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Articles by Wilfredo Escala in JoVE
JoVE Neuroscience
Testmetoder motoriskt, inlärning och minne Brister i Drosophila Modeller för neurodegeneration
Department of Molecular and Cellular Pharmacology, University of Miami, Miller School of Medicine
Beteende-analyser för att mäta rörelseorganens funktioner, lärande och förmågor minne i
Other articles by Wilfredo Escala on PubMed
BMAA Neurotoxicity in Drosophila
We report the establishment of an in vivo model using the fruit fly Drosophila melanogaster to investigate the toxic effects of L-BMAA. We found that dietary intake of BMAA reduced the lifespan as well as the neurological functions of flies. Furthermore, we have developed an HPLC method to reliably detect both free and protein-bound BMAA in fly tissue extracts.
β-N-Methylamino-L-alanine Induces Neurological Deficits and Shortened Life Span in Drosophila
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.
