In recent decades, cyanobacteria-dominated Harmful Algal Blooms (cyanoHABs) have increased in regularity and persistence, leading to increased concerns over water quality and human health. The buoyant cyanobacteria that form cyanoHABs are the main producers of cyanobacterial toxins (cyanotoxins), and the biochemical role of the well-documented cyanotoxins (e.g., microcystin and saxitoxin) is a focus of ongoing research, as identifying function is a prerequisite to enumerating the ecological drivers of toxin production. The atypical amino acid, Î²-N-methylamino-L-alanine (BMAA), diverges from other cyanotoxins in that it lacks acute toxicity, and as such, has received comparatively less attention from scientists and regulatory agencies. However, mounting evidence suggests that environmental and food web exposure to BMAA is causal to the increased incidence of a histopathologically distinct form of Alzheimer's disease (AD) and/or amyotrophic lateral sclerosis/Parkinsonism-dementia complex (ALS/PDC) observed in multiple geographically isolated populations. As BMAA is the only cyanotoxin thus far detected in axenic cultures of representative species from all five cyanobacteria "Orders," the compound may play a fundamental role within the canonical cyanobacterial metabolon, warranting investigation into its metabolic function. To date, conclusive evidence of an ecological function, biosynthetic pathway, or environmental driver of production has not been presented for BMAA.