Are Mitochondria the Key to Cracking Parkinson’s Disease? - European Medical Journal

Are Mitochondria the Key to Cracking Parkinson’s Disease?

2 Mins

THE MITOCHONDRIA of dopamine-producing cells have been linked to Parkinson’s disease, with researchers finding that affected individuals have dopamine cells in their brains less able to protect their mitochondrial DNA against age-related damage, compared with cells in healthy individuals. Parkinson’s disease is believed to be a combination of both genetic and environmental factors, the exact combination of which can vary greatly between individuals.

As a brain-wasting, progressive disease, Parkinson’s predominantly influences dopamine-producing neurons or nerve cells in a brain structure known as the substantia nigra; this causes these cells to malfunction and die and levels of dopamine are thus depleted, resulting in symptoms such as restricted movement, speech impediment, and impaired balance. Study leader Dr Charalampos Tzoulis, Department of Neurology, Haukeland University Hospital and Institute of Clinical Medicine, University of Bergen, Bergen, Norway, stated that these issues become more prominent with age, commenting, “It is known that the DNA of mitochondria is damaged during aging, causing failure in the power generators, lack of energy, and disease.”

Dr Tzoulis and his researchers investigated mitochondrial DNA, comparing the brains of patients with Parkinson’s disease and healthy, older individuals. Their findings suggested that the mitochondrial DNA of healthy dopamine-producing cells in the brain was efficiently protected against aging-induced damage. By contrast, the dopamine-producing cells of individuals with Parkinson’s disease could not replenish their DNA as successfully, which led to a gradual loss of healthy DNA within their mitochondria.

These results imply the existence of an important mechanism that would normally defend the brain against aging-induced damage. However, individuals that suffer from Parkinson’s disease seem to have malfunctioning, weaker mechanisms, causing their brains to become more vulnerable to the effects of aging. Dr Tzoulis believes that this research has allowed himself and other researchers to better understand the development and pathogenesis of Parkinson’s disease. Concluding, he stated, “There is generally very little knowledge about the mechanisms causing Parkinson’s disease. Now, we are a step closer to understanding these mechanisms and we may have a target to strike at for therapy.”


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