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A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam

2004· article· en· 409 citations· W2025541331 on OpenAlex· 10.1073/pnas.0404926101

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A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

About CanadaIts subject is Canada, wherever its authors sit.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

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Opus teacher head0.047
GPT teacher head0.283
Teacher spread
0.236 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

As root symbionts of cycad trees, cyanobacteria of the genus Nostoc produce beta-methylamino-l-alanine (BMAA), a neurotoxic nonprotein amino acid. The biomagnification of BMAA through the Guam ecosystem fits a classic triangle of increasing concentrations of toxic compounds up the food chain. However, because BMAA is polar and nonlipophilic, a mechanism for its biomagnification through increasing trophic levels has been unclear. We report that BMAA occurs not only as a free amino acid in the Guam ecosystem but also can be released from a bound form by acid hydrolysis. After first removing free amino acids from tissue samples of various trophic levels (cyanobacteria, root symbioses, cycad seeds, cycad flour, flying foxes eaten by the Chamorro people, and brain tissues of Chamorros who died from amyotrophic lateral sclerosis/Parkinsonism dementia complex), we then hydrolyzed the remaining fraction and found BMAA concentrations increased 10- to 240-fold. This bound form of BMAA may function as an endogenous neurotoxic reservoir, accumulating and being transported between trophic levels and subsequently being released during digestion and protein metabolism. Within brain tissues, the endogenous neurotoxic reservoir can slowly release free BMAA, thereby causing incipient and recurrent neurological damage over years or even decades, which may explain the observed long latency period for neurological disease onset among the Chamorro people. The presence of BMAA in brain tissues from Canadian patients who died of Alzheimer's disease suggests that exposure to cyanobacterial neurotoxins occurs outside of Guam.

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The record

Venue
Proceedings of the National Academy of Sciences
Topic
Cassava research and cyanide
Field
Agricultural and Biological Sciences
Canadian institutions
Funders
Keywords
CycadBiomagnificationBiologyCyanobacteriaTrophic levelFood chainBotanyEcologyBacteriaGenetics
Has abstract in OpenAlex
yes