In January 2016, several news outlets reported on research findings that a toxic substance found in food eaten by people living on the island of Guam was linked to the development of a rare neurodegenerative condition.
While this research provides substantial evidence that this condition, which included symptoms of dementia, was linked to the diet of the Guam islanders, it did not provide any evidence that dementia can be passed on this way in any other population.
What is the background to this story?
The paper was the result of the researchers spending several years studying a group of people called Chamorro villagers, who live on the island of Guam in the Pacific. They had previously reported that the villagers were eating a toxin called BMAA, which is made by an algae-like organism called cyanobacteria, and is found on the seeds of a local plant.
The Chamorro villagers are known to be affected by a rare condition called amyotrophic lateral sclerosis/parkinsonism dementia. This condition has elements of amyotrophic lateral sclerosis (also known as motor neurone disease), Parkinson’s disease dementia and some of the hallmarks seen in the brains of people with Alzheimer’s disease. The condition affects nerve cells, causing the villagers problems with their movement and symptoms of dementia. The researchers have previously thought that the occurrence of this rare condition could be related to the BMAA in the islanders’ diet.
BMAA is toxic because it affects the way that nerve cells work, causing them to die. It can also be mistaken for a similar chemical, called L-serine, which is important for building proteins in the body. Cells may accidentally use BMAA instead of L-serine when making proteins, and this can cause the proteins to behave incorrectly.
What are today’s results?
In order to see whether BMAA is linked to the islanders’ condition, vervet monkeys were fed fruit that contained BMAA for 140 days. When the researchers examined the brains of the monkeys, they found that there were deposits of two proteins often associated with dementia, called amyloid and tau. These protein deposits are also found in the brains of the islanders who were affected by the neurodegenerative condition. The protein deposits were not found in the brains of monkeys who had not been fed BMAA. This result indicates that BMAA is responsible for the appearance of the protein deposits in the brains of the monkeys, and suggests that this may also be the case for the islanders.
None of the monkeys, even those with the protein deposits in their brain, showed symptoms of dementia such as memory loss. However, this may be due to the fact that not enough time had passed for symptoms to develop.
The researchers fed some of the monkeys both BMAA and L-serine at the same time. They found that these monkeys did not have the protein deposits in their brain.
What does this result mean?
This research gives us important insight into the mechanisms behind the development of this particular neurodegenerative condition. However, there is no evidence that BMAA is linked to the development of Alzheimer’s disease or other common forms of dementia.
BMAA has been found in some other foods, including certain oysters and mussels from a particular part of Southern France. More research is needed to understand whether eating these is linked to the risk of developing dementia or any other neurodegenerative conditions.
This is not the first time that a toxin has been linked to a neurodegenerative condition in a small, specific group of people. So far it is unclear what relevance these findings have for wider populations.
We need more research to understand exactly how toxins such as BMAA affect nerve cells and how this relates to risk of developing conditions such as amyotrophic lateral sclerosis.
The researchers are conducting a trial into whether giving L-serine can help to treat amyotrophic lateral sclerosis. The results of this trial will give us new information in how we can treat certain neurodegenerative conditions. So far there is no evidence that L-serine can be used as a way to treat or prevent Alzheimer’s disease.