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Mol Cells. 2015 May;38(5):381-9. doi: 10.14348/molcells.2015.0034. Epub 2015 Apr 20.

Autophagy in neurodegenerative diseases: from mechanism to therapeutic approach.

Author information

1
Global Research Laboratory, School of Biological Science, Seoul National University, 1 Gwanak-ro, Gwanak-gu, Seoul 151-747, Korea.
2
Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115-5730, USA.

Abstract

Autophagy is a lysosome-dependent intracellular degradation process that allows recycling of cytoplasmic constituents into bioenergetic and biosynthetic materials for maintenance of homeostasis. Since the function of autophagy is particularly important in various stress conditions, perturbation of autophagy can lead to cellular dysfunction and diseases. Accumulation of abnormal protein aggregates, a common cause of neurodegenerative diseases, can be reduced through autophagic degradation. Recent studies have revealed defects in autophagy in most cases of neurodegenerative disorders. Moreover, deregulated excessive autophagy can also cause neurodegeneration. Thus, healthy activation of autophagy is essential for therapeutic approaches in neurodegenerative diseases and many autophagy-regulating compounds are under development for therapeutic purposes. This review describes the overall role of autophagy in neurodegeneration, focusing on various therapeutic strategies for modulating specific stages of autophagy and on the current status of drug development.

KEYWORDS:

ALS; HD; PD; autophagy; therapeutics

PMID:
25896254
PMCID:
PMC4443278
DOI:
10.14348/molcells.2015.0034
[Indexed for MEDLINE]
Free PMC Article

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