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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.

Neurotoxicity Research
|May 26, 2017
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
ALSAlzheimer’sAmyotrophic lateral sclerosisBMAACyanotoxinsGuamanian ALS/PDCNeurodegenerationParkinson’s dementia complex

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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.