|CAS number||, S|
|PubChem||, R, S|
|ChemSpider||, R , S|
|Jmol-3D images||Image 1
|Molar mass||118.13 g mol−1|
|Related alkanoic acids|
| (what is: / ?)
Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa)
BMAA is considered a possible cause of the amyotrophic lateral sclerosis/parkinsonism–dementia complex (ALS/PDC) that has an extremely high rate of incidence among the Chamorro people of Guam. The Chamorro call the condition lytico-bodig.
In the 1950s, ALS/PDC prevalence ratios and death rates for Chamorro residents of Guam and Rota were 50–100 times that of developed countries, including the United States. No demonstrable heritable or viral factors were found for the disease, and a subsequent decline of ALS/PDC after 1955 on Guam, led to the search for responsible environmental agents. The use of cycad (Cycas circinalis) seeds in food and traditional medicine had decreased as the Chamorro population became more Americanized following World War II.
In addition to eating the seeds directly, BMAA may have found its way into human diets by way of biomagnification. Fruit bats, a Chamorro delicacy, may feed on cycad seeds and concentrate the toxin in their flesh. Three museum specimen bats, collected in Guam in the 1950s, contained hundreds of times more BMAA, gram for gram, than cycad seeds.
Recent studies have begun to shed light on the effects of BMAA and the possible link to ALS and Alzheimer's. In 2009 neuroscientist Deborah Mash, who is the director of the University of Miami's Brain Endowment Bank, began working with colleague John Pablo. Together they conducted an independent study of ALS and Alzheimer's brains using samples from the brain bank. The results that followed were shocking; the team found BMAA in 23 out of the 24 samples derived from 12 Alzheimer's patients and also found that from the 13 samples that were taken from ALS patients all of the samples tested positive for BMAA. Studies like this one are still being conducted to see if the results can be reproduced to show that there is a link between BMAA and ALS and Alzheimer's. Unequivocal evidence implicating BMAA as a causative factor in human sporadic or familial ALS and AD has not been forthcoming. The multifocal nature of neurodegenerative processes in human ALS and AD suggests multiple etiologies.
A new study by University of Miami (UM) scientists in the journal Marine Drugs has discovered high concentrations of BMAA in shark fins, a neurotoxin possibly linked to neurodegenerative diseases in humans, including Alzheimer's and Lou Gehrig Disease (ALS). The study suggests that consumption of shark fin soup and cartilage pills may pose a health risk for degenerative brain diseases, but further research is necessary.
BMAA neurotoxic effects
Degenerative locomotor diseases had been described in animals grazing on cycad species, fueling interest in a possible link between the plant and the etiology of ALS/PDC . Subsequent laboratory investigations discovered the presence of BMAA. BMAA induced severe neurotoxicity in rhesus macaques, including:
- limb muscle atrophy
- nonreactive degeneration of anterior horn cells
- degeneration and partial loss of pyramidal neurons of the motor cortex
- behavioral dysfunction
- conduction deficits in the central motor pathway
- neuropathological changes of motor cortex Betz cells
There are reports that low BMAA concentrations can selectively kill cultured motor neurons from mouse spinal cords. In the motor neurons, BMAA activates AMPA-kainate glutamate receptors and boosted production of oxygen radicals.
The presence of BMAA in cyanobacteria, among the most populous organisms in the world, has raised concerns that humans worldwide may be exposed to levels of BMAA that could be potentially harmful. Cyanobacteria from soil and water samples collected around the world produce BMAA, giving rise to speculative biomagnification in food chains. Scientists have also found that newborn rats treated with BMAA showed early neurotoxicity and impaired learning and memory as adults 
- Oxalyldiaminopropionic acid, a related toxin
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- Spencer, P.S., P.B. Nunn, J. Hugon, A.C. Ludolph, S.M. Ross, D.N. Roy, and R.C. Robertson (1987). "Guam amyotrophic lateral sclerosis-parkinsonism-dementia linked to a plant excitant neurotoxin". Science 31 (237): 517–522. doi:10.1126/science.3603037. PMID 3603037.
- Karlsson O, Roman E, Berg AL, Brittebo EB. (2011). "Early hippocampal cell death, and late learning and memory deficits in rats exposed to the environmental toxin BMAA (β-N-methylamino-L-alanine) during the neonatal period". Behav Brain Res 219: 310–320. doi:10.1016/j.bbr.2011.01.056. PMID 21315110.