Exposure to environmental toxin may lead to Alzheimer’s

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Chamorro villagers living on the Pacific Island of Guam – a territory of the US – have led scientists to an important discovery; an environmental toxin present in some soils and lakes of the island may increase the risk for Alzheimer’s disease and other neurodegenerative disorders.

[A freshwater lake with algae]
BMAA is a toxin produced by cyanobacteria – a type of blue-green algae that live in oceans, soil and lakes.

In a study published in the journal Proceedings of the Royal Society B, researchers found exposure to the toxin beta-Methylamino-L-alanine (BMAA) may be associated with the development of beta-amyloid plaques and tau tangles in the brain.

These plaques and tangles are hallmarks of Alzheimer’s disease, and they are also found in the brains of some patients with Parkinson’s disease.

BMAA is a toxin produced by cyanobacteria – a type of blue-green algae that live in oceans, soil and lakes. The toxin is present in various marine life, including sharks and shellfish, which ingest cyanobacteria.

The toxin can also be found in plants, such as cycads; flying foxes consume the seeds of this plant, so BMAA is often present in the animals.

Since flying foxes and fish form a key component of the diet of Chamorro villagers, their diet is highly contaminated with BMAA. Interestingly, these villagers are prone to an unusual paralytic illness, and many individuals with this illness experience symptoms similar to Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis (ALS).

Previously, Paul Alan Cox, PhD, an ethnobotanist at the Institute for EthnoMedicine in Provo, UT, and colleagues had identified beta-amyloid plaques and tau tangles in the brains of Chamorro villagers who had died of paralytic illness.

These villagers had been exposed to high levels of dietary BMAA, primarily from consumption of flying foxes.

For this latest study, Cox and colleagues set out to establish whether there is a link between dietary exposure to BMAA and development of neurodegenerative diseases.

Dietary BMAA linked to development of plaques, tangles in monkeys

Over 140 days, the team conducted two experiments on vervet monkeys, in which they exposed the animals to various doses of dietary BMAA.

Fast facts about Alzheimer’s

  • Alzheimer’s is the most common form of dementia
  • In the US, Alzheimer’s is the sixth leading cause of death
  • Almost two thirds of people diagnosed with Alzheimer’s are women.

Learn more about Alzheimer’s

In the first experiment, the researchers fed the monkeys fruit containing BMAA. Another group of monkeys was fed fruit containing equal levels of BMAA and L-serine – a dietary amino acid – while another group was fed fruit containing a placebo.

On analyzing the monkeys’ brain tissue, the researchers found that those fed fruit containing only BMAA showed development of tau tangles and beta-amyloid plaques.

“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,” notes study coauthor Deborah Mash, PhD, director of the University of Miami Brain Endowment Bank in Florida.

The monkeys that consumed equal amounts of BMAA and L-serine, however, showed reduced tangles, while those that were fed the placebo did not develop tangles and plaques.

These findings were replicated in the second experiment, in which the monkeys were divided into four groups.

The first group was fed fruit containing BMAA at a dose similar to that consumed by Chamorro villagers, while the second group consumed fruit that contained a tenth of that dose. Fruit containing equal amounts of BMAA and L-serine was given to the third group, while the fourth group was fed fruit containing a placebo.

At the end of the 140 days, the researchers found all monkeys that consumed BMAA had developed tau tangles and beta-amyloid plaques.

Commenting on their results, Cox says:

“Our findings show that chronic exposure to BMAA can trigger Alzheimer’s-like brain tangles and amyloid deposits.

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.”

Could L-serine help treat Alzheimer’s?

However, as seen in the first experiment, monkeys that consumed an equal amount of L-serine alongside BMAA showed a significant reduction in tau tangles, suggesting the amino acid may hold promise for the treatment of Alzheimer’s.

The researchers note that in the US, the Food and Drug Administration (FDA) have not approved L-serine for the treatment of neurodegenerative conditions, and they say much more research is required before the amino acid can be recommended for such diseases.

Still, work is in progress; the Institute for EthnoMedicine are conducting a phase 1 clinical trial alongside Dartmouth Medical School in Hanover, NH, in which they are evaluating the effects of L-serine among patients diagnosed with mild cognitive impairment (MCI) or Alzheimer’s.

Medical News Today recently reported on a study in which researchers revealed how a urine test for Alzheimer’s may be within reach.