How α-Synuclein Aggregration Kills Neurons in Parkinson's Disease
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13

Jun

2018

13

Jun

2018

How α-Synuclein Aggregration Kills Neurons in Parkinson’s Disease

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Parkinson’s disease is strongly linked to quality control of mitochondria in neurons. The condition is characterized by the loss of a vital population neurons responsible for generating the neurotransmitter dopamine, and it is this loss that produces the tremors and other motor dysfunction observed in patients. Parkinson’s disease is also a proteopathy, however, in which α-synuclein clumps together to form solid deposits that harm brain cells. In the research noted here, scientists show that this α-synuclein aggregation kills neurons by damaging mitochondria and triggering mitochondrial mechanisms that produce the form of cell death called apoptosis. This might suggest a link to what is already known of the important portions of the biochemistry of Parkinson’s disease; more active mitochondrial quality control might slow the harm done by α-synuclein by removing damaged mitochondria before they can trigger apoptosis.

Parkinson’s disease isn’t the only synucleinopathy in which α-synuclein aggregation harms the function of the brain. Synucleinopathies are not the only class of proteopathy in the brain: amyloids and tau also form aggregates that are involved in the development of neurodegenerative conditions such as Alzheimer’s disease. Finding ways to

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