Scientists discovered a potential link between Parkinson’s disease and a gene that is affected by a neurotoxin made by blue-green algae. The discovery adds to a growing body of evidence that Parkinson’s can be influenced by environmental factors.
The study, “Analysis of DNA methylation associates the cystine–glutamate antiporter SLC7A11 with risk of Parkinson’s disease,” was published in the peer-reviewed journal Nature Communications.
Both environmental and genetic risk factors are thought to contribute to Parkinson’s, but how this happens and the degree to which each contributes remain poorly understood.
Researchers from Australia and New Zealand scanned two Parkinson’s-specific genetic databases for evidence of epigenetic modifications to genes related to the disease.
Unlike mutations, wherein the DNA sequence of gene undergoes a direct change, epigenetic modifications are caused by the addition of certain chemical groups (methyl) to the DNA sequence that are able to “turn off” a gene, or prevent it from being expressed. This is known as methylation.
If a mutation in the genetic code is like exchanging one ingredient for another in a recipe, an epigenetic modification is like a garnish placed on top of the original recipe that changes the flavor.
Epigenetic modifications can be caused by environmental factors such as smoking, exercise, and exposure to some pesticides. Environmental factors capable of triggering Parkinson’s have been a topic of intense research.
From a pool of 1,132 Parkinson’s cases and 999 control subjects, the researchers discovered a gene called SLC7A11, the activity of which was slowed in Parkinson’s cases. The lower activity appeared to be due to hypermethylation rather than a specific genetic change within Parkinson’s patients, and the effect of medication was ruled out. This suggested an environmental origin.
SLC7A11 is involved in signaling between neurons and in synthesizing glutathione, an important antioxidant. Oxidative stress is an imbalance between the production of free radicals and the ability of cells to detoxify them. These free radicals, or reactive oxygen species, are harmful to the cells and are associated with a number of diseases, including Parkinson’s.
“Disruption of glutamate signaling,” the researchers wrote, “has been associated with multiple neurodegenerative diseases, and for reasons that are not yet understood, dopaminergic neurons in the substantia nigra appear to be especially susceptible to damage by reactive oxygen species.”
Parkinson’s disease is characterized by the death of dopaminergic neurons in the substantia nigra.
SLC7A11 is the target of an environmental neurotoxin known as BMAA, which is produced by blue-green algae found in inland waterways. BMAA resulting from algal blooms poses a known health risk to both people and domestic animals.
While the study does not provide a direct link between BMAA and Parkinson’s, the toxin is associated with other neurodegenerative and motor neuron disorders. Past research has suggested that chronic dietary exposure to BMAA could have caused an outbreak of amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) among the Chamorro people of Guam in the 1950s.
The ASCC1 gene was identified as a second candidate for epigenetic modification in Parkinson’s. A mutation in this gene is implicated in some cases of spinal muscular atrophy, and has been shown to impair nerve growth in mice.
“More work is needed to confirm our findings, and to explore other possible explanations for the link between this gene and Parkinson’s disease, such as pesticides,” said Peter Visscher, one of the study’s lead authors, in a University of Queensland press release.
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