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Neuronal autophagy and neurodegenerative diseases

Title
Neuronal autophagy and neurodegenerative diseases
Authors
Son J.H.Shim J.H.Kim K.-H.Ha J.-Y.Han J.Y.
Ewha Authors
손형진
SCOPUS Author ID
손형진scopus
Issue Date
2012
Journal Title
Experimental and Molecular Medicine
ISSN
1226-3613JCR Link
Citation
vol. 44, no. 2, pp. 89 - 98
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
Autophagy is a dynamic cellular pathway involved in the turnover of proteins, protein complexes, and organelles through lysosomal degradation. The integrity of postmitotic neurons is heavily dependent on high basal autophagy compared to non-neuronal cells as misfolded proteins and damaged organelles cannot be diluted through cell division. Moreover, neurons contain the specialized structures for intercellular communication, such as axons, dendrites and synapses, which require the reciprocal transport of proteins, organelles and autophagosomes over significant distances from the soma. Defects in autophagy affect the intercellular communication and subsequently, contributing to neurodegeneration. The presence of abnormal autophagic activity is frequently observed in selective neuronal populations afflicted in common neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. These observations have provoked controversy regarding whether the increase in autophagosomes observed in the degenerating neurons play a protective role or instead contribute to pathogenic neuronal cell death. It is still unknown what factors may determine whether active autophagy is beneficial or pathogenic during neurodegeneration. In this review, we consider both the normal and pathophysiological roles of neuronal autophagy and its potential therapeutic implications for common neurodegenerative diseases. © 2012 by the The Korean Society for Biochemistry and Molecular Biology.
DOI
10.3858/emm.2012.44.2.031
Appears in Collections:
약학대학 > 약학과 > Journal papers
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