BMAA and Neurodegenerative Illness

  • Neurotox Res. 2018 Jan;33(1):178-183. doi: 10.1007/s12640-017-9753-6.
Paul Alan Cox  1 ,  Richard M Kostrzewa  2 ,  Gilles J Guillemin  3
Affiliations
  • 1. Brain Chemistry Labs, Institute for Ethnomedicine, PO Box 3464, Jackson Hole, WY, 83001, USA. [email protected].
  • 2. Department of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, PO Box 70577, Johnson City, TN, 37614, USA.
  • 3. Macquarie University, MND Research Centre, FMHS, 2 Technology Place, Sydney, NSW, 2109, Australia.
PMID: 28540663 DOI: 10.1007/s12640-017-9753-6
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.

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