ReviewNeuroscience letters2019
Endo-lysosomal pathway and ubiquitin-proteasome system dysfunction in Alzheimer's disease pathogenesis.
Review in Neuroscience letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 3 syntheses or guidelines pooled it, 75 citations in OpenAlex.
- Interplay between frailty and cardiometabolic disorders: from pathophysiology to clinical implications.Cardiovascular diabetology · 2025Pooled it
- The proteasome as a druggable target with multiple therapeutic potentialities: Cutting and non-cutting edges.Pharmacology & therapeutics · 2020Pooled it
- Targeting Ubiquitin-Proteasome Pathway by Natural Products: Novel Therapeutic Strategy for Treatment of Neurodegenerative Diseases.Frontiers in physiology · 2020Pooled it
- UPS-mediated P-glycoprotein regulation in Alzheimer's disease: pharmacological implications for the amyloid pathology.Molecular biology reports · 2026Review
- Overexpression of WNT3a in the Hippocampus Can Partly Alleviate Deficits in Animal Models of Alzheimer's Disease.Neurochemical research · 2026Article
- Protein Modifications and Quality Control System: Target for Alzheimer's Disease Therapy.International journal of molecular sciences · 2026Review
- Article
- Ubiquitin-Proteasome System Dysregulation in Alzheimer's Disease Impacts Protein Abundance.bioRxiv : the preprint server for biology · 2025Article
- Unveiling the therapeutic potential of natural products in Alzheimer's disease: insights fromFrontiers in pharmacology · 2025Review
- Role of Tau Protein Hyperphosphorylation in Diabetic Retinal Neurodegeneration.Journal of ophthalmology · 2025Review
- Truncated tau interferes with the autophagy and endolysosomal pathway and results in lipid accumulation.Cellular and molecular life sciences : CMLS · 2024Article
- DAP12 interacts with RER1 and is retained in the secretory pathway before assembly with TREM2.Cellular and molecular life sciences : CMLS · 2024Article
- Modeling reveals the strength of weak interactions in stacked-ring assembly.Biophysical journal · 2024Article
- Glua1 Ubiquitination in Synaptic Plasticity and Cognitive Functions: Implications for Neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Role of 14-3-3 protein family in the pathobiology of EBV in immortalized B cells and Alzheimer's disease.Frontiers in molecular biosciences · 2024Article
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Preserved autophagy in cognitively intact non-demented individuals with Alzheimer's neuropathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- The Proteome Profile of Olfactory Ecto-Mesenchymal Stem Cells-Derived from Patients with Familial Alzheimer's Disease Reveals New Insights for AD Study.International journal of molecular sciences · 2023Article
- Integrative metabolomics science in Alzheimer's disease: Relevance and future perspectives.Ageing research reviews · 2023Review
- 24-Hydroxycholesterol Induces Tau Proteasome-Dependent Degradation via the SIRT1/PGC1α/Nrf2 Pathway: A Potential Mechanism to Counteract Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Several lines of evidence have shown that defects in the endo-lysosomal autophagy degradation pathway and the ubiquitin-proteasome system play a role in Alzheimer's Disease (AD) pathogenesis and pathophysiology. Early pathological changes, such as marked enlargement of endosomal compartments, gradual accumulation of autophagic vacuoles (AVs) and lysosome dyshomeostasis, are well-recognized in AD. In addition to these pathological indicators, many genetic variants of key regulators in the endo-lysosomal autophagy networks and the ubiquitin-proteasome system have been found to be associated with AD. Furthermore, altered expression levels of key proteins in these pathways have been found in AD human brain tissues, primary cells and AD mouse models. In this review, we discuss potential disease mechanisms underlying the dysregulation of protein homeostasis governing systems. While the importance of two major protein degradation pathways in AD pathogenesis has been highlighted, targeted therapy at key components of these pathways has great potential in developing novel therapeutic interventions for AD. Future investigations are needed to define molecular mechanisms by which these complex regulatory systems become malfunctional at specific stages of AD development and progression, which will facilitate future development of novel therapeutic interventions. It is also critical to investigate all key components of the protein degradation pathways, both upstream and downstream, to improve our abilities to manipulate transport pathways with higher efficacy and less side effects.
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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.