ReviewFrontiers in aging neuroscience2023
Proteostasis and neurodegeneration: a closer look at autophagy in Alzheimer's disease.
Review in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 61 citations in OpenAlex.
- Serum Autophagy-Related Protein 5 and Clinically Defined Cognitive Status in Older Adults: A Plate-Stratified Cross-Sectional Study Across: Normal Cognition, Mild Cognitive Impairment, and Alzheimer's Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Novel Insights into the Pleiotropic Neuroprotective Action of Synthetic Halogen Free Thyronamine-like Analogues.Molecules (Basel, Switzerland) · 2026Article
- Zinc-mediated lysosomal activation by 1H10 enhances autophagy and attenuates tau pathology in Alzheimer's disease models.Molecular brain · 2026Article
- Emerging New Pathways in Malignant Neoplasms and Neurodegenerative Disorders: Perspectives for Therapeutics.Cells · 2026Review
- Putatively Identified Sarmentoside-B Removes Oligomerized Amyloid Peptide from Neurons by Inhibiting mTOR and Restoring Lysosomal Function, in In Vitro Alzheimer's Disease Model.Pharmaceutics · 2026Article
- LLPS Inflammasome Metabo-Proteostatic Failure Axis in AD: Mechanistic and Translational Insights.Molecular neurobiology · 2026Review
- Review
- Integration of aged brain multi-omics reveals cross-system mechanisms underlying Alzheimer's disease heterogeneity.Cell reports · 2026Article
- Wdfy3-dependent autophagy impairment recapitulates presymptomatic neurodegenerative signatures in mice.Scientific reports · 2026Article
- CRISPR-Cas9 and next-generation gene editing strategies for therapeutic intervention of neurodegenerative pathways in Alzheimer's disease: a state-of-the-art review.Acta neurologica Belgica · 2026Review
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- A Multi-Network Approach Identifies Proteins Related to Dendritic Spines in Alzheimer's Disease.eNeuro · 2026Article
- Locus- and Gene-Level Insights into the Inverse Association Between Alzheimer's Disease and Cancer.International journal of molecular sciences · 2026Article
- Misfolded Proteins and Cognitive Decline: Mechanistic Insights into Neurodegenerative Disorders.Neurology international · 2026Review
- Systems biology of Alzheimer's Disease: a scoping review of key pathways and mechanisms.Molecular neurodegeneration · 2026Article
- Research trends and hotspots of nanomaterials in Alzheimer's disease: bibliometric analysis.Discover nano · 2026Review
- Brain and circulating EV proteome signatures in schizophrenia as prognostic markers for age-related dementia.Acta neuropathologica communications · 2026Article
- Artificial Intelligence for Natural Products Drug Discovery in Neurodegenerative Therapies: A Review.Biomolecules · 2026Review
- Unveiling the neuroprotective effects of pomegranate extract and/or physical activity against aluminum chloride-induced Alzheimer's disease in rats: modulation of multitude pathways.Frontiers in pharmacology · 2026Article
- Chronic stress, cortisol dysregulation, and neurodegenerative vulnerability: mechanistic pathways linking HPA-axis dysfunction to Alzheimer's disease risk.Frontiers in aging neuroscience · 2026Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by the accumulation of misfolded amyloid-beta and tau proteins. Autophagy acts as a proteostasis process to remove protein clumps, although it progressively weakens with aging and AD, thus facilitating the accumulation of toxic proteins and causing neurodegeneration. This review examines the impact of impaired autophagy on the progression of AD disease pathology. Under normal circumstances, autophagy removes abnormal proteins and damaged organelles, but any dysfunction in this process can lead to the exacerbation of amyloid and tau pathology, particularly in AD. There is increasing attention to therapeutic tactics to revitalize autophagy, including reduced caloric intake, autophagy-stimulating drugs, and genetic therapy. However, the translation of these strategies into clinical practice faces several hurdles. In summary, this review integrates the understanding of the intricate role of autophagy dysfunction in Alzheimer's disease progression and reinforces the promising prospects of autophagy as a beneficial target for treatments to modify the course of Alzheimer's disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.