A major discovery sheds light on the underlying mechanisms of Parkinson’s disease, opening the door to new therapeutic approaches.
Until recently, our understanding of Parkinson’s disease has been quite limited, manifested in limited treatment options and management strategies for this debilitating disease.
Our knowledge has primarily focused on genetic factors associated with familial cases, with causal factors in the majority of patients remaining elusive.
However, in a new study, researchers from the University of Copenhagen have revealed new insights into how the brain functions in patients with Parkinson’s disease. Professor Shohreh Issazadeh-Navikas is at the helm of this groundbreaking discovery.
“For the first time, we can show that mitochondria, the producers of vital energy within brain cells, particularly neurons, are damaged, leading to disruptions in mitochondrial function. DNA. This triggers and spreads the disease like wildfire in the brain,” explains Shohreh Issazadeh-Navikas and adds:
“Our results establish that the spread of damaged genetic material, mitochondrial DNA, causes symptoms reminiscent of Parkinson’s disease and its progression to dementia.”
Parkinson’s disease is a chronic disease that affects the central nervous system and causes symptoms such as difficulty walking, tremors, cognitive difficulties and, eventually, dementia.
The disease affects more than 10 million people worldwide. Although there is currently no cure, certain medical treatments can relieve its symptoms.
Small fragments of mitochondrial DNA spread disease
By examining human and mouse brains, researchers found that damage to mitochondria in brain cells occurs and spreads when those cells have defects in antiviral response genes. They sought to understand why this damage occurred and how it contributed to disease.
Their research led to a remarkable revelation.
“Small fragments – 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,” explains Shohreh Issazadeh-Navikas.
“Given the interconnected nature of brain cells, these toxic DNA fragments spread to neighboring and distant cells, like an uncontrolled wildfire started by the occasional bonfire,” she adds.
The dream is a blood sample
Shohreh Issazadeh-Navikas believes that this study marks the first step towards a better understanding of the disease and the development of future treatments, diagnostics and measures of treatment effectiveness for Parkinson’s disease.
She also expressed hope that “detection of damaged mitochondrial DNA may serve as an early biomarker for disease development.”
Biomarkers are objective indicators of specific medical conditions observed in patients. While some biomarkers are common, like blood pressure, body temperature, and body mass index, others provide information about particular diseases, like genetic mutations in cancer or blood sugar levels for diabetes. The identification of a biomarker for Parkinson’s disease holds great promise for improving future treatments.
“It is possible that damage to mitochondrial DNA in brain cells escapes from the brain into the blood. This would allow a small sample of blood to be taken from a patient in order to make an early diagnosis or establish a favorable response to future treatments.”
Professor Issazadeh-Navikas also envisions the possibility of detecting damaged mitochondrial DNA in the bloodstream, which would make it possible to diagnose the disease or assess responses to treatment with a simple blood test.
The researchers’ next endeavor is to study how mitochondrial DNA damage can serve as predictive markers for different stages and progressions of the disease. “Additionally, we are committed to exploring potential therapeutic strategies aimed at restoring normal mitochondrial function to rectify the mitochondrial dysfunctions implicated in the disease. »
Reference: “Mitochondrial DNA damage triggers spread of Parkinson’s disease-like pathology” by Emilie Tresse, Joana Marturia-Navarro, Wei Qi Guenevere Sew, Marina Cisquella-Serra, Elham Jaberi, Lluis Riera-Ponsati , Natasha Fauerby, Erling Hu, Oliver Kretz, Susana Aznar and Shohreh Issazadeh-Navikas, October 2, 2023, Molecular Psychiatry.