A study published in the Journal of Toxicology on the 14th of March of this year has demonstrated that glyphosate exposure acts as a neurotoxin. The study demonstrated that roundup had a severe neurotoxic effect on the hippocampus of mice during acute exposure and chronic exposure during pregnancy.
The results found that acute exposure to Roundup induces calcium influx into neurons (primarily, by activating NMDA receptors and voltage-dependent Ca2+ channels), leading to oxidative stress and neural cell death. They also found that the herbicide affected the enzymes ERK and CaMKII, the later of which is an enzyme whose dysregulation has been linked to Alzheimer’s disease. Additionally, acute exposure was observed to have the following three effects:
1. Increase the amino acid glutamate into the junctions through which neurons communicate (synaptic cleft), which, when released in excess levels, can exert excitotoxic/neurotixc effects in neurons.
2. Decrease the neuroprotective antioxidant glutathione.
3. Increase ‘brain rancidity,’ i.e. lipoperoxidation, characterized by excitotoxicity (over-stimulation of the neurons) and oxidative damage.
Previous studies have correlated pesticide exposure to Parkinson’s disease and other neurological diseases. Researchers from the University of California have found that the risk to Parkinson is increased by exposure to pesticide. The risk of the disease is dependent on an individual’s genetic make up which can increase the risk for developing Parkinson’s disease. The study was published in the Journal of Neurology and also found that people with a modified genetic variant of the ALDH2 gene, (the gene implicated in increasing the risk of Parkinson), are particularly sensitive to the effects pesticides that inhibit the gene.
A prior study by the same team published last year discovered a link between Parkinson’s and the pesticide benomyl, a fungicide that has been banned by the U.S. Environmental Protection Agency. That study found that benomyl inhibited an enzyme called aldehyde dehydrogenase (ALDH), which converts aldehydes highly toxic to dopamine cells into less toxic agents, and therefore contributed to the development of Parkinson’s.
The exposure to pesticides starts a molecular chain reaction, preventing ALDH from controlling DOPAL, a toxin that naturally occurs in the brain. When ALDH does not detoxify DOPAL sufficiently, it accumulates, damages neurons and increases an individual’s risk of developing Parkinson’s.
The purpose of this study was to test the impact of other pesticides and found 11 other substances that also inhibit ALDH and increased the risk of Parkinson’s. In this case the levels used to trigger a response were substantially lower that the levels applied in every day use according to lead author Jeff Bronstein, a professor of neurology and director of movement disorders at UCLA. The study examined 360 Parkinson patients compared to 816 healthy people who all lived in a pesticide rich region in central California
“We were very surprised that so many pesticides inhibited ALDH and at quite low concentrations, concentrations that were way below what was needed for the pesticides to do their job,” Bronstein said. “These pesticides are pretty ubiquitous, and can be found on our food supply and are used in parks and golf courses and in pest control inside buildings and homes. So this significantly broadens the number of people at risk.”
“ALDH inhibition appears to be an important mechanism by which these environmental toxins contribute to Parkinson’s pathogenesis, especially in genetically vulnerable individuals,” said study author Beate Ritz, a professor of epidemiology at the Fielding School of Public Health at UCLA. “This suggests several potential interventions to reduce Parkinson’s occurrence or to slow its progression.”
The studies are especially concerning in light of the trend to produce genetically modified organisms that have been engineered to be pesticide resistant and which have been linked to increased pesticide exposure and application.
A. G. Fitzmaurice, S. L. Rhodes, M. Cockburn, B. Ritz, J. M. Bronstein. Aldehyde dehydrogenase variation enhances effect of pesticides associated with Parkinson disease. Neurology, 2014; 82 (5): 419 DOI: 10.1212/WNL.0000000000000083
Daiane Cattani, Vera Lúcia de Liz Oliveira Cavalli, Carla Elise Heinz Rieg, Juliana Tonietto Domingues, Tharine Dal-Cim, Carla Inês Tasca, Fátima Regina Mena Barreto Silva, Ariane Zamoner. MECHANISMS UNDERLYING THE NEUROTOXICITY INDUCED BY GLYPHOSATE-BASED HERBICIDE IN IMMATURE RAT HIPPOCAMPUS: INVOLVEMENT OF GLUTAMATE EXCITOTOXICITY. Toxicology. 2014 Mar 14. Epub 2014 Mar 14. PMID: 24636977