BMAA and Neurodegenerative Illness

Paul Alan Cox; Richard M. Kostrzewa; Gilles J. Guillemin

doi:10.1007/s12640-017-9753-6

BMAA and Neurodegenerative Illness

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

^*Corresponding author for this work

Macquarie University Centre for Motor Neuron Disease Research

Research output: Contribution to journal › Article › peer-review

29 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 language	English
Pages (from-to)	178–183
Number of pages	6
Journal	Neurotoxicity Research
Volume	33
Issue number	1
DOIs	https://doi.org/10.1007/s12640-017-9753-6
Publication status	Published - Jan 2018

Keywords

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

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BMAA and Neurodegenerative Illness

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