Abstract
Neurons, long-lived postmitotic cells, are highly dependent on quality control mechanisms to maintain a healthy intracellular environment. A continuous evaluation of protein and organelle “quality” allows a coordinated action between repair and clearance of damage proteins and dysfunctional organelles. A great body of evidence links mitochondrial and lysosomal dysfunction, and protein misfolding to Parkinson’s disease (PD) etiopathogenesis. Although the mechanism underlying protein accumulation remains unclear, it is believed that impaired autophagy can trigger downstream pathogenic events, leading to neurodegeneration of different subset of neurons. Indeed, it has been described that age-dependent impairments in the intracellular clearance mechanisms result in the progressive accumulation of damaged organelles and aggregates of aberrant proteins. In view of this, we review the latest advances on autophagy involvement in PD etiopathogenesis and discuss potential disease-modifying strategies.
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