A neurotoxin found in a common species of algae that grows in freshwater lakes and ponds between July and October has been linked to Alzheimer’s-like brain changes, according to a recent study. However, the new research, published in Proceedings of The Royal Society B, suggests that there may be an antidote.

The findings build upon prior research conducted in the late 1990s by current study author Dr. Paul Alan Cox to figure out the cause of a mysterious paralytic illness, which was first noticed by the U.S. military in the 1950s, among Chamorro villagers on the Pacific island of Guam.

The disease, which has similarities to Parkinson's, ALS, (Lou Gehrig's disease), and dementia, ran rife in a few remote villages, but had no clear pattern of inheritance. Dr. Ralph Garruto, who also traveled to the Pacific island in the late 90s, found that outsiders who moved in with Chamorro families were also at risk of developing the disease, CBS News reported. So what, then, was causing the illness?

"Our field work was sort of like reading an Agatha Christie novel. Who is the murderer?" Cox told CBS News. "We knew that other peoples on Guam, including the Filipinos, the Caroline islanders, U.S. military personnel, and expatriate Japanese did not get the disease, only the Chamorro villagers. So as ethnobotanists, we spent our time in the villages, rather than in the clinic, trying to figure out who the hidden killer is."

While looking for possible environmental causes, researchers discovered that cycad seeds, a staple of the Chamorro villager’s diet, contained the neurotoxin β-N-methylamino-L-alanine (BMAA.) The toxin also made its way into their diets through contaminated meat, largely in the tissue of flying foxes, animals who also consumed the seed, according to The Los Angeles Times. However, it was unclear whether this neurotoxin, which can be found in blue-green algae, caused the paralytic illness.

For the current study, researchers fed vervet monkeys BMAA-dosed fruit for 140 days in an effort to examine the link between the neurotoxin and neurodegenerative disease. Another group of monkeys was fed fruit with 651 mg of L-serine, a third cohort was fed fruit dosed with 651 mg of L-BMAA plus 651 mg of L-serine, and a fourth control cohort received a piece of fruit dosed with 651 mg of rice flour as a placebo.

Researchers found that chronic exposure to BMAA triggered the development of neurofibrillary tangles (NFT) and β-amyloid plaques — neurological hallmarks of both Alzheimer's disease and the unusual paralytic illness suffered by Chamorro villagers. The vervet monkeys who were fed fruit dosed with BMAA developed NFT and plaques in their brains.

"This study takes a leap forward in showing causality — that BMAA causes disease," Dr. Deborah Mash, director of the University of Miami Brain Endowment Bank and co-author of the current study, said in a statement. "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."

The group of monkeys that received both the dietary amino acid L-serine with L-BMAA had a reduced density of NFT, suggesting that while chronic exposure to the environmental toxin BMAA can trigger neurodegeneration in vulnerable individuals, increasing the amount of L-serine in the diet can reduce the risk. Some foods high in L-Serine include soy beans, eggs, and lentils.

Source: Cox P, Davis D, Mash D, Metcalf J, Banack S. Dietary Exposure to an Environmental Toxin Triggers Neurofibrillary Tangles and Amyloid Deposits in the Brain. Proceedings Of The Royal Society B. 2016.