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Research reveals a cause of Parkinson’s disease

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Researchers in Denmark have unveiled new insights into the workings of the brain in Parkinson’s patients.

The discovery was led by University of Copenhagen Professor Shohreh Issazadeh-Navikas.

The researcher said:

“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 .

“This initiates and spreads the disease like a wildfire through the brain.

“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.”

Parkinson’s disease is a chronic condition that affects the central nervous system, leading to symptoms such as tremors, difficulty walking, cognitive challenges, and, eventually, dementia.

The condition afflicts over 10 million people worldwide and while there is currently no cure, certain medical treatments can offer relief from its symptoms.

By examining both human and mouse brains, the researchers learned that the damage to mitochondria in brain cells occurs and spreads when these cells have defects in anti-viral response genes.

The scientists sought to understand why this damage occurred and how it contributed to the disease.

Their search led to a remarkable discovery.

Issazadeh-Navikas said:

“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 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.

Issazadeh-Navikas envisions that this study marks the initial stride towards a better understanding of Parkinson’s disease and the development of future treatments, diagnostics, and measurement of treatment efficacy for the condition.

The researcher also expressed hope that “detecting the damaged mitochondrial DNA could serve as an early biomarker for disease development”.

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