Macroautophagy is a cellular catabolic process that involves the sequestration 
of cytoplasmic constituents into double-membrane vesicles known as 
autophagosomes, which subsequently fuse with lysosomes, where they deliver their 
cargo for degradation. The main physiological role of autophagy is to recycle 
intracellular components, under conditions of nutrient deprivation, so as to 
supply cells with vital materials and energy. Selective autophagy also takes 
place in nutrient-rich conditions to rid the cell of damaged organelles or 
protein aggregates that would otherwise compromise cell viability. Mitophagy is 
a selective type of autophagy, whereby damaged or superfluous mitochondria are 
eliminated to maintain proper mitochondrial numbers and quality control. While 
mitophagy shares key regulatory factors with the general macroautophagy pathway, 
it also involves distinct steps, specific for mitochondrial elimination. Recent 
findings indicate that parkin and the phosphatase and tensin homolog-induced 
putative kinase protein 1 (PINK1), which have been implicated in the 
pathogenesis of neurodegenerative diseases such as Parkinson's disease, also 
regulate mitophagy and function to maintain mitochondrial homeostasis. Here, we 
survey the molecular mechanisms that govern the process of mitophagy and discuss 
its involvement in the onset and progression of neurodegenerative diseases 
during aging.