DNA mutations linked to Gulf War Illness could apply to Parkinson’s
Study ties mitochondrial DNA damage to disease severity
Genetic variants found in the DNA of mitochondria, the cell compartments that produce energy, were associated with the severity of Gulf War Illness (GWI), a chronic condition seen in Gulf War veterans that’s associated with environmental toxin exposure, a study found.
The research team, led by scientists at the University of California San Diego, said the study could implicate mitochondrial DNA changes in other conditions that are associated with environmental exposures, such as Parkinson’s disease.
“The findings shed new light on how GWI, which is thought to be triggered by environmental toxins, develops,” the university said in a research alert. “The findings could also have implications for other diseases with environmental triggers, such as Parkinson’s disease and certain types of cancer.”
The study, “Gulf war illness: a tale of two genomes,” was published in BMC Research Notes.
GWI refers to a group of chronic and unexplained symptoms experienced by veterans of the Gulf War, an armed conflict against Iraq that ran from 1990-1991. Symptoms may include chronic fatigue, gastrointestinal problems, pain, sleep issues, and other medically unexplained issues.
Chemical exposure
While it is not known exactly what causes GWI, the condition is associated with certain chemical exposures during the war, including a class of nerve agents called acetylcholinesterase inhibitors.
Such chemicals cause toxicity to mitochondria, the parts of cells responsible for creating the energy necessary to sustain normal cellular function. This drives an energy deficiency that especially causes problems for tissues with high energetic demands, including the brain.
There are some similarities between Parkinson’s and GWI. Like GWI, exposure to certain environmental toxins is believed to contribute to Parkinson’s. Evidence also suggests that mitochondrial dysfunction contributes to Parkinson’s disease progression.
Diseases like Parkinson’s and GWI are also associated with accelerated aging processes in the body.
While the majority of the body’s DNA is found in a cell’s nucleus, and is inherited from both mother and father, mitochondria have their own DNA that’s solely inherited from a person’s mother.
In their study, the researchers aimed to explore the possible role of a particular group of genetic variants found in mitochondrial DNA, called haplotype U, in GWI. This group of variants has been linked to an increased risk of aging-related conditions.
GWI severity was evaluated for 52 Gulf War veterans, 45 of whom also had mitochondrial DNA assessments. All had nuclear DNA assessments.
Results showed that haplotype U variants were significantly associated with GWI, with veterans who had those mutations scoring significantly higher on a measure of GWI severity.
Nuclear DNA variants associated with reduced activity of the butyrylcholinesterase (BChE) enzyme have also been linked to GWI. Here, those variants were also independent predictors of GWI severity, but the link was not as strong as with mitochondrial DNA variants.
“Our data, for the first time, implicate mitochondrial genetics in GWI,” the researchers wrote, noting that the significant findings despite the small number of participants indicate the strength of the observed relationship.
Although the study was focused on GWI, the researchers suggested that similar associations could be observed for these symptoms in the general population who hadn’t been in the Gulf War. “Implications are likely to extend beyond GWI — with anticipated relevance both to conditions promoted by environmental toxins, and to those entailing impaired bioenergetics,” they wrote.
Research has in fact started to uncover a possible role for mitochondrial DNA in Parkinson’s disease. Studies suggest that mitochondrial DNA damage may begin to accrue before clinical disease onset, and contributes to the spread of neurodegeneration.
About the Author
