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tau-protein
387 studies tagged tau-protein, dated 1987-01-01 to 2026-10-31. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- APH-1A and CDK5 Expression Correlates with Tau Hyperphosphorylation and Its Attenuation by Brahmi and Donep-M in STZ induced Alzheimer’s Disease Model 2026-10-31
- Opposing Regulation of Tau Condensation by Phosphorylation Levels and Molecular Chaperone Interactions 2026-10-30
- The Alzheimer's disease-associated rs28834970 variant in PTK2B impairs electrical activity and regulates Tau phosphorylation and APP processing in human neuronal cultures 2026-10-30
Studies
387 studies carry this tag.
Date range
1987 to 2026
Top journals
- Acta neuropathologica 16
- Alzheimer's & dementia : the journal of the Alzheimer's Association 12
- bioRxiv 12
- Molecular neurodegeneration 10
- Research Square 10
173 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses.
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αSyn SAA positivity was more common in Aβ + vs. Aβ- subjects and increased with clinical severity (p < 0.001).
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In Alzheimer's disease (AD), tau undergoes abnormal post-translational modifications and aggregations.
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Experimental drugs lowering brain tau are heralded as improvements in the treatment of Alzheimer's disease.
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Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) and other tauopathies.
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Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB.
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We found a strong, positive correlation between all the measurements.
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The transmission of tau pathology has been proposed as one of the major mechanisms for the spatiotemporal spreading of tau pathology in neurodegenerative diseases.
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In Alzheimer's disease (AD), tau dissociates from microtubules (MTs) due to hyperphosphorylation and misfolding.
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We found that the AL04 treatment decreases hyperphosphorylated tau at PP2A-sensitive epitope Ser202/Thr205 in the hippocampus of the brain.
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Alzheimer's disease (AD) is the most common cause of dementia.
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Alzheimer's disease (AD) is a debilitating neurodegenerative disorder characterized by brain aggregation of β-amyloid (Aβ) peptides and phosphorylated tau (P-tau) proteins.
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Unlike other aggregation inhibitors, RI-AG03 effectively suppresses aggregation of multiple Tau species containing both hotspots in vitro and in vivo, is non-toxic, and suppresses aggregation-dependent neurodegenerative and behavioral phenotypes.
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Tau protein accumulation is one of the characteristic features of Alzheimer's disease (AD).
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Positron Emission Tomography (PET) ligands have advanced Alzheimer's disease (AD) diagnosis and treatment.
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Activation of the NLRP3 pathway was observed in the mouse organotypic slice culture (OSC) model following stimulation with LPS and nigericin or exposure to tau seeds.
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Tau interacts with α-Synuclein (α-Syn) and co-localizes with it in the Lewy bodies, influencing α-Syn pathology in Parkinson's disease (PD).
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Pathological tau disrupts protein homeostasis (proteostasis) within neurons in Alzheimer's disease (AD) and related disorders.
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16/100
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®).
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This study investigates various pathological tau isoforms in the retina of individuals with early and advanced Alzheimer's disease (AD), exploring their connection with disease status.
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Pathological tau aggregates cause cognitive decline in neurodegenerative tauopathies, including Alzheimer's disease (AD).
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Anti-ac-tauK174 treatment mitigates neurobehavioral impairment and reduces tau pathology in PS19 mice.
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N-terminal p-tau was increased in CJD versus SCD (p < 0.0001) and correlated with total tau (t-tau) in the presence of AD and PART co-pathology (rho = 0.758-0.952, p ≤ 001).
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the loss of neural connections and decreased brain tissue volume.
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Alzheimer's disease (AD) involves reduced glutathione levels, causing oxidative stress and contributing to neuronal cell death.
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Tauopathies, a group of neurodegenerative disorders, are characterized by disrupted homeostasis of the microtubule binding protein tau.
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We identified significant clusters of tau-aggregation in praxis-related regions (e.g., supramarginal gyrus, angular gyrus, temporal, parietal and occipital regions) that were associated with apraxia.
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Monoclonal antibodies have emerged as a leading therapeutic agent for the treatment of disease, including Alzheimer's disease.
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Neuronal loss is the central issue in Alzheimer's disease (AD), yet no treatment developed so far can halt AD-associated neurodegeneration.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment, a loss of cholinergic neurons, and cognitive decline that insidiously progresses to dementia.
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Neurons with lower basal UPS activity were more vulnerable to tau accumulation following mild UPS inhibition.
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The hypothesis that neurodegenerative diseases are proteinopathies due to toxic effect of different underlying proteins, such as amyloid-beta and 3+4R-tau in Alzheimer's disease (AD) and alpha-synuclein in Parkinson's disease (PD), while still controversial is supported by several studies in the literature.
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Alzheimer's disease (AD) and non-AD tauopathies such as chronic traumatic encephalopathy (CTE), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) are characterized by the abnormal aggregation of three-repeat (3R) and/or four-repeat (4R) tau isoforms.
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The levels of p-tau217 and p-tau231 in cerebrospinal fluid (CSF) are associated with early amyloid beta (Aß) changes in the brain, while the CSF levels of p-tau205 are foremost related to tau pathology in the later stages of the disease.
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Microtubule-associated protein tau is an intrinsically disordered protein (IDP) that forms characteristic fibrillar aggregates in several diseases, the most well-known of which is Alzheimer's disease (AD).
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We and others have shown that [18F]-Flortaucipir, the most validated tau PET tracer thus far, binds with strong affinity to tau aggregates in Alzheimer's (AD) but has relatively low affinity for tau aggregates in non-AD tauopathies and exhibits off-target binding to neuromelanin- and melanin-containing cells, and to hemorrhages.
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By employing the hybridoma technique, 49 mAbs recognizing Tau (1-22), nine mAbs targeting p-Tau231, one mAb targeting p-Tau217, and two mAbs targeting p-Tau181 were developed.
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Tau is a microtubule-associated protein essential for microtubule assembly and stability in neurons.
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Alzheimer's disease (AD) is a significant 21st-century public health challenge.
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Amyloid-β (Aβ) plaques and neurofibrillary tangles containing phosphorylated tau protein are major hallmarks of Alzheimer's disease (AD).
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Aggregation of tau protein is a pathological hallmark of Alzheimer's disease and other neurodegenerative tauopathies.
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54/100
Serum concentrations of semorinemab were consistent across studies and showed a dose-proportional increase across the evaluated dose range.
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The prediction model achieved PPV of 97.7% for amyloid, 96.2% for tau. 119 participants in the full analysis set (70 treatment and 49 placebo) were classified as A+T+.
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In Alzheimer's disease, the spread of aberrantly phosphorylated tau is an important criterion in the Braak staging of disease severity and correlates with disease symptomatology.
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The common marmoset (Callithrix jacchus), a small South American monkey, is an important nonhuman primate model in the study of aging and age-related neurodegenerative disease, including Alzheimer's disease, Parkinson's disease, and related dementias.
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Over the last decade, there has been a growing interest in intrabodies and their therapeutic potential.
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To simply and rapidly detect the highly phosphorylated tau protein at threonine 217 (p-tau217) as a precautionary measure against Alzheimer's disease and distinguish it from other neurodegenerative diseases, a novel immunosensor was prepared using luminol as the electrochemiluminescent (ECL) sensing probe reinforced by Au-Cu nanoparticles (Au-Cu NPs).
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Triggering receptor expressed on myeloid cells 2 (TREM2), a pattern recognition receptor abundantly expressed on microglia, has been identified as one of the risk factors for Alzheimer's disease (AD).
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Alzheimer disease (AD) is the most common cause of dementia in older individuals.
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This study focused on designing and evaluating Tau-PET tracers for noninvasive positron emission computed tomography (PET) imaging of neurofibrillary tangles (NFTs), a hallmark pathology of Alzheimer's disease (AD).
From across this tag
8 of the 387 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 8. The same 8 appear here every time.
- Tauvid™: The First FDA-Approved PET Tracer for Imaging Tau Pathology in Alzheimer's Disease
- Alz-50/Gallyas-positive lysosome-like intraneuronal granules in Alzheimer's disease and control brains
- MARK/PAR1 kinase is a regulator of microtubule-dependent transport in axons
- Anti-Tau Trials for Alzheimer's Disease: A Report from the EU/US/CTAD Task Force
- Soluble pathogenic tau transmission to astrocytes drives cellular senescence and neurovascular uncoupling in a model of Alzheimer’s tauopathy
- Effect of Metformin on tau pathology and proteostasis in cellular and a Drosophila model of Tauopathy
- Distinct binding of PET ligands PBB3 and AV-1451 to tau fibril strains in neurodegenerative tauopathies
- Microglia-mediated T cell infiltration drives neurodegeneration in tauopathy