Autophagic/lysosomal dysfunction in Alzheimer’s disease
Open accessAbstract
Autophagy serves as the sole catabolic mechanism for degrading organelles and protein aggregates. Increasing evidence implicates autophagic dysfunction in Alzheimer's disease (AD) and other neurodegenerative diseases associated with protein misprocessing and accumulation. Under physiologic conditions, the autophagic/lysosomal system efficiently recycles organelles and substrate proteins. However, reduced autophagy function leads to the accumulation of proteins and autophagic and lysosomal vesicles. These vesicles contain toxic lysosomal hydrolases as well as the proper cellular machinery to generate amyloid-beta, the major component of AD plaques. Here, we provide an overview of current research focused on the relevance of autophagic/lysosomal dysfunction in AD pathogenesis as well as potential therapeutic targets aimed at restoring autophagic/lysosomal pathway function.
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Autophagy-lysosomal dysfunction is a critical mechanism impairing clearance of pathological proteins in AD.
“Autophagy–lysosomal dysfunction has emerged as a critical mechanism impairing the clearance of pathological proteins [16].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [16]
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Self-citationIntracellular amyloid-β in Alzheimer's disease
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- Authors
- Orr, M. E., & Oddo, S.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Corresponding author
- Oddo, Salvatore
- Venue
- Alzheimer's Research & Therapy
- Published
- 2013
- Volume
- 5
- Issue
- 5
- Pages
- 53
- ISSN
- 1758-9193 (ISSN-L)
- PMC
- PMC3979020
- OpenAlex
- W2127312027
- Cited by
- 199
- References
- 5
- Citations by year
- 2026: 17 · 2025: 22 · 2024: 16 · 2023: 12 · 2022: 12 · 2021: 26 · 2020: 20 · 2019: 15 · 2018: 20 · 2017: 15 · 2016: 11 · 2015: 7 · 2014: 6
- FWCI
- 0.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Alzheimer s Research & Therapy (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- UA Campus Repository (The University of Arizona) (acceptedVersion)
- Funders
- National Institutes of Health (AG037637-03)
- National Institute on Aging (AG021890, AG037637, T32AG021890, R01AG037637)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Keywords
- autophagy, lysosomal dysfunction, Alzheimer's disease, protein aggregation, amyloid-beta, lysosomal enzymes, neurodegeneration, therapeutic target
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