| Literature DB >> 28540663 |
Paul Alan Cox1, Richard M Kostrzewa2, Gilles J Guillemin3.
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.Entities:
Keywords: ALS; Alzheimer’s; Amyotrophic lateral sclerosis; BMAA; Cyanotoxins; Guamanian ALS/PDC; Neurodegeneration; Parkinson’s dementia complex
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Year: 2017 PMID: 28540663 DOI: 10.1007/s12640-017-9753-6
Source DB: PubMed Journal: Neurotox Res ISSN: 1029-8428 Impact factor: 3.911