Environmental Toxin May Increase Risk for Alzheimer’s Disease
A collaboration between researchers at the Institute for EthnoMedicine and the University of Miami Brain Endowment Bank revealed that chronic exposure to an environmental toxin has the potential to increase the risk for neurodegenerative illnesses such as Alzheimer’s disease.
The research paper, “Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain,” was published in Proceedings of the Royal Society B.
Neurofibrillary tangles (NFT) and β-amyloid plaques in the brain are hallmarks of several neurodegenerative diseases, including Alzheimer’s, along with an unusual illness suffered by the Chamorro villagers on the Pacific island of Guam.
The villagers often have symptoms related to other neurological diseases, such as dementia. The disorder pathogenesis, called Guamanian amyotrophic lateral sclerosis/Parkinsonism dementia complex (ALS/PDC), is poorly understood, especially the relevance of environmental factors, another trait common with Alzheimer’s.
Researchers studied a cyanobacterial toxin present in the traditional Chamorro diet, called BMAA (β-N-methylamino-L-alanine), of which scientists have long suspected to be connected with the neurodegeneration observed in the population and the illnesses. Through experiments conducted on vervet monkeys, researchers found that chronic dietary exposure to this toxin leads to development of neuropathology.
For 140 days a group of vervets was fed fruit dosed with BMAA, developing neurofibrillary tangles and amyloid protein plaques similar to the Pacific islanders who died from the disease. A second group was fed equal amounts of L-BMAA and the dietary amino acid L-serine, which lead to a reduced level of plaque formation, while vervets fed with a placebo did not develop brain issues. In a second experiment, a dose of BMAA similiar to the amount Chamorro villagers would be exposed to in their lifetime was fed to the animals.
The study’s conclusions point to a causative role of BMAA, since amyloid deposits and NFT were found in all animals that consumed the toxin. However, a significant reduction was observed when the animals also consumed an equal amount of L-serine. Researchers highlight that the FDA has not approved the treatment of neurodegenerative diseases with L-serine aminoacid but, even so, this animal model might constitute a valuable platform for evaluation of neurological drugs.
“Our findings show that chronic exposure to BMAA can trigger Alzheimer’s-like brain tangles and amyloid deposits,” lead author Paul Alan Cox, Ph.D., an ethnobotanist at the Institute for EthnoMedicine, 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.”