“I lose a patient every couple of weeks from the disease, and I see the devastating effects it has on patients and families—it’s very sad,” says Elijah Stommel, MD, PhD, a professor of neurology at Dartmouth’s Geisel School of Medicine and a neurologist at Dartmouth-Hitchcock Medical Center.
Dr. Stommel is talking about ALS (amyotrophic lateral sclerosis), or Lou Gehrig’s disease, a progressive and lethal neurodegenerative disorder affecting nerve cells in the brain and spinal cord. As of yet, no cure has been found and no effective treatments have been developed for ALS.
But more is now understood about potential causes of the disease, thanks to the research efforts of Stommel and his colleagues at Geisel and other institutions. Over the past several years, they’ve made key contributions to a growing body of evidence linking exposure to environmental toxins—particularly those produced by cyanobacteria, the blue-green algae commonly found in and around bodies of water—to neurodegenerative disease.
Findings from a compelling new study related to this research were announced last week in the journal Proceedings of the Royal Society B. Below, Stommel comments on the importance of the new findings and its impact on his own research efforts.
Q: Can you tell us about the new study and its findings?
Stommel: The researchers tested dietary exposure of BMAA (a nerve toxin produced by cyanobacteria), comparing it to exposure of both BMAA and L-serine (an amino acid which has been shown to block the neurotoxic effects of BMAA), and a control group in animal model study.
The study showed a direct link between dietary exposure to BMAA and the development of neuropathological abnormalities. Researchers were able to reproduce almost the same histopathology—development of brain tangles and amyloid deposits—that had been found in a group of human villagers that were studied years ago on the Pacific island of Guam. These villagers ate cycad seeds, which contain BMAA, and many were stricken with neurodegenerative disease, suffering from symptoms that resembled aspects of Alzheimer’s disease, ALS, Parkinson’s disease, and dementia. The new study also showed that when the dietary exposure included L-serine, there was less evidence of disease.
Q: How significant are these findings?
Stommel: I think they’re very enlightening and important. They fill in another piece of the puzzle, in terms of helping us understand more about the mechanisms that are at play with dietary exposure of BMAA. The findings also suggest that L-serine may have some potential as a neuroprotective agent.
That said, it’s a little early to tell whether BMAA may be promoting diseases like ALS, since the disease can take as long as 30 years to develop, and that was shown in Guam. It’s also important to note that exposure to BMAA is probably a risk factor for those who are genetically predisposed to develop neurodegenerative disease. Not everyone who gets exposed develops clinical disease, just like not all smokers get lung cancer.
Q: How does this new study impact your own research efforts?
Stommel: It certainly confirms something that I’ve already come to believe—that BMAA is capable of triggering neurodegeneration in vulnerable individuals. And it plays into what we’re looking at with cyanobacteria, which is a major source of BMAA.
Using a number of research methodologies, we’ve established a statistically significant correlation between the ALS clusters we’ve defined (areas with an unusually high number of ALS cases) and bodies of water containing cyanobacterial blooms across northern New England.
Identifying risk factors is critical. We know that people can be exposed to BMAA in a variety of ways, from eating certain kinds of fish to breathing in the microbes in the air—we’ve found BMAA in aerosol filter collectors we’ve set up near the water. In fact, aerosolization is an area we want to look into further, to better understand how proximity (how close people live to the water) may affect exposure.
While this new study doesn’t necessarily validate what we’ve found in our research, it definitely raises the level of concern over this worrisome link between exposure to BMAA and the development of neurodegeneration. More research still needs to be done, but we’re making progress.
