Neurology · 1992 · 129 citations · 0 references
PharmacyFood ScienceToxicologyFood AnalysisFood ChemistryFood ToxicologyBiomarkers Of NeurotoxicityDementia BiomarkersNeurodegeneration MechanismsNeurodegenerative DiseasesNeurodegenerative DisordersNeurotoxicity AssessmentAmyotrophic Lateral Sclerosis PathologyDementia With ParkinsonismEtiologic HypothesisHigh-performance Liquid ChromatographyMethod Detection LimitNeurotoxic Food ContaminantsNeurotoxic Plant Compounds
Exposure to cycad seed kernel is an etiologic factor for the western Pacific amyotrophic lateral sclerosis (ALS) and parkinsonism-dementia complex (PDC). Traditionally processed cycad flours (n = 17) obtained from Chamorro residents of Guam and the adjacent island of Rota at risk for neurodegenerative disease were extracted and analyzed by high-performance liquid chromatography for content of beta-N-methylamino-L-alanine (BMAA) and methyl-azoxymethanol beta-D-glucoside (cycasin). Cycasin (detection limit: picomole) was present in concentrations of 0.004 to 75.93 micrograms/g (mean, 12.45 +/- 5.0 micrograms/g), and levels of BMAA (detection limit: subpicomole) ranged from 0.00 to 18.39 micrograms/g (mean, 5.44 +/- 1.56 micrograms/g). On average, cycasin content was approximately 10 times higher than that of BMAA. The largest concentrations of cycasin were found in samples from villages with a high reported prevalence of ALS/PDC. Ingestion of cycad-derived food would result in estimated human exposure to milligram amounts of cycasin per day. The cytotoxic properties of cycasin merit consideration in relation to the etiology of western Pacific ALS/PDC.