ReviewJournal of neurochemistry2019
Redox proteomics and amyloid β-peptide: insights into Alzheimer disease.
Review in Journal of neurochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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
66 citing papers in PubMed, 103 citations in OpenAlex.
- Review
- Linking Experimental Models to Pathophysiology: Oxidative Stress and DNA Damage in Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- Treatment of age-related decreases in GTP levels restores endocytosis and autophagy.GeroScience · 2026Article
- Proteostasis breakdown and aggregate diversity in aging and neurodegenerative disease.Frontiers in aging neuroscience · 2026Review
- The Research of Proteomics in Neurodegenerative Diseases Based on Bibliometric Analysis.Brain and behavior · 2025Article
- Investigating the oxidative stress-vascular brain injury axis in mild cognitive impairment of the Alzheimer's type.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Oxidative Stress-mediated Lipid Peroxidation-derived Lipid Aldehydes in the Pathophysiology of Neurodegenerative Diseases.Current neuropharmacology · 2025Review
- Altered Heme and Redox Homeostasis Underpin Late-onset Alzheimer's Disease.International journal of biological sciences · 2025Article
- The double life of glucose metabolism: brain health, glycemic homeostasis, and your patients with type 2 diabetes.BMC medicine · 2024Review
- The effect of azelaic acid on AlClActa neuropsychiatrica · 2024Article
- Metformin effectively alleviates the symptoms of Alzheimer in rats by lowering amyloid β deposition and enhancing the insulin signal.Metabolic brain disease · 2024Article
- Nitric Oxide Signaling and Sensing in Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- The Effects of PICALM rs3851179 and Age on Brain Atrophy and Cognition Along the Alzheimer's Disease Continuum.Molecular neurobiology · 2024Article
- Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers.Antioxidants (Basel, Switzerland) · 2024Review
- Protein Oxidation in Aging and Alzheimer's Disease Brain.Antioxidants (Basel, Switzerland) · 2024Review
- Normal-Tension Glaucoma and Potential Clinical Links to Alzheimer's Disease.Journal of clinical medicine · 2024Review
- Exosomal Dynamics and Brain Redox Imbalance: Implications in Alzheimer's Disease Pathology and Diagnosis.Antioxidants (Basel, Switzerland) · 2024Review
- Reactive oxygen species in biological systems: Pathways, associated diseases, and potential inhibitors-A review.Food science & nutrition · 2024Review
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders.Progress in neurobiology · 2023Review
6 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
Abstract
Alzheimer disease (AD) is a progressive neurodegenerative disorder associated with aging and characterized pathologically by the presence of senile plaques, neurofibrillary tangles, and neurite and synapse loss. Amyloid beta-peptide (1-42) [Aβ(1-42)], a major component of senile plaques, is neurotoxic and induces oxidative stress in vitro and in vivo. Redox proteomics has been used to identify proteins oxidatively modified by Aβ(1-42) in vitro and in vivo. In this review, we discuss these proteins in the context of those identified to be oxidatively modified in animal models of AD, and human studies including familial AD, pre-clinical AD (PCAD), mild cognitive impairment (MCI), early AD, late AD, Down syndrome (DS), and DS with AD (DS/AD). These redox proteomics studies indicate that Aβ(1-42)-mediated oxidative stress occurs early in AD pathogenesis and results in altered antioxidant and cellular detoxification defenses, decreased energy yielding metabolism and mitochondrial dysfunction, excitotoxicity, loss of synaptic plasticity and cell structure, neuroinflammation, impaired protein folding and degradation, and altered signal transduction. Improved access to biomarker imaging and the identification of lifestyle interventions or treatments to reduce Aβ production could be beneficial in preventing or delaying the progression of AD. This article is part of the special issue "Proteomics".
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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.