Arguing for Mitochondrial DNA Damage to Spread Between Neurons in Parkinson ' s Disease

The most noticeable symptoms of Parkinson's disease occur because of the loss of a small but vital population of dopamine-generating neurons in the brain. The condition is associated with the spread of misfolded, aggregated α-synuclein throughout brain tissue. α-synuclein is one of the few molecules in the body capable of misfolding in ways that encourage other molecules o α-synuclein to also misfold in the same way. It can thus spread from cell to cell, perhaps carried in extracellular vesicles. It is thought that misfolding of α-synuclein often first occurs in the intestines, and only then spreads to the brain through the nervous system. Dopaminergenic neurons are in some way more vulnerable than other cells to the pathological biochemistry that accompanies the presence of misfolded α-synuclein. This vulnerability also appears strongly connected to the function of mitochondria, the power plants of the cell, hundreds found in every neuron. Genetic variants that increase the risk of suffering Parkinson's disease are connected to loss of mitochondrial function and loss of mitochondrial quality control, suggesting that mitochondrial dysfunction is important to the death of neurons in this condition. One of the mechanisms thought to cause age-related declines in mitochondrial function is mitochondrial DNA damage. Mitochondria are the descendants of ancient symbiotic bacteria, and they still carry their own circular genome. In today's open access paper, the aut...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs