ArticleRedox biology2014
Aβ and tau toxicities in Alzheimer's are linked via oxidative stress-induced p38 activation: protective role of vitamin E.
Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 2 of them syntheses that pooled it.
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
152 citing papers in PubMed, 2 syntheses or guidelines pooled it, 261 citations in OpenAlex.
- Association of vitamin E intake in diet and supplements with risk of dementia: A meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- Pathophysiology and Therapeutic Perspectives of Oxidative Stress and Neurodegenerative Diseases: A Narrative Review.Advances in therapy · 2020Pooled it
- Oxidative stress and inflammation in neurodegenerative disorders.Archives of toxicology · 2026Review
- Hesperidin attenuates aluminum chloride-induced cognitive impairment by modulating ERK/MAPK Signaling, tau protein immunoexpression, neuroinflammation, and microglial activation in mice.Metabolic brain disease · 2026Article
- Amelioration of behavioral and neural deficits in animal models of neurodegenerative disease by nanoformulations of curcumin and quercetin.Neural regeneration research · 2026Article
- Circadian gatekeepers of the gut-brain-immune axis: implications for neuroinflammation and neurodegeneration.Journal of neuroinflammation · 2026Review
- Circulating Sphingomyelins Correlate With Plasma T-Tau in Cognitively Unimpaired Older Adults at Risk of Developing Alzheimer's Disease.Journal of neurochemistry · 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
- CAR Treg therapies for neurodegenerative diseases.iScience · 2026Review
- Protective effects of vitamin B12 against LPS-induced cognitive impairment through modulation of neuroinflammation, oxidative stress, and cholinergic dysfunction.Iranian journal of basic medical sciences · 2026Article
- Tolcapone Interferes With Key Pathological Features in Alzheimer's Disease.Bioinorganic chemistry and applications · 2026Article
- Vitamin deficiencies and Alzheimer's disease: evidence and implications for supplementation.Frontiers in nutrition · 2026Review
- Plant-derived exosome-like nanovesicles: mechanisms and molecular understanding in neurological disorders with potential therapeutic applications.Drug delivery and translational research · 2025Review
- Senescent-like border-associated macrophages regulate cognitive aging via migrasome-mediated induction of paracrine senescence in microglia.Nature aging · 2025Article
- Review
- Interplay Between Aging and Tau Pathology in Alzheimer's Disease: Mechanisms and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Oxidative Stress: Pathological Driver in Chronic Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Epigallocatechin-3-Gallate Inhibits Oxidative Stress Through the Keap1/Nrf2 Signaling Pathway to Improve Alzheimer Disease.Molecular neurobiology · 2025Review
- Exploring nutraceutical approaches linking metabolic syndrome and cognitive impairment.iScience · 2025Review
- RhoA/ROCK/GSK3β Signaling: A Keystone in Understanding Alzheimer's Disease.Current issues in molecular biology · 2025Review
92 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is a hallmark of Alzheimer's disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E). We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 transgenic mice exhibit a high level of P-p38 in the hippocampus but not in cortex and this is prevented by feeding animals with a diet supplemented with vitamin E. Our results underpin the role of oxidative stress in the altered cell signaling in AD pathology and suggest that antioxidant prevention may be useful in AD therapeutics.
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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.