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|Molar mass||118.14 g·mol−1|
Related alkanoic acids
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Structure and properties
Sources and detection
BMAA is produced by cyanobacteria in marine, freshwater and terrestrial environments. In cultured non-nitrogen-fixing cyanobacteria, BMAA production increases in nitrogen depleted medium. BMAA has been found in aquatic organisms and in plants with cyanobacterial symbionts such as certain lichens, the floating fern Azolla, the leaf petioles of the tropical flowering plant Gunnera, cycads as well as in animals that eat the fleshy covering of cycad seeds, including flying foxes.
High concentrations of BMAA are present in shark fins. Consumption of shark fin soup and cartilage pills may therefore pose a health risk. The toxin can be detected via several laboratory methods, including liquid chromatography, high-performance liquid chromatography, mass spectrometry, amino acid analyzer, capillary electrophoresis and NMR spectroscopy.
Although the mechanisms by which BMAA causes motor neuron dysfunction and death are not entirely understood, current research suggests that there are multiple mechanisms of action. Acutely, BMAA can act as an excitotoxin on glutamate receptors such as NMDA, calcium dependent AMPA and kainate receptors. The activation of the metabotropic glutamate receptor 5 is believed to induce oxidative stress in the neuron by depletion of glutathione.
BMAA may also misincorporate into nascent proteins in place of L-serine, possibly causing protein misfolding and aggregation, both hallmarks of tangle diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and Lewy body disease. In vitro research has shown that protein association of BMAA can be inhibited in presence of excess L-serine.
A study performed in 2015 with Green Monkey subjects found that animals orally administered BMAA developed hallmark histopathology features of Alzheimer's Disease including amyloid beta plaques and neurofibrillary tangle accumulation. Animal subjects in the trial fed smaller doses of BMAA were found to have correlative decreases in these pathology features. Additionally, animals that were co-administered BMAA with serine were found to have 70% less beta-amyloid plaques and neurofibrillary tangles than those administered BMAA alone, suggesting that serine may be protective against the neurotoxic effects of BMAA. This experiment represents the first in-vivo model of Alzheimer's Disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease.
Degenerative loco-motor diseases have 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
Scientists have also found that newborn rats treated with BMAA show a progressive neurodegeneration in the hippocampus, including fibril formation, and impaired learning and memory as adults.  In addition BMAA has been reported to be excreted into rodent breast milk, and subsequently transferred to the suckling offspring, suggesting mothers and cows milk might be other possible exposure routes.
BMAA is considered a possible cause of the amyotrophic lateral sclerosis/parkinsonism–dementia complex (ALS/PDC) that had 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 1963 on Guam led to the search for responsible environmental agents. The use of cycad (Cycas micronesica) seeds in food decreased as that plant became rarer and the Chamorro population became more Americanized following World War II.
In addition to eating the seeds directly, BMAA may be ingested by humans through biomagnification. Flying foxes, a Chamorro delicacy, may feed on cycad seeds and concentrate the toxin in their flesh. Twenty-four specimens of flying foxes from museum collections were tested for BMAA and BMAA was found in large concentrations in the flying foxes from Guam.
Studies on human brain tissue of ALS/PDC, ALS, Alzheimer's disease, Parkinson's disease, Huntington's disease and neurological controls indicated that BMAA is present in non-genetic progressive neurodegenerative disease but not in controls or genetic-based Huntington's disease.
- Oxalyldiaminopropionic acid, a related toxin
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- Determining the Safety of L-serine in ALS.
- Safety Study of High Doses of Zinc in ALS Patients (completed).