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Scientists link a toxic compound found in Guam with an increased risk of neurological diseases

Scientists have discovered a link between a toxin present in some soils and lakes on the Pacific Island of Guam and an increased risk of neurodegenerative disorders, including Alzheimer’s. The study suggested that exposure to certain environmental toxins may play a part in the growth of beta-amyloid plaques and tau tangles, both of which are associated with Alzheimer’s, and some cases of Parkinson’s disease.

The toxin, known as BMAA, is produced by algae living in soil, lakes and oceans, and is usually found in shellfish and sharks. As it’s also present in some native Guam plants, BMAA is often ingested by animals such as flying foxes, which eat the local vegetation. This in turn enters the human food chain, as the villagers’ diet consists mainly of seafood and flying foxes.

The scientists found that the residents of one particular village, Chamorro, developed an uncommon paralytic illness and exhibited similar symptoms to those associated with Alzheimer’s, Parkinson’s and ALS. Prior to this particular study, beta-amyloid plaques and tau tangles had already been seen in the brains of the villagers who had died of this illness. Now, the researchers, led by Paul Alan Cox, PhD, wanted to ascertain whether there was a relationship between such neurodegenerative diseases and the ingestion of BMAA.

Researchers try to establish a link

To establish this link the researchers carried out two experiments where they gave vervet monkeys a variety of doses of BMAA. Some of the monkeys were given fruit containing BMAA, while others received fruit with both BMAA and another dietary amino acid. A third group were fed fruit which contained a placebo.

The scientists discovered that tau tangles and beta-amyloid plaques had developed in the brains of the monkeys who had eaten fruit with just BMAA, and that these were almost identical to the tangles and amyloid deposits found in the brains of the Chamorro residents who had died as a result of the paralytic illness. The monkeys in the second group had fewer tangles, and the placebo group showed no development of tangles or plaques.

The experiment was replicated a second time, with the results showing tau tangles and beta-amyloid plaques in all monkeys that had eaten fruit with BMAA, whether the dose of BMAA was small or large. This led the researchers to conclude that brain tangles and amyloid deposits usually associated with Alzheimer’s disease were triggered by long-term exposure to BMAA.

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