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Researchers have given new insights into the working of the brain in Parkinson's sufferers in a new study. Professor Shohreh Issazadeh-Navikas is at the helm of this ground-breaking discovery.
The study was published in Molecular Psychiatry. Until recently, our understanding of Parkinson's disease was relatively restricted, which was reflected in the devastating condition's limited therapy options and care. Our current understanding has centred mostly on the genetic elements responsible for familial cases, leaving the vast majority of patients' causal causes unclear. For the first time, we can show that mitochondria, the vital energy producers within brain cells, particularly neurons, undergo damage, leading to disruptions in mitochondrial DNA[LP1]. This initiates and spreads the disease like a wildfire through the brain, says Shohreh Issazadeh-Navikas and adds: Our findings establish that the spread of the damaged genetic material, the mitochondrial DNA, causes the symptoms reminiscent of Parkinsons disease and its progression to dementia. Parkinson's disease is a chronic condition that affects the central nervous system, leading to symptoms such as difficulty walking, tremors, cognitive challenges, and, eventually, dementia.[LP2] The disease afflicts over 10 million people worldwide. While there is currently no cure, certain medical treatments can offer relief from its symptoms. By examining both human and mouse brains, researchers discovered that the damage to mitochondria in brain cells occurs and spreads when these cells have defects in anti-viral response genes. They sought to understand why this damage occurred and how it contributed to the disease. Their search led to a remarkable revelation. Small fragments of actually DNA from the mitochondria are released into the cell. When these fragments of damaged DNA are misplaced, they become toxic to the cell, prompting nerve cells to expel this toxic mitochondrial DNA, Shohreh Issazadeh-Navikas explains. Given the interconnected nature of brain cells, these toxic DNA fragments spread to neighbouring and distant cells, similar to an uncontrolled forest fire sparked by a casual bonfire she adds. Shohreh Issazadeh-Navikas envisions that this study marks the initial stride towards a better understanding of the disease, and the development of future treatments, diagnostics, and measurement of treatment efficacy for Parkinsons disease. She also expressed hope that detecting the damaged mitochondrial DNA could serve as an early biomarker for disease development. Biomarkers are objective indicators of specific medical conditions observed in patients. While some biomarkers are common, such as blood pressure, body temperature and body mass index, others provide insights into particular diseases, like gene mutations in cancer or the level of blood sugar for diabetes. Identifying a biomarker for Parkinsons disease holds significant promise for enhancing future treatments. It could be possible that the damage of the mitochondrial DNA in the brain cells leaks from the brain into the blood. That would make it possible to take a small sample of a patients blood as a way of diagnosing early on or to establish the favourable response to future treatments. Professor Issazadeh-Navikas also envisions the possibility of detection of damaged mitochondrial DNA in the bloodstream, making it feasible to diagnose the disease or gauge treatment responses through a simple blood test. The researchers' next endeavour involves investigating how mitochondrial DNA damage can serve as predictive markers for different disease stages and progression. Furthermore, we are dedicated to exploring potentialcaimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in the disease. (ANI)
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