On the pacific island of Guam, some of the local Chamorro villagers exhibit a unique, endemic neurodegenerative disease known locally as Lytico-bodig and described by neuroscientists as amyotrophic lateral sclerosis-parkinsonism-dementia complex (ALS-PDC). Many characteristics of this disease resemble aspects of Amyotrophic Lateral Sclerosis, Parkinson's disease and Alzheimer's disease, and like these diseases, the cause of ALS-PDC is largely unknown.

One theory involves a neurotoxic amino acid, BMAA, that is produced by symbiotic cyanobacteria on the roots of Guamanian cycads. When ALS-PDC was most common, in the mid-twentieth century, Chamorro regularly consumed both local flour, which was made from cycad seeds, and flying foxes, which feed on the cycads and accumulate BMAA in their body fat. As flying foxes were hunted to near-extinction, the occurrence of ALS-PDC also declined to the degree that it is now considered a rare disease.

Researchers have examined different types and amounts of exposure to BMAA, but with mixed findings. Most recently, scientist Paul Cox and colleagues at the Institute for EthnoMedicine (Provo, UT) and the University of Miami Brain Endowment Bank (Miami, FL) studied how chronic dietary exposure to BMAA affected the neuropathology of vervets (Proc. R. Soc. B 283, 20152397; 2015). Over a 140 day period, vervets were given fruit dosed with either a high dose of BMAA or a low dose that resembled the cumulative exposure to BMAA that a Chamorro might experience over a lifetime.

These treatments produced neuropathy in vervets that resembled that of Chamorros who died with ALS-PDC. Chronic dietary exposure to BMAA resulted in the formation of neurofibrillary tangles and β-amyloid deposits that are also found in Alzheimer's disease. As Deborah Mash, one of the study's coauthors, described in a press release, “the tangles and amyloid deposits produced were nearly identical to those found in the brain tissue of the Pacific Islanders who died from the Alzheimer's-like disease.”

These findings help cement the role of BMAA in ALS-PDC, demonstrating how chronic dietary exposure can produce the neurodegenerative effects that precede this uncommon disease. This study could spur medical advances beyond the island of Guam, however, as Cox also noted that, “as far as we are aware, this is the first time researchers have been able to successfully produce [neurofibrillary] tangles and amyloid deposits in an animal model through exposure to an environmental toxin.” This could provide researchers with a new model of key neuropathies that accompany and potentially cause many neurodegenerative conditions, including Alzheimer's disease.