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phosphorylated
738 studies tagged phosphorylated, dated 1986-05-01 to 2026-10-19. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
Studies
738 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
231 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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The pathological hallmark of neurodegenerative diseases is the formation of toxic oligomers by proteins such as alpha-synuclein (aSyn) or microtubule-associated protein tau (Tau).
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This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions.
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The advent of PET ligands that bind tau pathology has enabled the quantification and visualization of tau pathology in aging and in Alzheimer disease (AD).
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We evaluated the relationship between baseline CSF p-tau181 and the rate of tau PET change in the temporal meta-ROI and entorhinal cortex (ERC) and how it varied by amyloid level (CSF Aβ42 or amyloid PET) among 143 individuals from the Mayo Clinic Study of Aging and Mayo Alzheimer Disease Research Center.
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This study examined plasma phosphorylated tau 181 (P-tau181) and 217 (P-tau217) in 1,329 individuals aged 30-98 years from the population-based Mayo Clinic Study of Aging.
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60/100
Neuroimaging and biofluid tau markers hold potential for optimising such clinical trials by augmenting participant selection, providing evidence of target engagement, and monitoring treatment efficacy.
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Well-authenticated biomarkers can provide critical insights into the biological basis of Alzheimer disease (AD) to enable timely and accurate diagnosis, estimate future burden and support therapeutic trials.
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Aβ(+) patients with TES (N = 10), but not Aβ(-) TES, had significantly higher plasma P-tau levels than HC (P-tau181: p d = 1.34; P-tau217: p d = 1.59).
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Our results indicate good diagnostic and prognostic performance of the plasma p-tau217+ Janssen assay, similar to the p-tau217 Lilly assay.
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However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s).
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In DIAD, clinical disease stage and BDNF Met66 were associated with cognitive impairment and levels of site-specific tau phosphorylation.
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61/100
Brain regions with higher synaptic density are associated with a higher 18F-AV-1451 binding in progressive supranuclear palsy/corticobasal degeneration, but this association diminishes with disease severity.
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72/100
Of 343 participants, the mean (SD) age was 72.56 (7.24) years, and 157 (51.1%) were female.
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Of 4,150 studies screened, 26 were eligible for inclusion, of which 17 were human studies, 8 were preclinical animal studies, and 1 included both human and preclinical animal studies.
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Tau (MAPT) drives neuronal dysfunction in Alzheimer disease (AD) and other tauopathies.
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Alzheimer disease comorbid pathologic characteristics are common and are associated with more rapid cognitive decline in patients with dementia with Lewy bodies (DLB); therefore, it is anticipated that plasma p-tau concentrations may have utility in assessing cognitive impairment in individuals with this disorder.
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Total tau protein (T-Tau) and neurofilament light chain (NfL) have emerged as candidate plasma biomarkers of neurodegeneration, but studies have not compared how these biomarkers cross-sectionally or longitudinally associate with cognitive and neuroimaging measures.
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Although recent clinical trials targeting amyloid-β in Alzheimer's disease have shown promising results, there is increasing evidence suggesting that understanding alternative disease pathways that interact with amyloid-β metabolism and amyloid pathology might be important to halt the clinical deterioration.
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43/100
The human tau protein is implicated in a wide range of neurodegenerative "tauopathy" diseases, consisting of Alzheimer's disease (AD) and frontotemporal lobar degeneration which includes progressive supranuclear palsy, corticobasal degeneration, Pick's disease, and FTLD-tau (frontotemporal dementia with parkinsonism caused by MAPT mutations).
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69/100
For early detection of Alzheimer's disease, it is important to find biomarkers with predictive value for disease progression and clinical manifestations, such as cognitive decline.
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62/100
In Alzheimer's disease, post-mortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with Brodmann area 35, and the entorhinal cortex.
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The ordered assembly of tau protein into filaments characterizes several neurodegenerative diseases, which are called tauopathies.
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA).
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Although all p-tau variants increased across the AD continuum, p-tau217 Lilly showed the greatest dynamic range (13-fold increase vs 1.9-5.4-fold increase for other p-tau variants for AD dementia vs non-AD).
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Plasma-based biomarkers would be potential biomarkers for early diagnosis of Alzheimer's disease (AD) because they are more available and cost-effective than cerebrospinal fluid (CSF) or neuroimaging.
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In this largely presymptomatic population, these results suggest subtle differences across plasma p-tau species and platforms for the prediction of amyloid and tau PET and magnetic resonance imaging measures of cerebrovascular and Alzheimer-related pathology.
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Plasma p-tau217 and p-tau181 were correlated (r=0·90, p diff =0·31) and in pathology-confirmed Alzheimer's disease (n=15, mean age 73 years [SD 12]) versus pathologically confirmed FTLD (n=68, mean age 67 years [SD 8]; AUC=0·96 [0·92-1·00] for p-tau217, AUC=0·91 [0·82-1·00] for p-tau181; p diff =0·22).
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Patients with essential tremor (ET) frequently develop concurrent dementia, which is often assumed to represent co-morbid Alzheimer disease (AD).
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40/100
The microtubule-associated protein tau oligomerizes, but the actions of oligomeric tau (oTau) are unknown.
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Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD).
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In this longitudinal study, we included 396 cognitively normal to dementia subjects with 18 F-Florbetapir/ 18 F-Florbetaben-amyloid-PET, 18 F-Flortaucipir-tau-PET and ~ 2-year cognitive follow-up.
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Primary age-related tauopathy (PART) is a form of Alzheimer-type neurofibrillary degeneration occurring in the absence of amyloid-beta (Aβ) plaques.
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New technology is convenient for measuring blood total tau concentrations and provides a unique and increased opportunity for early intervention to slow cognitive decline.
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Among 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male.
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PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers.
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Traumatic brain injury (TBI) constitutes one of the strongest environmental risk factors for several progressive neurodegenerative disorders of cognitive impairment and dementia that are characterized by the pathological accumulation of hyperphosphorylated tau (p-Tau).
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To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer's disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer's Disease Neuroimaging Initiative (ADNI).
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In Alzheimer's disease (AD) models, AD risk variants in the microglial-expressed TREM2 gene decrease Aβ plaque-associated microgliosis and increase neuritic dystrophy as well as plaque-associated seeding and spreading of tau aggregates.
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A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer's disease (AD) dementia.
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61/100
Alzheimer's disease is characterized by β-amyloid plaques and tau tangles.
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Overall visual ratings showed complete concordance between radiotracers for both the medial temporal lobe and the neocortex.
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47/100
Tauopathies consist of over 25 different neurodegenerative diseases that include argyrophilic grain disease (AGD), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and Pick's disease (PiD).
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Exclusion criteria included any significant neurologic disorder other than suspected AD; presence of infection, infarction, or multiple lacunes as detected by magnetic resonance imaging; and any significant systemic condition that could lead to difficulty complying with the protocol.
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Regional sex-related differences in tau PET burden may contribute to the disparities in AD prevalence between males and females.
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Alzheimer's disease (AD) is a devastating condition with no effective treatments, with promising findings in rodents failing to translate into successful therapies for patients.
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Tau and Aβ assemblies of Alzheimer's disease (AD) can be visualized in living subjects using positron emission tomography (PET).
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These results suggest that the presence of objective memory impairment in patients with probable CAA could serve as a marker for underlying tau pathology.
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Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by abnormal extracellular aggregates of amyloid-β and intraneuronal hyperphosphorylated tau tangles and neuropil threads.
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56/100
DCTclock discriminates between diagnostic groups and improves upon traditional cognitive tests for detecting biomarkers of amyloid and tau pathology in CN older adults.
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Furthermore, plasma p-tau231 was significantly increased in amyloid-β PET quartiles 2-4, whereas CSF p-tau217 and plasma p-tau181 increased only at quartiles 3-4 and 4, respectively.
From across this tag
9 of the 733 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.
- The Cell and Molecular Pathology of Tau Protein in Alzheimer’s Disease
- Global neuropathologic severity of Alzheimer's disease and locus coeruleus vulnerability influences plasma phosphorylated tau levels
- Synergistic interaction between amyloid and tau predicts the progression to dementia
- Argyrophilic grain disease: a late-onset dementia with distinctive features among tauopathies
- Passive immunization targeting the N-terminal projection domain of tau decreases tau pathology and improves cognition in a transgenic mouse model of Alzheimer disease and tauopathies
- Frontotemporal dementia with the V337M MAPT mutation: Tau-PET and pathology correlations
- Inhibition of heparin-induced tau filament formation by phenothiazines, polyphenols, and porphyrins
- CSF beta-amyloid 1-42 and tau in Tunisian patients with Alzheimer's disease: the effect of APOE epsilon4 allele
- Genetic Architecture of Plasma Amyloid and Tau Biomarkers in the Amish