Cyanobacteria are some of the oldest organisms on
earth, and have evolved to produce a battery of toxic metabo-
lites, including hepatotoxins, dermatoxins, and neurotoxins. In
this review, we focus on the occurrence and mechanisms of
toxicity of a number of neurotoxins synthesised by these an-
cient photosynthetic prokaryotes. We discuss the evidence
linking β-methylamino-L-alanine (BMAA), a non-protein ami-
no acid, to an unusual neurological disease complex reported
on the island of Guam in the 1950s, and how 60 years later, the
role that BMAA plays in human disease is still unclear. There is
now evidence that BMAA is also produced by some eukary-
otes, and can bioaccumulate in food chains; this combined with
higher frequency of cyanobacterial blooms globally, increases
the potential for human exposure. Three BMAA isomers that
often co-occur with BMAA have been identified, and the cur-
rent knowledge on the toxicity of these molecules is presented.
The acute alkaloid toxins; anatoxin-a, homoanatoxin-a and the
saxitoxins, and the organophosphate neurotoxin anatoxin-a(S)
are also discussed. In many cases, human exposure to a cocktail
of cyanobacterial neurotoxins is likely; however, the implica-
tions of combined exposure to these toxins have not been fully
explored. Increased understanding of the combined effects of
cyanobacterial neurotoxins is required to fully understand how
these molecules impact on human health.

• Cyanobacterial Neurotoxins: Their Occurrence and Mechanisms of Toxicity