BMAA and Neurodegenerative Illness

Paul Alan Cox*, Richard M. Kostrzewa, Gilles J. Guillemin

*Corresponding author for this work

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)178–183
Number of pages6
JournalNeurotoxicity Research
Volume33
Issue number1
DOIs
Publication statusPublished - Jan 2018

Keywords

  • ALS
  • Alzheimer’s
  • Amyotrophic lateral sclerosis
  • BMAA
  • Cyanotoxins
  • Guamanian ALS/PDC
  • Neurodegeneration
  • Parkinson’s dementia complex

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