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Related Concept Videos

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Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
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Autophagic Cell Death01:18

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
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In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells
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[Multiple system atrophy and autophagy].

Koichi Wakabayashi1, Kunikazu Tanji

  • 1Department of Neuropathology, Hirosaki University School of Medicine.

Rinsho Shinkeigaku = Clinical Neurology
|December 19, 2014
PubMed
Summary
This summary is machine-generated.

Autophagy gene homologues LC3 and GABARAPs are altered in Lewy body disease (LBD) and multiple system atrophy (MSA), indicating impaired autophagy. Strategies to enhance autophagy may treat these neurodegenerative diseases.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Macroautophagy is a crucial cellular process for degrading cellular components via autophagosomes.
  • Two key mammalian autophagy-related gene (Atg) 8 homologues, LC3 and GABARAPs, are essential for autophagosome formation.
  • Dysregulation of autophagy is implicated in various neurodegenerative diseases.

Purpose of the Study:

  • To investigate the alterations of Atg8 homologues (LC3 and GABARAPs) in Lewy body disease (LBD) and multiple system atrophy (MSA).
  • To determine the role of these autophagy-related proteins in the pathogenesis of LBD and MSA.

Main Methods:

  • Biochemical analysis of brain tissue fractions from patients with LBD and MSA.
  • Quantification of LC3 and GABARAPs levels in soluble and insoluble fractions.
  • Immunohistochemical staining to localize LC3 and GABARAPs in pathological inclusions.

Main Results:

  • LC3 levels were elevated in the insoluble fraction of LBD brains, while GABARAPs levels decreased.
  • Matured GABARAPs were significantly reduced in the cerebellum of MSA patients.
  • Increased levels of matured and lipidated LC3 were observed in the insoluble fraction of MSA brains.
  • LC3 and GABARAPs were found within Lewy bodies and glial cytoplasmic inclusions in MSA.

Conclusions:

  • Autophagic function appears to be impaired in LBD and MSA due to alterations in Atg8 homologues.
  • These findings suggest that modulating autophagy could be a potential therapeutic strategy for LBD, MSA, and other neurodegenerative conditions.