A team of researchers from the University of Miami has discovered that chronic exposure to a particular environmental toxin can increase the risk of neurodegenerative diseases such as Alzheimer's. The study focused on the brain tangles and amyloid plaques that are present in those with Alzheimer's as well as an illness suffered by villagers on the Pacific Island of Guam who possess a diet that is contaminated by the environmental toxin BMAA. The villagers suffering from this illness show symptoms that mirror those with dementia such as Alzheimer's as well as ALS and Parkinson's.
Although the exact cause of neurodegenerative disease has yet to be uncovered, one of the most poorly understood aspects is the role of environment, although the current study points to BMAA, a neurotoxin found in some algae, as a potential factor.
"Our findings show that chronic exposure to BMAA can trigger Alzheimer's-like brain tangles and amyloid deposits," Paul Cox, lead author of the study, said in a press release. "As far as we are aware, this is the first time researchers have been able to successfully produce brain tangles and amyloid deposits in an animal model through exposure to an environmental toxin."
The team examined vervets, a species of monkey, in two different experiments. In the first, researchers fed one group of vervets BMAA, and they subsequently developed neurofibrillary tangles and amyloid deposits similar to those seen in the Pacific Islanders who died from the unusual disease. A separate group was fed an equal amount of L-serine, a dietary amino acid, which led to reduced tangle density.
The second experiment was a repetition experiment with an additional dose of BMAA in one group and a lesser amount in the second group while the third group was dosed equal amounts of BMAA and L-serine and the fourth group was a control that received just fruit.
The results showed that after 140 days, all vervets that were dosed with BMAA developed tangles and amyloid deposits in their brains, whereas those that were dosed an equal amount of L-serine showed a reduced density of these deposits and plaques.
"This study takes a leap forward in showing causality - that BMAA causes disease," said Deborah Mash, co-author of the study. "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."
The findings were published in the Jan. 20 issue of the Proceedings of the Royal Society B.
