Neuronal autophagy: a housekeeper or a fighter in neuronal cell survival?
Open accessAbstract
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.
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Autophagy is protective for neuronal survival in neurodegenerative diseases.
“Autophagy is now recognized as protective for neuronal survival in neurodegenerative diseases (Hara et al., 2006; Komatsu et al., 2006; Lee, 2012).”
From Downregulation of MicroRNA-193b-3p Promotes Autophagy and Cell Survival by Targeting TSC1/mTOR Signaling in NSC-34 Cells (2017) · cites this paper as Lee, 2012
The Conclusion and Perspectives section says neuronal autophagy can protect cells under disease conditions, supporting its protective role. But it also says excessive autophagy or defective autophagic flux can contribute to neurodegeneration and neuronal death, so the unqualified claim overstates the review's context-dependent account. The supplied passages do not specify page numbers. (LLM, conf=0.84)
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References 76 · Cited by 119
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- Authors
- Lee, J.-A.
- Affiliations
- Hannam University (KR)
- Corresponding author
- Lee, Jin-A
- ORCID
- Lee, Jin-A
- Venue
- Experimental Neurobiology
- Published
- 2012-03-31
- Volume
- 21
- Issue
- 1
- Pages
- 1-8
- ISSN
- 1226-2560 (ISSN-L)
- 2093-8144
- PMC
- PMC3294068
- OpenAlex
- W2155463891
- Cited by
- 119
- References
- 76
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 6 · 2023: 5 · 2022: 4 · 2021: 8 · 2020: 14 · 2019: 11 · 2018: 11 · 2017: 12 · 2016: 11 · 2015: 7 · 2014: 8 · 2013: 9 · 2012: 5
- FWCI
- 6.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Experimental Neurobiology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuronal autophagy, autophagic flux, neurodegeneration, autophagosomes, lysosomal degradation, protein quality control, Alzheimer's disease, Huntington's disease, Parkinson's disease, frontotemporal dementia, neuronal survival, neurodegenerative disease treatment
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