BMAA and Neurodegenerative Illness

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

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    39 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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