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

Xianchong Zhou, Wilfredo Escala, Spyridon Papapetropoulos, R. Grace Zhai

Research output: Contribution to journalArticle

16 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)2663-2679
Number of pages17
JournalToxins
Volume2
Issue number11
DOIs
StatePublished - Nov 2010

Keywords

  • Amyotrophic lateral sclerosis
  • Dementia
  • Neurodegeneration

ASJC Scopus subject areas

  • Toxicology
  • Health, Toxicology and Mutagenesis

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