Damaged genetic material of mitochondrial DNA –the vital energy producers within brain cells-- spreads like a wildfire through the brain causing Parkinson’s disease like symptoms, a team of researchers have found in a first of its kind study published in the journal Molecular Psychiatry.
Professor Shohreh Issazadeh-Navikas said, “Our findings establish that the spread of the damaged genetic material, the mitochondrial DNA, causes the symptoms reminiscent of Parkinson's disease and its progression to dementia.”
The study offers the potential for innovative treatments in the future. 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.
The disease which afflicts over 10 million people worldwide, currently has no cure, but certain medical treatments can offer relief from its symptoms.
The understanding of Parkinson's disease has been quite limited.
It primarily revolved around the genetic factors responsible for familial cases, while the causative factors in the vast majority of patients remained unknown.
Researchers from the University of Copenhagen in Denmark found that small fragments of mitochondrial DNA spreads the disease.
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.
In the paper, published in the journal Molecular Psychiatry, they sought to understand why this damage occurred and how it contributed to the disease.
“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,” Issazadeh-Navikas explained.
“Given the interconnected nature of brain cells, these toxic DNA fragments spread to neighboring and distant cells, similar to an uncontrolled forest fire sparked by a casual bonfire” she added.
Issazadeh-Navikas envisions that the 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 Parkinson's disease.
She also expressed hope that “detecting the damaged mitochondrial DNA could serve as an early biomarker for disease development”.