The basic and pathogenic role of neuronal autophagy. Neurons have highly specialized structures for intercellular communication, which typically include the soma, axon, dendrites and synapses. In the soma, the central region of the neuron containing the nucleus, basal levels of autophagy, including macroautophagy, mitophagy and chaperone-mediated autophagy (CMA), occur to maintain normal cellular homeostasis. The axon, a specialized structure to conduct nerve impulses, transfers proteins and organelles over significant distances by axoplasmic transport. Axotomy and excitotoxic insult trigger the accumulation of autophagosomes in dystrophic axonal swellings. Autophagic vaculoes (AVs) have also been observed in dysfunctional axons in alzheimer's disease (AD), parkinson's disease (PD) and huntington's disease (HD). Synapse, the region of contact where a neuron transferring information to another cell, represents a region of high energy demand and protein turnover; They contain abundant mitochondria and polyribosomes. Autophagy is known to play an important role in synapse development as autophagy is induced in response to many developmental and environmental cues. Thus, autophagy may play an important role in the synapse growth and plasticity required for learning and memory.