Algae blooms may be slowly eating away at our memories.
Chronic exposure to a commonplace algae toxin in crabs, shellfish and other seafood increases risk of Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS), a new study suggests.
The study, published Tuesday in the biological research journal Proceedings of the Royal Society B, found similar "brain tangles" and protein deposits in the brains of monkeys fed fruit dosed with the same amino acid produced by blue-green algae species common to Florida and elsewhere.
The researchers examined an amino acid known as BMAA, produced by most blue-green algae and known to accumulate in shellfish from contaminated marine waters. They looked for proteins in the monkey's brains called amyloid deposits, associated with Alzheimer's and other nuerodegenerative diseases in humans.
"Our findings show that chronic exposure to BMAA can trigger Alzheimer's-like brain tangles and
amyloid deposits," Paul Alan Cox, Ph.D., an ethnobotanist at the Institute for EthnoMedicine and lead author of the study, said in a release. "As far as we are aware, this is the first time researchers have been able to successfully replicate brain tangles and amyloid deposits in an animal model through exposure to an environmental toxin."
The research was conducted by scientists at the Institute for EthnoMedicine, a non-profit medical research organization, and the University of Miami Brain Endowment Bank.
Scientists long have suspected an association between BMAA and neurodegenerative illness. But the causes remain mostly unknown, and the role of environmental factors poorly understood.
The researchers conducted two experiments on vervet monkeys that lasted for 140 days.
In the first experiment, monkeys fed fruit dosed with BMAA developed brain tangles and amyloid deposits similar to Pacific Islanders who died from the disease.
They found brain tangles and amyloid deposits — hallmarks of both Alzheimer's disease and an unusual illness suffered by Chamorro villagers on the Pacific Island of Guam.
Pacific Islanders with this unusual condition also suffer from dementia and symptoms similar to Alzheimer's disease, ALS and Parkinson's disease.
Army physicians first described the mysterious ALS-like disease among the indigenous Chamorro villagers in the 1950s. The BMAA toxin is biomagnified in flying foxes, eaten by the villagers.
"This study takes a leap forward in showing causality — that BMAA causes disease," said Deborah Mash, director of the University of Miami Brain Endowment Bank and co-author of the study. "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."
Vervet monkeys fed equal amounts of BMAA and the naturally occurring dietary amino acid L-serine had a reduced density of tangles, suggesting diets with L-serine could lower the risk of neurological diseases.
The body synthesizes serine — one of the non-essential amino acids that makes up protein — from food. Foods high in serine include soy, eggs and nuts.
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Humans aren't the only mammals at risk. BMAA toxin may also be harming the neurological health of dolphins, manatees and other wildlife, causing them to wander far astray from usual routes.
"It's not an acute toxin. It's something that accumulates over time," said Larry Brand, a biologist at the University of Miami, who's studied the toxin but was not involved with the Institute of Ethnomedicine's study.
But in his own research Brand's recently found levels of BMAA in lagoon dolphin tissues similar to what is seen in brains of humans with Alzheimer's disease. "They accumulate more and more of the entangled protein in their brain," Brand said of the dolphins.
In a 2010 study, Brand found the highest levels of BMAA in blue crabs, shrimp and pufferfish among the samples he examined in South Florida.
"I myself would not eat any seafood from Indian River Lagoon or Florida Bay, for several reasons," he said.
Brand likens the risk to mercury in fish, and suggests similarly limiting consumption of certain types of seafood high in BMAA.
"We've probably all been exposed to this to some extent, but we're not going to all die of Alzheimer's," Brand said. "Some of us are just more susceptible."
Cox does not advocate patients taking L-serine. "The FDA has not approved its use for the treatment of neurodegenerative illness, and much more research is needed," he said. "However, this new animal model may prove useful in evaluating other potential new Alzheimer's drugs."
The Institute for EthnoMedicine has sponsored FDA-approved human clinical trials to study the effects of L-serine in people with ALS, and is working with Dartmouth Medical School to begin human clinical trial of L-serine for patients diagnosed with mild cognitive impairment or early stage Alzheimer's disease.
Follow Jim Waymer on Twitter: @JWayEnviro
