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Toxins (Basel). 2010 Nov;2(11):2663-79. doi: 10.3390/toxins2112663. Epub 2010 Nov 3.

β-N-methylamino-L-alanine induces neurological deficits and shortened life span in Drosophila.

Author information

1
Department of Molecular and Cellular Pharmacology, Miller School of Medicine, University of Miami, Miami, Florida, USA. zhouxchong@gmail.com

Abstract

The neurotoxic non-protein amino acid, β-N-methylamino-L-alanine (BMAA), was first associated with the high incidence of Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) in Guam. Recently, BMAA has been implicated as a fierce environmental factor that contributes to the etiology of Alzheimer's and Parkinson's diseases, in addition to ALS. However, the toxicity of BMAA in vivo has not been clearly demonstrated. Here we report our investigation of the neurotoxicity of BMAA in Drosophila. We found that dietary intake of BMAA reduced life span, locomotor functions, and learning and memory abilities in flies. The severity of the alterations in phenotype is correlated with the concentration of BMAA detected in flies. Interestingly, developmental exposure to BMAA had limited impact on survival rate, but reduced fertility in females, and caused delayed neurological impairment in aged adults. Our studies indicate that BMAA exposure causes chronic neurotoxicity, and that Drosophila serves as a useful model in dissecting the pathogenesis of ALS/PDC.

KEYWORDS:

Amyotrophic Lateral Sclerosis; dementia; neurodegeneration

PMID:
22069570
PMCID:
PMC3153171
DOI:
10.3390/toxins2112663
[Indexed for MEDLINE]
Free PMC Article
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