Abstract
Autophagy is a nonspecific catabolic process that plays an important role in controlling cellular homeostasis by degradation of misfolded proteins, protein aggregates and damaged organelles. Nutrient starvation causes increased activation of autophagy and it maintains cellular metabolism by recycling intracellular components.
Many recent studies have focused on autophagy and its role in neurodegeneration, such as Alzheimer, Parkinson and Huntington disease. Neurodegenerative diseases are characterized by aggregation of specific forms of proteins that disrupt cell functions and cause death of specific groups of neurons in different neurodegenerative diseases.
Many studies have shown that autophagy is the major degradation pathway for aggregated proteins and through regulation of autophagy it is possible to control the extent of protein aggregation. Targeted induction of autophagy causes increased degradation of pathological forms of proteins and thus alleviation of neurodegenerative process in selected model organisms.
On the contrary, inhibition of autophagy causes increased formation and accumulation of protein aggregates. Stimulation of autophagy has a neuroprotective effect by degrading aggregated or otherwise altered proteins.
Regulation of autophagy is a potential therapeutic target for treatment of neurodegenerative diseases.