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7442007 
Journal Article 
Review 
BMAA and Neurodegenerative Illness 
Cox, PA; Kostrzewa, RM; Guillemin, GJ 
2018 
1 
Neurotoxicity Research
ISSN: 1029-8428
EISSN: 1476-3524 
Springer New York LLC 
33 
1 
178-183 
English 
28540663 
WOS:000417881600017 
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. 
ALS; Alzheimer’s; Amyotrophic lateral sclerosis; BMAA; Cyanotoxins; Guamanian ALS/PDC; Neurodegeneration; Parkinson’s dementia complex; 2 amino 3 methylaminopropionic acid; amino acid receptor stimulating agent; beta-N-methylamino-L-alanine; diamino acid; amyotrophic lateral sclerosis; Article; cyanobacterium; degenerative disease; dementia; disease association; Guamanian amyotrophic lateral sclerosis; human; long term exposure; neurotoxicity; nonhuman; parkinsonism; parkinsonism dementia complex; priority journal; risk; amyotrophic lateral sclerosis; animal; chemically induced; chemistry; parkinsonism; Amino Acids, Diamino; Amyotrophic Lateral Sclerosis; Animals; Excitatory Amino Acid Agonists; Humans; Parkinsonian Disorders 
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