Chronic exposure to an environmental toxin known as BMAA may significantly increase the risk of developing Alzheimer’s and other neurodegenerative diseases. The findings from this research were recently published in the journal
Proceedings of the Royal Society B.
The neurological hallmark features of Alzheimer’s disease (AD) are neurofibrillary tangles and β–amyloid plaques. Scientists have noticed that these pathological features are also present for a group of indigenous people, the Chamorro villagers, who live on the Pacific Island of Guam. The link was first described in the 1950s, when US Army physicians noted amyotrophic lateral sclerosis-like (ALS-like) and Parkisonism dementia complex (PDC) symptoms in the Chamorro villagers. Brain autopsies of afflicted villagers show the abnormal protein deposits in the brain, even before symptoms manifested. Additionally, outsiders who adopted the Chamorro lifestyle also experienced an increased risk of illness, pointing to environmental causes for the disease.
Since the 1960s, researchers have noted that the Chamorro diet included a neurotoxic amino acid known as b-N-methylamino-L-alanine or BMAA. This chemical is produced by symbiotic cyanobacteria and is contained in cycad seeds. The seeds are used by the Chamorros to prepare tortilla flour, dumplings, and soups. In addition, the Chamorros’ diet also includes animals like flying foxes, feral deer, and pigs that feed on the cycad seeds.
Until now, the link between BMAA and neurological disease has been strongly suspected, but not proven. To definitively establish BMAA as a neurotoxin, researchers exposed vervet monkeys to fruit dosed with BMAA. The exposure lasted for 140 days. These animals developed neurofibrillary tangles and amyloid deposits that were similar to those found in brain tissues of the afflicted Chamorros.
The researchers also tested BMAA in the presence of another compound, L-serine, which has been found to counteract the effects of BMAA. Vervets fed a diet with both compounds showed reduced levels of pathological brain deposits. And finally, the researchers noted that vervets fed with a placebo diet did not develop any brain abnormalities.
"Our findings show that chronic exposure to BMAA can trigger Alzheimer's-like brain tangles and amyloid deposits," said Paul Alan Cox, Ph.D., an ethnobotanist at the Institute for EthnoMedicine and lead author of the study. "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."
There are numerous other studies that link environmental toxins and neurodegenerenative illnesses. For example, a neurological condition known as Minimata disease was caused by chronic dietary exposure to fish living in water contaminated with methyl-mercury. Furthermore, exposures to certain pesticides, metals, and solvents have been linked to Parkinson’s disease. But so far, this study is the first to give causal evidence for BMAA and disease.
And though L-serine seemed to reduce the pathological effects of BMAA, the scientists do not endorse the compound as an anti-Alzheimer’s drug just yet. "The FDA has not approved its use for the treatment of neurodegenerative illness, and much more research is needed," said Cox. "However, this new animal model may prove useful in evaluating other potential new Alzheimer's drugs."
Additional Source:
EurekAlert
