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tau
751 studies tagged tau, dated 1986-05-01 to 2026-10-19. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
751 studies carry this tag.
Date range
1986 to 2026
Top journals
- Neurology 52
- Alzheimer s & Dementia 50
- JAMA neurology 42
- Brain : a journal of neurology 24
- The Journal of biological chemistry 22
233 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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TAR-DNA-binding protein 43 (TDP-43) has been identified as a major component protein of ubiquitin-positive inclusions in brains from patients with frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-U) and amyotrophic lateral sclerosis.
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40/100
Intraneuronal accumulation of phosphorylated Tau protein is a molecular pathology found in many forms of dementia, including Alzheimer disease.
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Cerebrospinal fluid (CSF) total Tau levels vary widely in neurodegenerative disorders, thus being not useful in their discrimination over Alzheimer disease.
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57/100
Many potential treatments for Alzheimer's disease target amyloid-beta peptides (Abeta), which are widely presumed to cause the disease.
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Intracellular aggregation of the microtubule-associated protein tau into filamentous inclusions is a defining characteristic of Alzheimer disease.
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Neurofibrillary tangles (NFTs) are a pathological hallmark of Alzheimer's disease and other tauopathies, but recent studies in a conditional mouse model of tauopathy (rTg4510) have suggested that NFT formation can be dissociated from memory loss and neurodegeneration.
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The objective of this study was to investigate the levels of tau protein in neurosyphilis.
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44/100
Cerebrospinal fluid (CSF) concentrations of amyloid beta(42) (Abeta(42)) peptides and tau proteins may serve as biomarkers for Alzheimer disease (AD).
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Intraneuronal accumulation of hyperphosphorylated protein tau in paired helical filaments together with amyloid-beta peptide (Abeta) deposits confirm the clinical diagnosis of Alzheimer disease.
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As a potential disease-modifying treatment for Alzheimer disease (AD), 3-amino-1-propanesulfonic acid (3APS) is a compound that binds to amyloid beta (Abeta), a toxic protein known to aggregate, leading to amyloid plaque deposition in the brain.
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43/100
These results provide a link between tau autoimmunity and tauopathy-like abnormalities and indicate potential dangers of using tau for immunotherapy.
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Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease.
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Frontotemporal dementia (FTD) is the second most common cause of dementia in people under the age of 65 years.
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Neurofibrillary tangles form in a specific spatial and temporal pattern in Alzheimer's disease.
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The microtubule binding protein tau is implicated in neurodegenerative tauopathies, including frontotemporal dementia (FTD) with Parkinsonism caused by diverse mutations in the tau gene.
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Neurodegenerative diseases are often classified based on the abnormal accumulation of synuclein or tau.
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Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of tauopathies.
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Here, we describe the generation of a novel transgenic mouse model of human tauopathy.
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Discovery of various mutations in the tau gene among frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) families suggests gain-of-toxic function of wild-type or mutant tau as the mechanism for extensive neuronal loss.
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We generated several cell models of tauopathy in order to study the mechanisms of neurodegeneration in diseases involving abnormal changes of tau protein.
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Microtubule-associated protein tau is the major component of the neurofibrillary tangles of Alzheimer disease (AD) and is genetically linked to frontotemporal dementias (FTDP-17).
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Neurofibrillary tangles (NFTs) are the most common intraneuronal inclusion in the brains of patients with neurodegenerative diseases and have been implicated in mediating neuronal death and cognitive deficits.
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Familial frontotemporal dementia (FTD), characterized by tau-negative, ubiquitin-positive inclusions at autopsy, is linked to a chromosomal region at 17q21 (FTDU-17), encompassing the gene encoding the microtubule associated protein tau, MAPT.
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The microtubule-associated tau protein abnormally phosphorylated at threonine 231 (p-tau231) has been investigated as a potential marker of Alzheimer disease.
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49/100
Transgenic mice overexpressing the P301L mutant human tau protein exhibit an accumulation of hyperphosphorylated tau and develop neurofibrillary tangles.
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Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies.
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Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial Alzheimer disease, in Down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of Guam.
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Hyperphosphorylated microtubule-associated protein tau is the major protein component of neurofibrillary tangles in the brain of patients with Alzheimer's disease (AD).
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Tau is the major component of the intracellular filamentous deposits that define a number of neurodegenerative diseases.
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Just as neuronal activity is essential to normal brain function, microtubule-associated protein tau appears to be critical to normal neuronal activity in the mammalian brain, especially in the evolutionary most advanced species, the homo sapiens.
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49/100
Tau protein is the major component of the intraneuronal filamentous inclusions that constitute defining neuropathological characteristics of Alzheimer's disease and other tauopathies.
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36/100
Argyrophilic grain disease (AgD) is a late-onset dementia morphologically characterized by the presence of abundant spindle-shaped argyrophilic grains (ArG) in neuronal processes and coiled bodies in oligodendrocytes.
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The INNO-BIA AlzBio3 selectively and specifically measured Abeta((1-42)), T-TAU, and P-TAU((181P)) in the CSF.
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Neurofibrillary tangles (NFTs) are a pathological hallmark of many neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP17).
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We have reported that the ambient gyrus is the site with the greatest accumulation of argyrophilic grains (AGs) and that the degeneration of the ambient gyrus is responsible for dementia with grains.
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Mild cognitive impairment is considered to be a transitional stage between normal aging and dementia.
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Neurofibrillary degeneration (ND) is both a pivotal and a primary lesion of Alzheimer disease (AD) and related tauopathies.
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36/100
Alzheimer's disease (AD) is characterized histopathologically by beta-amyloid-containing plaques, neurofibrillary tangles (NFT), reduced synaptic density, and neuronal loss in selected brain areas.
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Neurofibrillary tangles (NFTs) are composed of abnormal aggregates of the cytoskeletal protein tau.
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36/100
Intracellular accumulations of filamentous tau inclusions are neuropathological hallmarks of neurodegenerative diseases known as tauopathies.
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Inflammation is a process that has been actively related with the onset of several neurodegenerative disorders including Alzheimer disease (AD).
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The p-tau proteins in CSF come closest to fulfilling the criteria of a biological marker of AD.
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Loss of synapses and dying back of axons are considered early events in brain degeneration during Alzheimer's disease.
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In Alzheimer's disease and related disorders, the microtubule-associated protein Tau is abnormally hyperphosphorylated and aggregated into neurofibrillary tangles.
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Tau protein is a microtubule-associated protein located in neuronal axons, which has been used in various configurations as a diagnostic marker of degenerative changes in the CNS.
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Frontotemporal dementia (FTD) is a pathologically heterogeneous group of presenile neurodegenerative disorders, with or without the deposition of hyperphosphorylated tau protein in affected brain regions.
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40/100
We report a case of rapidly progressive frontotemporal dementia presenting at age 33 years.
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36/100
Frontotemporal dementia with parkinsonism chromosome 17 type (FTDP-17) is caused by mutations in MAPT, the gene encoding tau.
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The major protein constituent of Lewy bodies (LBs), the pathological hallmark of Parkinson disease and dementia with Lewy bodies, is considered to be alpha-synuclein, but other proteins, in particular the microtubule-associated protein tau, have been implicated in the pathogenesis of LBs.
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The identification of mutations in the Tau gene in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has made it possible to express human tau protein with pathogenic mutations in transgenic animals.
From across this tag
9 of the 746 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 9. The same 9 appear here every time.
- Lack of tau proteins rescues neuronal cell death and decreases amyloidogenic processing of APP in APP/PS1 mice
- Role of tau protein in Alzheimer's disease: The prime pathological player
- Appoptosin-Mediated Caspase Cleavage of Tau Contributes to Progressive Supranuclear Palsy Pathogenesis
- Sex Differences in the Associations of Obesity with Tau, Amyloid PET, and Cognitive Outcomes in Preclinical Alzheimer's Disease: Cross-Sectional A4 Study
- Outcome associations of CSF total tau in suspected non-Alzheimer pathophysiology
- Prognostic Value of Blood-Based P-Tau217 Levels for Progression to Cognitive Impairment
- Mutations of tau protein in frontotemporal dementia promote aggregation of paired helical filaments by enhancing local beta-structure
- Association of Memory Impairment With Concomitant Tau Pathology in Patients With Cerebral Amyloid Angiopathy
- White matter hyperintensities: relationship to amyloid and tau burden