Exp Neurobiol 2012; 21(1): 1-8
Published online March 31, 2012
© The Korean Society for Brain and Neural Sciences
Department of Biotechnology, College of Life Science and Nanotechnology, Hannam University, Dajeon 305-811, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-42-629-8785, FAX: 82-42-629-8769
Neurons have highly dynamic cellular processes for their proper functions such as cell growth, synaptic formation, or synaptic plasticity by regulating protein synthesis and degradation. Therefore, the quality control of proteins in neurons is essential for their physiology and pathology. Autophagy is a cellular degradation pathway by which cytosolic components are sequestered in autophagosomes and degraded upon their fusion with lysosomal components. Thus, the autophagic pathway may play important roles in neuronal cell survival and neuronal function under physiological condition and pathological conditions. Recent several findings suggest that the loss of basal autophagy or imbalance of autophagic flux leads to neurodegeneration. Autophagosomes accumulate abnormally in affected neurons of several neurodegenerative diseases such as Alzheimer's disease (AD), Huntington's disease (HD), Parkinson's disease (PD), or Frontotemporal dementia (FTD). Thus, the understanding how autophagy is associated with several neurological diseases would be the first step for new therapeutic intervention in neurological disorders. In this review, I will discuss the molecular mechanism of autophagy in neurons and autophagy-associated neurodegenerative diseases.
Keywords: neuron, autophagy, neurodegenerative disease, homeostasis