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A Norwegian study shows that impairment in mitochondria may actually protect the brain in Parkinson’s disease. Mitochondria are microscopic power stations found inside human cells. They convert foodstuffs into fuel, providing the required energy. Studies in brain tissue from individuals with Parkinson’s disease showed that an essential component of the mitochondrial energy generators, called respiratory complex-I, becomes impaired in an area of the brain called the “substantia nigra” .
A new study from the University of Bergen (UiB), in Norway, in collaboration with the University of Cambridge, shows that the function of mitochondria, the microscopic powerhouses of the cell, is altered throughout the entire brain of individuals with Parkinson’s disease. This new study shows that complex I deficiency is a global phenomenon in the brain of people with Parkinson’s disease, and is found indiscriminately in both affected and healthy brain regions.
Intriguingly, brain cells (neurons) with decreased complex I levels are significantly less likely to contain Lewy bodies, the abnormal protein-aggregates that characterize Parkinson’s disease. These discoveries suggest that, contrary to mainstream theory, mitochondrial complex I deficiency may not be entirely deleterious for the brain in Parkinson’s disease. It is possible that complex I deficiency is part of a compensatory regulation attempting to protect the brain in Parkinson’s disease.
Parkinson’s disease is one of the most common brain disorders. It affects millions of people worldwide. It starts after the age of 50 and causes a combination of debilitating symptoms, including shaking and other abnormal movements, loss of balance, low blood pressure, bladder and intestinal problems, sleeping disorders and dementia. Presently, there is no cure and patients die prematurely due to increasing disability.
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