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Published on: June 28, 2019
BMAA and Neurodegenerative Illness
Paul Alan Cox1, Richard M Kostrzewa2, Gilles J Guillemin3
1Brain Chemistry Labs, Institute for Ethnomedicine, PO Box 3464, Jackson Hole, WY, 83001, USA. paul@ethnomedicine.org.
The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) is linked to Guamanian ALS/PDC. Its global production and neurotoxic effects raise concerns about its role in other neurodegenerative diseases.
Area of Science:
- Neuroscience
- Toxicology
- Environmental Health
Background:
- Cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) is implicated in Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC).
- BMAA is produced by cyanobacteria globally.
- Multiple neurotoxic mechanisms of BMAA, especially for motor neurons, are known.
Purpose of the Study:
- To provide an overview of existing BMAA research.
- To introduce a collection of manuscripts focused on BMAA.
Main Methods:
- Literature review of BMAA studies.
- Introduction to a special issue on BMAA.
Main Results:
- BMAA is a significant factor in Guamanian ALS/PDC.
- Increased global interest in BMAA exposure as a neurodegenerative risk factor.
- This collection of manuscripts explores various facets of BMAA.
Conclusions:
- BMAA's role in neurodegeneration warrants further investigation.
- Understanding BMAA's impact is crucial for public health.
- This special issue provides a comprehensive resource on BMAA research.
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