|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 (77 °F), 100 kPa)
Structure & Properties
Sources & 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.
A University of Miami study in the journal Marine Drugs discovered high concentrations of BMAA in shark fins. The study suggests that consumption of shark fin soup and cartilage pills may 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 kainite receptors. The activation of the metabotropic glutamate receptor 5 is believed to induce oxidative stress in the neuron by depletion of glutathione.
BMAA is also known to misincorporate into nascent proteins in place of L-Serine, causing protein misfolding and aggregation, both hallmarks of tangle diseases, including Alzheimer's, Parkinson's and ALS, PSP and Lewy Body Disease. In-vitro research has shown that tRNA mischarging of L-BMAA for L-Serine can be inhibited in presence of excess L-Serine.
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
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 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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