ReviewOxidative medicine and cellular longevity2015
Tau Hyperphosphorylation and Oxidative Stress, a Critical Vicious Circle in Neurodegenerative Tauopathies?
Review in Oxidative medicine and cellular longevity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.
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Who cites it
160 citing papers in PubMed, 300 citations in OpenAlex.
- Tau protein differentially affects Piezo1 and Kir2.1 channels in brain capillary endothelial cells.Biophysical journal · 2026Article
- RNA-based therapeutics for Alzheimer's disease and related tauopathies: challenges and opportunities.The journal of prevention of Alzheimer's disease · 2026Review
- Gut Microbiome Changes in Preclinical Alzheimer's Disease.Nutrients · 2026Review
- Limited Detectability of Network Functional Alterations in a Tauopathy Model Using Mouse Primary Cortical Cultures.Biomedicines · 2026Article
- Life Cycle and Circadian Rhythms in Central Resident Immunity and Neuropsychiatric Pathology.Neuroscience bulletin · 2026Review
- Tau profiling of brain extracellular vesicles reveals PHF6 peptide as core for pathological tau seeding in Alzheimer's disease.Journal of biomedical science · 2026Article
- Metabolic Brain Disorders: Prodromes, Symptoms, and Syndromes.International journal of molecular sciences · 2026Review
- Cannabidiol attenuates tau hyperphosphorylation and cognitive deficits in an experimental model of Alzheimer's disease and is associated with restoration of PP2A expression.Metabolic brain disease · 2026Article
- Integration of Transcriptional Signatures from Brain Tissue and Plasma Extracellular Vesicles of a Preclinical Tauopathy Mouse Model.International journal of molecular sciences · 2026Article
- From Food Additives to Neurodegeneration: The Emerging Role of Polyphosphates in Tauopathies.ACS chemical neuroscience · 2026Review
- Hexaraphane as a potential therapeutic strategy for tauopathies.Redox biology · 2026Article
- The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases.Journal of personalized medicine · 2026Review
- From Lipids to Mitochondria: Shared Metabolic Alterations in Obesity and Alzheimer's Disease.Cells · 2026Review
- Tau Pathology in Chronic Traumatic Encephalopathy: Mechanisms and Diagnostic Advances.The Yale journal of biology and medicine · 2026Review
- Long-term adherence and changes in the Mediterranean and MIND diets in relation to dementia risk and cognitive function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Tau Protein Aggregation Inhibitors-Therapeutic Strategy for Concurrent Tau and Amyloid Aggregation Inhibition.Biomedicines · 2026Review
- Article
- Standardized Hydroxytyrosol-Enriched Olive Pomace Juice Modulates Metabolic and Neurotrophic Signaling Pathways to Attenuate Neuroinflammation and Protect Neuronal Cells.Molecules (Basel, Switzerland) · 2026Article
- Neuroprotective effect of selenium in rats subjected to chronic intermittent cold and immobilization stress: The role of phosphorylated tau.Iranian journal of basic medical sciences · 2026Article
- A Review on the Pathophysiology of Alzheimer's Disease.Current protein & peptide science · 2026Review
100 more citing papers are in PubMed but not listed here.
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
Hyperphosphorylation and aggregation of the microtubule-associated protein tau in brain, are pathological hallmarks of a large family of neurodegenerative disorders, named tauopathies, which include Alzheimer's disease. It has been shown that increased phosphorylation of tau destabilizes tau-microtubule interactions, leading to microtubule instability, transport defects along microtubules, and ultimately neuronal death. However, although mutations of the MAPT gene have been detected in familial early-onset tauopathies, causative events in the more frequent sporadic late-onset forms and relationships between tau hyperphosphorylation and neurodegeneration remain largely elusive. Oxidative stress is a further pathological hallmark of tauopathies, but its precise role in the disease process is poorly understood. Another open question is the source of reactive oxygen species, which induce oxidative stress in brain neurons. Mitochondria have been classically viewed as a major source for oxidative stress, but microglial cells were recently identified as reactive oxygen species producers in tauopathies. Here we review the complex relationships between tau pathology and oxidative stress, placing emphasis on (i) tau protein function, (ii) origin and consequences of reactive oxygen species production, and (iii) links between tau phosphorylation and oxidative stress. Further, we go on to discuss the hypothesis that tau hyperphosphorylation and oxidative stress are two key components of a vicious circle, crucial in neurodegenerative tauopathies.
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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.