New Alzheimer’s drug: Study linking environmental toxin to Alzheimer’s, opens up new drug possibility
Alzheimer’s may be caused by environmental toxin (BMAA) produced by cyanobacteria, commonly known as blue-green algae. However, researchers, who have linked chronic exposure to the environmental toxin BMAA to increased risk of Alzheimer’s and other neurodegenerative diseases, believe that the study can prove to be useful in evaluating potential new Alzheimer’s drugs.
The study, published in the science journal Proceedings of the Royal Society B, was carried out by scientists from the Institute for EthnoMedicine, a non-profit medical research organisation, and the University of Miami Brain Endowment Bank. The study provides a foundation for future research and drug development of Alzheimer's disease, Parkinson's disease and ALS.
“As far as we are aware, this is the first time researchers have been able to successfully produce brain tangles and amyloid deposits in an animal ... through exposure to an environmental toxin,” Dr. Paul Alan Cox, lead study author and ethnobotanist at the Institute for EthnoMedicine, was quoted by the ABC as saying.
Two experiments were conducted on vervets by researchers and which lasted 140 days. In the first experiment, the vervets were fed fruits with the BMAA and they developed neurofibrillary tangles and amyloid deposits, like that of the Pacific Islanders who died from the Alzheimer’s disease due to over-exposure to blue-green algae.
Amyloid deposits and brain tangles are trademarks of an unusual illness and Alzheimer’s disease in Chamorro villagers on the Pacific Island of Guam. Their diet is contaminated by BMAA.
Interestingly, vervets who were fed with equal amounts of dietary amino acid L-serine and L-BMAA had reduces tangle density. Vervets fed with a placebo dose didn’t develop neuropathology.
In a replication experiment, BMAA dose was added in quantity similar to the amount Chamorro villagers would be exposed to over a lifetime, reports EurekAlert. Four groups were created. The first group had fruits containing L-BMAA. The second group had fruits with one-tenth of the regular L-BMAA dose. The third group had fruits containing equal amounts of L-BMAA and L-serine, while the fourth group received fruits containing placebo.
Although tangles and amyloid deposits were found in all vervet brains who consumed BMAA, the tangle density was significantly less in vervets who consumed equal amounts of L-serine.
When asked on this finding, Cox said he does not advise patients to take L-serine immediately as the FDA hasn’t approved it yet to treat neurodegenerative illnesses.
“However, this new animal model may prove useful in evaluating other potential new Alzheimer's drugs,” he added.
