Toxin From Algae Blooms May Cause Alzheimer's, Other Diseases
Exposure to an environmental toxin linked to algae blooms may up one’s risks of neurodegenerative disease, warned a new study.
Brain tangles as well as plaques – both common markers of Alzheimer’s disease – are noticed in an unusual condition suffered by Guam’s Chamorro villagers, whose diet is laced by the environmental toxin called BMAA. The Pacific Island villagers suffered from symptoms such as dementia and those seen in Alzheimer’s, Parkinson’s disease, and Lou Gehrig’s disease (ALS).
The findings were published in the Journal Proceedings of the Royal Society B.
In the late 1990s, study author Dr. Paul Alan Cox of the Institute for EthnoMedicine started to interview Chamorro villagers suffering from an unknown condition that showed symptoms similar to neurodegenerative diseases. In the 1950s, the U.S. military first noted the existence of the illness.
Dr. Cox’s colleague and neurologist Dr. Leonard Kurland saw that the illness prevailed in a few remote villages, with no apparent inheritance pattern. Outsiders who moved in with families in the village also developed the condition.
Looking at the environmental aspect, the researchers saw that the Chamorro people were exposed something that none of the others on the island encountered. Cycad seeds – used for making tortilla flour and consumed by flying foxes, a Chamorro diet staple – contained the toxin BMAA.
Neurotoxin in Harmful Algae Blooms
BMAA is a neurotoxin detected in certain harmful algae blooms, also referred to as blue-green algae. According to other studies, BMAA can collect in fish and shellfish with algae blooms, including South Florida.
The researchers established a link between the toxin and the villagers’ sickness. "Our findings show that chronic exposure to BMAA can trigger Alzheimer's-like brain tangles and amyloid deposits," said Dr. Cox.
The team held two monkey experiments that lasted 140 days: one where monkeys were fed fruits with BMAA, and the other given equal amounts of L-BMAA and amino acid L-serine. The former developed tangles and amyloid deposits similar to the villagers who died from the illness, while the latter had a decreased tangle density.
They obtained the same results in a follow-up experiment, with every BMAA-fed animal developing tangles and plaques.
Cox, however, said the U.S. Food and Drug Administration has not approved the use of L-serine for treating neurodegenerative disease, thus needing more research into its therapeutic effects.
He added that their animal research, however, may be useful when evaluation new Alzheimer’s drug treatments.
Photo: Eutrophication & Hypoxia | Flickr