PT  - JOURNAL ARTICLE
AU  - Glen E. Kisby
AU  - Mike Ellison
AU  - Peter S. Spencer
TI  - Content of the neurotoxins cycasin (methylazoxymethanol β‐D‐glucoside) and BNLAA (β‐<em>N</em>‐methylamino‐L‐alanine) in cycad flour prepared by Guam Chamorros
AID  - 10.1212/WNL.42.7.1336
DP  - 1992 Jul 01
TA  - Neurology
PG  - 1336--1336
VI  - 42
IP  - 7
4099  - http://n.neurology.org/content/42/7/1336.short
4100  - http://n.neurology.org/content/42/7/1336.full
SO  - Neurology1992 Jul 01; 42
AB  - 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 β-N-methylamino-L-alanine (BMAA) and methylazoxymethanol β-D-glucoside (cycasin). Cycasin (detection limit: picomole) was present in concentrations of 0.004 to 75.93 μg/g (mean, 12.45 ± 5.0 μg/g), and levels of BMAA (detection limit: subpicomole) ranged from 0.00 to 18.39 μg/g (mean, 5.44 ± 1.56 μg/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.