ReviewOxidative medicine and cellular longevity2020
Proteostasis Failure in Neurodegenerative Diseases: Focus on Oxidative Stress.
Review in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
What it found
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The trial behind it
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Who cites it
103 citing papers in PubMed, 181 citations in OpenAlex.
- The Potential Effects of Oxidative Stress-Related Plasma Abnormal Protein Aggregate Levels on Brain Volume and Its Neuropsychiatric Consequences in Parkinson's Disease.Oxidative medicine and cellular longevity · 2021Trial
- Rodent Models of Alzheimer's Disease: Bridging the Translational Gap Through Systems-Level Integration.Biomedicines · 2026Review
- A Rapamycin Pharmacogenomic Approach for the Childhood Dementia Niemann-Pick C.Journal of inherited metabolic disease · 2026Article
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- A next-generation HDAC6 inhibitor for amyotrophic lateral sclerosis and frontotemporal dementia.Brain : a journal of neurology · 2026Article
- Natural Products as a Pipeline for Next-Generation Neurodegenerative Drugs: From Single-Target Failure to Multi-Target Opportunity in Alzheimer's and Parkinson's Disease.Molecules (Basel, Switzerland) · 2026Review
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Copper Dyshomeostasis Affects α-Synuclein Clearance Mechanisms in Parkinson's Disease: Insights from In Vitro Models and Translational Evidence.International journal of molecular sciences · 2026Review
- Structural signature of plasma proteins classifies the status of Alzheimer's disease.Nature aging · 2026Article
- Balanced deep learning on multi-omics networks identifies molecular subgroups of pathological brain aging.medRxiv : the preprint server for health sciences · 2026Article
- Shared molecular mechanisms in aging and neurodegenerative diseases: from mechanistic insights to therapeutic strategies.Frontiers in human neuroscience · 2026Review
- Editorial: Application of stem cells in degenerative orthopedic diseases.Frontiers in cell and developmental biology · 2026Article
- 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
- Proteostasis breakdown and aggregate diversity in aging and neurodegenerative disease.Frontiers in aging neuroscience · 2026Review
- Proteasome and Ribosome Ubiquitination in Retinal Pigment Epithelial (RPE) Cells in Response to Oxidized Low-Density Lipoprotein (OxLDL).Biomedicines · 2025Article
- SLP2/PHB Aggregates in ALS Mouse Models and Patients: Implications BeyondInternational journal of molecular sciences · 2025Article
- The Proteostasis Network in Proteinopathies: Mechanisms and Interconnections.The American journal of pathology · 2025Review
- Conserved Blood Transcriptome Patterns Highlight microRNA and Hub Gene Drivers of Neurodegeneration.Genes · 2025Article
- Adaptive Suppression of MAPT Transcription Maintains Tau Proteostasis in Developing Human Neurons.Research square · 2025Article
- Impacts of systemic milieu on cerebrovascular and brain aging: insights from heterochronic parabiosis, blood exchange, and plasma transfer experiments.GeroScience · 2025Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protein homeostasis or proteostasis is an essential balance of cellular protein levels mediated through an extensive network of biochemical pathways that regulate different steps of the protein quality control, from the synthesis to the degradation. All proteins in a cell continuously turn over, contributing to development, differentiation, and aging. Due to the multiple interactions and connections of proteostasis pathways, exposure to stress conditions may cause various types of protein damage, altering cellular homeostasis and disrupting the entire network with additional cellular stress. Furthermore, protein misfolding and/or alterations during protein synthesis results in inactive or toxic proteins, which may overload the degradation mechanisms. The maintenance of a balanced proteome, preventing the formation of impaired proteins, is accomplished by two major catabolic routes: the ubiquitin proteasomal system (UPS) and the autophagy-lysosomal system. The proteostasis network is particularly important in nondividing, long-lived cells, such as neurons, as its failure is implicated with the development of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. These neurological disorders share common risk factors such as aging, oxidative stress, environmental stress, and protein dysfunction, all of which alter cellular proteostasis, suggesting that general mechanisms controlling proteostasis may underlay the etiology of these diseases. In this review, we describe the major pathways of cellular proteostasis and discuss how their disruption contributes to the onset and progression of neurodegenerative diseases, focusing on the role of oxidative stress.
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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.