Neurology Central

Environmental toxin linked to Alzheimer’s pathology in new animal model

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Scientists from the Institute of Ethnomedicine (WY, USA) and the University of Miami Brain Endowment Bank (FL, USA) have today published results of a study investigating the role of the environmental toxin termed beta-Methylamino-L-alanine (BMAA) in increasing the risk of Alzheimer’s disease. The study, which was published in the Proceedings of the Royal Society B, suggests that chronic exposure to BMAA could cause the build up of protein deposits characteristic of Alzheimer’s and some other neurodegenerative diseases.

The potential significance of BMAA as an environmental toxin was first highlighted through the study of an indigenous population on the Pacific island of Guam. Scientists studying this population observed a high rate of a rare condition that was linked to dementia and presented some symptoms characteristic of Alzheimer’s disease, amyotrophic lateral sclerosis and Parkinson’s disease. One common theme across the island was the presence of high levels of BMAA within their diets, highlighting the potential link between environmental toxins and the development of neurodegenerative diseases.

In the current investigation, the research team evaluated the effects of BMAA and the amino acid L-serine on protein deposition in the brain in vervets for 140 days. The vervets were split into groups receiving either fruit dosed with BMAA, fruit dosed with equal amounts of L-BMAA and L-serine or placebo. Those receiving only BMAA and BMAA plus L-serine both developed neurofibrillary tangles and amyloid deposits after the 140 day period, however those receiving L-serine had a reduced density of the tangles. The placebo group exhibited no evidence of neuropathology.

In a follow-up replication, BMAA was administered at a dose similar to the amount ingested by Guam locals over a lifetime in one group, at a tenth of the dose in another group and in the third group equal amounts of L-BMAA and L-serine were administered. A fourth group again received a placebo.

Following a 140 day period, both tangles and amyloid deposits were present in the brains of all vervets that received BMAA. Despite this, there was again a significant reduction in tangle density in individuals that received equal L-serine.

“Our findings show that chronic exposure to BMAA can trigger Alzheimer’s-like brain tangles and amyloid deposits,” explained Paul Alan Cox (Institute of Etrhnomedicine). “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.”

Cox does not however advocate patients taking L-serine currently: “The FDA has not approved its use for the treatment of neurodegenerative illness, and much more research is needed. However, this new animal model may prove useful in evaluating other potential new Alzheimer’s drugs.”

The Institute of Ethnomedicine is currently sponsoring FDA-approved human clinical trials to investigate the effects of L-serine in people with ALS and is also hoping to begin a Phase I human clinical trial of L-serine in collaboration with Dartmouth Medical School (NH, USA) for patients diagnosed with mild cognitive impairment or early Alzheimer’s disease.

Look out for more insight into this study in Neurology Central’s exclusive interview with Dr Paul Cox, coming soon.

Sources: Institute of Ethnomedicine press release

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