BMAA and Neurodegenerative Illness

Neurotox Res. 2018 Jan;33(1):178-183. doi: 10.1007/s12640-017-9753-6. Epub 2017 May 24.


The cyanobacterial toxin β-N-methylamino-L-alanine (BMAA) now appears to be a cause of Guamanian amyotrophic lateral sclerosis/parkinsonism dementia complex (ALS/PDC). Its production by cyanobacteria throughout the world combined with multiple mechanisms of BMAA neurotoxicity, particularly to vulnerable subpopulations of motor neurons, has significantly increased interest in investigating exposure to this non-protein amino acid as a possible risk factor for other forms of neurodegenerative illness. We here provide a brief overview of BMAA studies and provide an introduction to this collection of scientific manuscripts in this special issue on BMAA.

Keywords: ALS; Alzheimer’s; Amyotrophic lateral sclerosis; BMAA; Cyanotoxins; Guamanian ALS/PDC; Neurodegeneration; Parkinson’s dementia complex.

Publication types

  • Review

MeSH terms

  • Amino Acids, Diamino / chemistry
  • Amino Acids, Diamino / toxicity*
  • Amyotrophic Lateral Sclerosis / chemically induced*
  • Amyotrophic Lateral Sclerosis / epidemiology
  • Animals
  • Cyanobacteria Toxins
  • Excitatory Amino Acid Agonists / chemistry
  • Excitatory Amino Acid Agonists / toxicity*
  • Humans
  • Parkinsonian Disorders / chemically induced*
  • Parkinsonian Disorders / epidemiology


  • Amino Acids, Diamino
  • Cyanobacteria Toxins
  • Excitatory Amino Acid Agonists
  • beta-N-methylamino-L-alanine