Researchers at the University of Miami have discovered that continuing exposure to a particular environmental toxin has the capacity to increase the risk of neurodegenerative diseases such as Alzheimer’s.
The team of researchers focused its research on the brain tangles and amyloid plaques, which are present in people suffering from Alzheimer’s as well as well as illness suffered by villagers living on the Pacific Island of Guam who possess a diet that is contaminated by the environmental toxin called BMAA. The villagers suffering from the illness have symptoms that are similar to those being shown by people suffering from dementia such as Alzheimer’s as well as ALS and Parkinson’s.
The exact cause of the neurodegenerative disease; but one of the most misunderstood aspects is the role being played by the environment. However, the current study is not shying away from pointing fingers to BMAA, which is a neurotoxin usually found in some algae, which could be 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 research team examined vervets, a species of monkey, in two different experiments. In the first examination conducted, they 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, reports HNGN. The team also conducted the examination on a separate group by feeding an equal amount of L-serine, a dietary amino acid, which led to reduced tangle density.
The team’s second experiment was a repetition with an additional dose of BMAA in one group, a lesser amount on the second group, while the third group was given an equal dose of BMAA and L-serine, and the fourth group was a control that received just fruit.
The results obtained by the group showed that all vervets that were dosed with BMAA developed tangles and amyloid deposits in their brains after 140 days. However, those who were given 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.”
Interest in finding the relationship that exists between environmental toxins and neurological disease heightened after residents of Minamata Bay, Japan, were sickened by chronic dietary exposure to methyl-mercury-laden fish. This has encouraged further research by medical experts to find out more about the disease.
More information on the history of the disease, research, and relationship with the environment can be found on this website.