ReviewFrontiers in neuroscience2019
Interplay Between Mitochondrial Oxidative Disorders and Proteostasis in Alzheimer's Disease.
Review in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 89 citations in OpenAlex.
- Amyloid-beta fibrils as active contributors to synaptic dysfunction in Alzheimer's disease.Acta pharmacologica Sinica · 2026Article
- Distinct single-nucleus RNA-seq changes among non-neuronal cells in ADNC, LATE-NC, and mixed pathologies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- DRP lyase deficient DNA polymerase beta impairs mitochondrial electron transport chain and compromise mitochondrial DNA integrity.Research square · 2026Article
- Review
- Multi-platform integration of brain and CSF proteomes reveals biomarker panels for Alzheimer's disease.Briefings in bioinformatics · 2026Article
- Neuroprotective Effect of Fresh Gac Fruit Parts Against β-Amyloid-Induced Toxicity and Its Influence on Synaptic Gene Expression in HT-22 Cell Model.Molecules (Basel, Switzerland) · 2025Article
- Neuronal Death and Biomolecular Condensates: Are There Any New Treatment Options for Alzheimer's Disease?Cells · 2025Review
- Modulatory Effects ofAntioxidants (Basel, Switzerland) · 2025Review
- Article
- Aging and Alzheimer's: the critical role of mitochondrial dysfunction and synaptic alterations.Frontiers in synaptic neuroscience · 2025Review
- Neurostimulation devices to treat Alzheimer's disease.Exploration of neuroscience · 2025Article
- Dietary supplementation and the role of phytochemicals against the Alzheimer's disease: Focus on polyphenolic compounds.The journal of prevention of Alzheimer's disease · 2025Review
- The Use of Natural Products for Preventing Cognitive Decline/Providing Neuroprotection.Handbook of experimental pharmacology · 2025Review
- From Fundamentals to Innovation in Alzheimer's Disease: Molecular Findings and Revolutionary Therapies.International journal of molecular sciences · 2024Review
- Review
- Ferroptosis regulation through Nrf2 and implications for neurodegenerative diseases.Archives of toxicology · 2024Review
- Metabolomic Changes in Rat Serum after Chronic Exposure to Glyphosate-Based Herbicide.Metabolites · 2024Article
- Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024Review
- Pathophysiological Aspects and Therapeutic Armamentarium of Alzheimer's Disease: Recent Trends and Future Development.Cellular and molecular neurobiology · 2023Review
- Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the basis of Alzheimer's disease (AD) etiology remains unknown, oxidative stress (OS) has been recognized as a prodromal factor associated to its progression. OS refers to an imbalance between oxidant and antioxidant systems, which usually consist in an overproduction of reactive oxygen species (ROS) and reactive nitrogen species (RNS) which overwhelms the intrinsic antioxidant defenses. Due to this increased production of ROS and RNS, several biological functions such as glucose metabolism or synaptic activity are impaired. In AD, growing evidence links the ROS-mediated damages with molecular targets including mitochondrial dynamics and function, protein quality control system, and autophagic pathways, affecting the proteostasis balance. In this scenario, OS should be considered as not only a major feature in the pathophysiology of AD but also a potential target to combat the progression of the disease. In this review, we will discuss the role of OS in mitochondrial dysfunction, protein quality control systems, and autophagy associated to AD and suggest innovative therapeutic strategies based on a better understanding of the role of OS and proteostasis.
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What 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.