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

Department of Biomedical Sciences

Institute for Ethnomedicine
Macquarie University

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

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	American English
Journal	Neurotoxicity Research
Volume	33
DOIs	https://doi.org/10.1007/s12640-017-9753-6
State	Published - Jan 1 2018

Keywords

ALS
Alzheimer’s
BMAA
Parkinson’s dementia complex
amyotrophic lateral sclerosis
cyanotoxins
guamanian ALS/PDC
neurodegeneration

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title = "BMAA and Neurodegenerative Illness",

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.",

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AU - Cox, Paul Alan

AU - Kostrzewa, Richard M.

AU - Guillemin, Gilles J.

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N2 - 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.

AB - 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.

KW - ALS

KW - Alzheimer’s

KW - BMAA

KW - Parkinson’s dementia complex

KW - amyotrophic lateral sclerosis

KW - cyanotoxins

KW - guamanian ALS/PDC

KW - neurodegeneration

UR - https://dc.etsu.edu/etsu-works/10356

UR - https://doi.org/10.1007/s12640-017-9753-6

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DO - 10.1007/s12640-017-9753-6

M3 - Article

VL - 33

JO - Neurotoxicity Research

JF - Neurotoxicity Research

ER -

BMAA and Neurodegenerative Illness

Abstract

Keywords

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