Beta-Methylamino-L-alanine

β-Methylamino- L -alanine, or BMAA, is a neurotoxin. This non-proteinogenic amino acid (very similar to the non-essential amino acid alanine) is produced by cyanobacteria.

Neurotoxicity
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.

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.

Worldwide concerns
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