Animal models of BMAA neurotoxicity: a critical review.

摘要: Of all the molecules reported to have toxicological effects, BMAA (beta-methylamino alanine) stands out as having most checkered past. In late 1960's it was be a toxic component of cycad flour consumed by Chamorros on Guam which caused high incidence amyotrophic lateral sclerosis (ALS) in Guam, that associated with Parkinson's disease-like dementia complex (ALS-PDC). However, because ALS-PDC is slow onset disease, manifesting itself long 30 years following exposure putative neurotoxin, and only acute effects were observed animal studies, interest waned. A seminal study Spencer et al., 1987 showing neurological impairments long-term BMAA-fed monkeys revived hypothesis could cause ALS-PDC. amounts used viewed being equivalent person consuming their body weight every day. Again, discarded. Recently third iteration has been proposed. It based discovery novel dietary source via biomagnification flying foxes, once great Chamorros. Also, reports can incorporated into plant proteins, heretofore unrecognized BMAA, further solidified this new hypothesis. again its detractors remains controversial. This manuscript critically evaluates vivo studies directed at establishing an model BMAA-induced implications for