Abstract
Cyanobacteria can generate molecules that are toxic to human health, including the production of neurotoxic substances. This chapter focuses on β-N-methylamino-Lalanine (BMAA) as an example of a high-exposure cyanobacterial neurotoxin that has been linked to occurrence of ALS-parkinsonism-dementia complex of Guam. The historical account of the BMAA hypothesis is presented, together with a discussion of possible mechanisms underlying the neurotoxic effects of this nonprotein amino acid. This chapter also alludes to the globalimportance of marine cyanobacterial blooms and the fate of BMAA in marine and freshwater ecosystems, which may contribute to sporadic neurodegenerative diseases occurring outsideof Guam.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 138-149 |
| Number of pages | 12 |
| Journal | CONTINUUM Lifelong Learning in Neurology |
| Volume | 14 |
| Issue number | 5 |
| DOIs | |
| State | Published - Oct 1 2008 |
ASJC Scopus subject areas
- Clinical Neurology
- Genetics(clinical)
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Cite this
Mash, D. C. (2008). Cyanobacterial toxins in neurodegeneration. CONTINUUM Lifelong Learning in Neurology, 14(5), 138-149. https://doi.org/10.1212/01.CON.0000337997.85667.1f