ReviewMolecular neurobiology2016
The Ubiquitin-Proteasome System and Molecular Chaperone Deregulation in Alzheimer's Disease.
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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.
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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
51 citing papers in PubMed, 94 citations in OpenAlex.
- FBXW7α regulates amyloid pathology by mediating ubiquitination and degradation of BACE1 in Alzheimer's disease.Cell death discovery · 2026Article
- ScFv T1 Protects Against Mitochondrial Damage of SH-SY5Y Cells Caused by Extracellular Tau Aggregates.Antioxidants (Basel, Switzerland) · 2026Article
- Heat shock proteins (Hsp70 and Hsp90) in neurodegeneration: pathogenic roles and therapeutic potential.Frontiers in aging neuroscience · 2026Review
- Gerobiotics: Exploring the Potential and Limitations of Repurposing Probiotics in Addressing Aging Hallmarks and Chronic Diseases.Probiotics and antimicrobial proteins · 2026Review
- Boosting Brain Clean-Up: Can Targeting UPS Genes Offer Neuroprotection?Molecular neurobiology · 2025Review
- Retinal vascular dysfunction in the MthfrAlzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The Ubiquitination and Degradation of SH2B3 Mediated by MEF2A/WWP2 Axis Restores Microglial Homeostasis to Alleviate Cerebral Microvascular Endothelial Cell Injury in Ischemic Stroke.Neurochemical research · 2025Article
- Proteasomes and Ubiquitin C-Terminal Hydrolase L1 as Biomarkers of Tissue Damage and Inflammatory Response to Different Types of Injury-A Short Review.Life (Basel, Switzerland) · 2025Review
- From molecules to medicine: a systematic review of Gastrodia elata's bioactive metabolites and therapeutic potential.Frontiers in pharmacology · 2025Review
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- Article
- Proteome-Wide Discovery of Cortical Proteins That May Provide Motor Resilience to Offset the Negative Effects of Pathologies in Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Cellular response to β-amyloid neurotoxicity in Alzheimer's disease and implications in new therapeutics.Animal models and experimental medicine · 2023Review
- Inhibition of histone methyltransferase Smyd3 rescues NMDAR and cognitive deficits in a tauopathy mouse model.Nature communications · 2023Article
- SUMO1 Modification of Tau in Progressive Supranuclear Palsy.Molecular neurobiology · 2022Article
- Deubiquitinating enzymes (DUBs): decipher underlying basis of neurodegenerative diseases.Molecular psychiatry · 2022Review
- Integrated Network Pharmacology and Comprehensive Bioinformatics Identifying the Mechanisms and Molecular Targets of Yizhiqingxin Formula for Treatment of Comorbidity With Alzheimer's Disease and Depression.Frontiers in pharmacology · 2022Article
- LISTERIN E3 Ubiquitin Ligase and Ribosome-Associated Quality Control (RQC) Mechanism.Molecular neurobiology · 2021Review
- Review
- Yuan‑zhi‑san inhibits tau protein aggregation in an AβMolecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the shared hallmarks of neurodegenerative diseases is the accumulation of misfolded proteins. Therefore, it is suspected that normal proteostasis is crucial for neuronal survival in the brain and that the malfunction of this mechanism may be the underlying cause of neurodegenerative diseases. The accumulation of amyloid plaques (APs) composed of amyloid-beta peptide (Aβ) aggregates and neurofibrillary tangles (NFTs) composed of misfolded Tau proteins are the defining pathological markers of Alzheimer's disease (AD). The accumulation of these proteins indicates a faulty protein quality control in the AD brain. An impaired ubiquitin-proteasome system (UPS) could lead to negative consequences for protein regulation, including loss of function. Another pivotal mechanism for the prevention of misfolded protein accumulation is the utilization of molecular chaperones. Molecular chaperones, such as heat shock proteins (HSPs) and FK506-binding proteins (FKBPs), are highly involved in protein regulation to ensure proper folding and normal function. In this review, we elaborate on the molecular basis of AD pathophysiology using recent data, with a particular focus on the role of the UPS and molecular chaperones as the defensive mechanism against misfolded proteins that have prion-like properties. In addition, we propose a rational therapy approach based on this mechanism.
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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.