Brain cells may prevent Parkinson's disease

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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HIV treatment prevents cognitive decline

HIV-positive patients have the same risk of dementia as any other person if they take viral-suppressing medication and live a healthy lifestyle. One of the most debilitating effects of HIV is the neurocognitive decline, which can range from memory and language issues to dementia. Until now, research suggested that even those who take anti-retroviral therapy, the viral suppressing drug, had a higher risk of brain disorders than the general population.

Those who successfully suppress their viral load and live healthily have the same lifetime risk of dementia and other brain disorders as any other person. Older patients' brains may already have been ravaged by the disease, and medication couldn't reverse the damage, which would typically trigger symptoms within three or four years.

Researchers examined adults with HIV treated with cART with good viral suppression as well as those who did not have HIV for comparison. Both groups were about half women, with an average age of around 48 for the HIV-positive adults and 51 for the HIV-negative adults. Over the course of two years, the researchers assessed their brain changes using MRI scans.

They focused on the cortical thickness and subcortical volumes. They also assessed their cognitive performance using neuropsychological assessments. Those with HIV had poorer cognition and reduced brain thickness and volume than adults without HIV. However, by the end of the study, there were barely any differences between the two groups.
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