- Researchers from the University of Copenhagen, in Denmark, have made an important breakthrough in our understanding of Parkinson’s disease.
- Their discovery centres around the damage of mitochondrial DNA in brain cells and its potential as an early biomarker for the disease.
- As this condition affects over 10 million individuals worldwide, these findings hold significant promise for the future of diagnostics and treatments.
- With the implications of these damaged DNA pieces likened to an unchecked forest blaze, the research provides hope and a fresh direction in understanding and treating this condition.
Parkinson’s disease is a neurological condition that impacts movement. Initial symptoms involve shaking, diminished sense of smell and difficulties with coordination.
The exact cause of Parkinson’s disease remains unclear but current theories suggest that genetic alterations and interactions with the environment, such as exposure to harmful substances, may significantly contribute to its onset.
In a new study, published in
This damage leads to problems in the mitochondrial DNA, which then spreads the disease throughout the brain rapidly.
The researchers point out that their study confirms that the transmission of this damaged genetic material results in symptoms similar to Parkinson’s and its evolution into dementia.
Lead author Prof. Shohreh Issazadeh-Navikas, group leader for Neuroinflammation Unit, Director of MoMeD PhD School, Faculty of Health and Medical Sciences at the University of Copenhagen, Denmark, spoke to Medical News Today about the study.
“We show that brain cells chop off parts of their own genetic material (mitochondrial DNA) and spit it out of the cells, this is taken up by other neighboring cells,” Prof. Issazadeh-Navikas explained.
“In this way, this damaged genetic material makes the new cell sick and thereby disease spreads like a wildfire,” she added.
“Normally antiviral genes help the brain cells to prevent the disease to start and spread. But if brain cells do not have good antiviral responses, then the disease can start,” Prof. Issazadeh-Navikas pointed out.
Biomarkers, which are tangible signs of specific health conditions in patients, can vary from commonly measured attributes like blood pressure and body temperature to more disease-specific indicators, such as genetic mutations in cancer or glucose levels for diabetes.
For example, based on this new research, there is a chance that damaged mitochondrial DNA in brain cells might seep into the bloodstream.
If this is the case, it could be possible to use a simple blood sample from a patient for early diagnosis or to monitor the effectiveness of upcoming treatments.
Prof. Issazadeh-Navikas highlighted that this could be a future possibility:
“The first step is to check small blood samples from patients with Parkinson and healthy individuals to make sure the damaged genetic materials are selective for Parkinson’s patients. This can help to diagnose Parkinson’s patients and the stages of their disease progression (as biomarker). The biomarker can help to check the treatment effects. The new knowledge can help to develop new drugs.”
Three experts, not involved in this research, spoke to MNT about their views on the study findings.
“With neurodegenerative diseases like Parkinson’s or sporadic Parkinson’s disease we don’t have definitive causes so there have been limits on treatments,” said psychiatrist Dr. Howard Pratt, board-certified medical director at Community Health of South Florida.
“We are often treating the symptoms rather than the cause so, more and more efforts are looking for that root cause. I’m excited about this different approach to looking at the cause of Parkinson’s,” added Dr. Pratt. “The implications are so significant because knowing the cause will guide us toward the best treatments.”
“This particular study looks at signaling pathways of mitochondrial DNA and how its disruption can potentially induce sporadic Parkinson’s disease-like symptoms. What’s interesting about that is that by injecting damaged mitochondrial DNA into mouse brains it induced sporadic Parkinson’s disease symptoms. This is huge. And potentially could guide us to curative treatments.”
– Dr. Howard Pratt
Dr. J. Wes Ulm, a bioinformatic scientific resource analyst, and biomedical data specialist at the National Institutes of Health, further noted that “the findings reported here are consistent with our mechanistic knowledge of central nervous system function and metabolism, on the one hand, and shed interesting new light on the role of subcellular processes in pathophysiology (the rise of disease) germane to Parkinson’s on the other.”
“This article, in its core findings, indicates that damage to this mitochondral DNA (mtDNA) may be one important subcellular trigger that can lead to the spread of the pathophysiology that is involved in Parkinson’s disease and other conditions like it,” Dr. Ulm explained.
Dr. Kathy Doubleday, doctor of physical therapy and clinical director at Physio Ed, agreed, saying that “the findings in this study show a mechanism for the spread of mitochondrial DNA damage in Parkinson’s disease-like knockout mice model.”
“The mechanism is important to find a molecular solution to the energy system and transcription problems that lead to death of neurons in the basal ganglia and then by projections to other areas of the brain. The study is one in a long list of new theories on the origin and progression of Parkinson’s disease and how it may be treated in the future.”
– Dr. Kathy Doubleday
More research is needed on the potential role of mitochondrial damage in neurodegenerative conditions. However, Dr. Doubleday highlighted that “in physical therapy we have changed our perspective on patients with degenerative neurologic conditions and have been turning them into ‘athletes’ by increasing their physical exercise and physical conditioning.”
“This trend is being seen in many gyms and therapy clinics that are designed for Parkinson’s clients to work hard on their fitness and function,” Dr. Doubleday explained. “The reasoning for this is that we see clinical gains in function with increasing demands on the physical body.”
“One of the most promising clinical treatments is high intensity aerobic exercise. The research on aerobic exercise shows an effect on the mitochondria and the cells ability to produce ATP for energy, messenger RNA and gene transcription of proteins.. In fact, several studies have shown that young and old adults have a similar oxidative capacity to produce energy from mitochondria but is dependent on physical activity levels.”
Dr. Kathy Doubleday
Dr. Doubleday noted that this study emphasizes the importance of prescribing exercise to Parkinson’s patients early in their diagnosis. This could potentially mitigate the damage caused by the disease’s effect on the mitochondria.
Physical therapists are researching the ideal exercise type, intensity, and timing for the most therapeutic benefit. Exercise as an early and frequent intervention can help combat the decline in function seen in Parkinson’s.
“My main takeaway from this study is that the aerobic exercise regimes that we implement in physical therapy may currently be our best way of intervening in this mitochondrial DNA and energy system,” Dr. Doubleday said.
“By progressing the intensity of aerobic exercise, adding functional challenges of all kinds, and educating patients on how exercise can make changes to how brain cells function, we can empower patients to influence the course of their own brain changes in Parkinson’s disease,” she emphasized.