7-dihydroxytryptamines were relatively selective for serotonin neurons. Additional neurotoxins were discovered, but it was MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) that predominated neurotoxicity research in the 1980s. Eventually, Clostridium botulinum neurotoxin (BoNT), discovered as a "poisonous" principle in the late 1800s, resurfaced in purified and standardized forms as a clinically useful drug. Neurotoxins represent chemical tools, useful not only for discerning neuronal mechanisms and animal modeling of neurological disorders, but also for their use in medicine and potential as treatments for medical disorders. This unit reviews the early discovery of neurotoxins, describes categories of neurotoxins, and finally characterizes their usefulness--first as research tools, and eventually as clinical therapeutic agents.

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Animal models of BMAA neurotoxicity: A critical review

Cited by 150 publications

References 83 publications

The non-protein amino acid β-N-methylamino-l-alanine in Portuguese cyanobacterial isolates

The non-protein amino acid β-N-methylamino-l-alanine in Portuguese cyanobacterial isolates

The neurotoxin BMAA in aquatic systems : analysis, occurrence and effects

Evolution of Neurotoxins: From Research Modalities to Clinical Realities

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