ReviewMolecular neurobiology2025
Roles of Ubiquitin Ligases and Deubiquitylases in Alzheimer's Disease.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- UCHL3 drives ferroptosis in nucleus pulposus cells by deubiquitinating HMGB1 to activate NCOA4-mediated ferritinophagy.Autophagy · 2026Article
- Proteomic Analysis of Human Chronic Traumatic Encephalopathy Brain Implicates Proteasome and Ribosome Dysfunction in Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Beyond Amyloid: Targeting Co-Aggregating Proteins and Targeted Degradation Strategies in Alzheimer's Disease.Biomedicines · 2026Article
- Post-translational modifications as a regulatory code for tau function in health and disease.Frontiers in dementia · 2026Review
- Proteomic analysis of human chronic traumatic encephalopathy brain implicates proteasome and ribosome dysfunction in disease severity.Molecular neurodegeneration advances · 2026Article
- The modifier matrix: emerging roles of ubiquitin-like proteins in Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Tau Liquid-Liquid Phase Separation in Alzheimer's Disease: Mechanisms, Pathogenesis, and Therapeutic Implications.Molecular neurobiology · 2025Review
- Alzheimer's Disease: From Molecular Mechanisms to Promising Therapeutic Strategies.International journal of molecular sciences · 2025Review
- UCH-L1 in Alzheimer's Disease: A Crucial Player in Dementia-Associated Mechanisms.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
The mechanisms responsible for the accumulation of Aβ plaques and neurofibrillary tangles, composed of phosphorylated Tau protein, in Alzheimer's disease (AD) remain a mystery. Dysfunction of the ubiquitin-proteasome system (UPS) largely contributes to abnormal protein aggregation. A cascade of ubiquitinating enzymes promotes protein ubiquitination, while deubiquitylases (DUBs) regulate its reversal. Disruptions in ubiquitination and deubiquitination processes result in abnormal protein aggregation and the formation of inclusion bodies, ultimately leading to neuronal damage. Recent studies have highlighted the significant role of protein ubiquitination and deubiquitination in the pathogenesis of AD. E3 ubiquitin ligases, which facilitate protein ubiquitination, are beneficial for Aβ clearance, synaptic function, gap junction maintenance, mitophagy, and neuroinflammation. Conversely, DUBs, responsible for removing ubiquitin from substrate proteins, inhibit Aβ and Tau degradation while promoting neuroinflammation in neurons. This review provides a thorough overview of the involvement of E3 ubiquitin ligases and DUBs in AD, highlighting their diverse roles in aspects of pathophysiological processes.
Indexed as
Identifiers
39932514What OpenQuestion holds
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.