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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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GWAS found associations between plasma biomarkers and the APOE gene.
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16/100
Plasma p-tau217 concentrations were positively associated with plasma TNF- (Kendalls {tau} = 0.339; P < .001) and IL-6 (Kendalls {tau} = 0.310; P < .001) concentrations.
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Of 822 individuals enrolled in the HEAD study, 681 participants spanning cognitively unimpaired to dementia were included.
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16/100
--Clinical trajectories after a diagnosis of mild cognitive impairment (MCI) vary widely, so prognostic models must account for both the timing of subsequent diagnoses and unequal follow-up.
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In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline.
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BackgroundTuberous sclerosis complex (TSC) is a rare autosomal dominant neurodevelopmental disorder caused by loss-of-function mutations in TSC1 or TSC2, resulting in chronic hyperactivation of the mechanistic target of rapamycin (mTOR) pathway.
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status.
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52/100
Prion disease and Alzheimer disease (AD) are common causes of rapidly progressive dementia (RPD).
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32/100
Defective mitochondrial quality control is increasingly implicated in tau-mediated neurodegeneration, but how distinct tau lesions in different cell types interact with PINK1-PRKN-mediated mitophagy remains unclear.
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ObjectivePlasma p-Tau217 leaves 30-50% of patients in an indeterminate "gray zone" often requiring A{beta}-PET.
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BackgroundPlasma phosphorylated tau at threonine 217 (p-Tau217) is a leading blood-based biomarker for Alzheimers disease (AD).
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A doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva cuja fisiopatologia envolve, entre outros mecanismos, o acúmulo cerebral de β-amiloide, associado a alterações da proteína tau, sua hiperfosforilação e formação de emaranhados neurofibrilares, contribuindo para a disfunção sináptica e a perda neuronal.
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INTRODUCTIONBiomarkers for monitoring disease activity and treatment response in peripheral neuropathies remain limited.
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The PS19 mouse model expressing the P301S tau mutation exhibits tau pathology associated with frontotemporal dementia.
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Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17).
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A major hurdle in Alzheimer disease research is the failure of mouse models to capture complexities of the human brain that contributes to repeated clinical trial failure.
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Amyloid immunotherapy with lecanemab and donanemab has been approved on the basis of statistically significant slowing of cognitive and functional decline in early Alzheimer's disease (1,2).
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The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]).
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Despite reductions in plasma p-tau217 with donanemab treatment, this biomarker cannot currently be used to accurately detect TRAC by PET (< 24.1 CL) in individuals with early symptomatic AD.
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The accumulation of pathological four-repeat (4R) tau is central to several frontotemporal dementia (FTD) subtypes, but human neuronal models amenable to high-throughput screening of 4R tau-targeting therapies remain very limited.
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Tau protein misfolding and deposition in the brain is a common factor across many neurodegenerative diseases, grouped under the term tauopathies.
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In older adults, temporal [18F]PI-2620 binding was higher in women (β = 0.543, P < 0.001) and APOE4 carriers (β = 0.395, P = 0.030) and was positively associated with plasma p-tau217 (β = 0.22, P = 0.008).
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Spatial analyses localised early hippocampal tau-PET signal predominantly to the anterior CA1.
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation.
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In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed.
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56/100
Characterizing the timing and progression of Alzheimer's disease biomarker onset in Down syndrome (DS) and contrasting potential timing differences with neurotypical adults is needed to identify optimal Alzheimer's disease therapeutic treatment windows in DS.
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Tau pathology spreads cell to cell, but the mechanisms of intercellular tau transmission remain unclear.
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Flortaucipir (FTP) PET imaging was developed to quantify tau burden in tauopathies such as Alzheimer’s disease (AD) and to distinguish AD from other dementias, including frontotemporal lobar degeneration (FTLD).
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Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling.
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Furthermore, we showed that phosphorylated tau accumulates within the endo-lysosomal system of the CHCHD10 V57E -expressing flies and mammalian cells.
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To evaluate plasma p-tau217 ability to detect pre-symptomatic Alzheimer disease (AD) in ethnoracially diverse cognitively normal individuals.
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60/100
We found that ApoE4 did not facilitate amyloid-PET-associated ptau increases, suggesting that amyloid-related ptau secretion is not altered by ApoE4 carriage.
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51/100
The final study sample comprised 8,797 participants (53.5% women, mean age at HUNT4 77.8 [SD 6.2]).
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This cross-sectional study evaluates the performance of the US Food and Drug Administration–cleared phosphorylated tau 217 (p-tau217) to β-amyloid 42 ratio cut points used to detect amyloid pathology associated with Alzheimer disease.
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Tauopathies are neurodegenerative diseases characterized by the accumulation of misfolded tau protein and include Alzheimer's disease (AD) and related dementia disorders.
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In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9).
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TDP-43 is a ubiquitously expressed, primarily nuclear DNA/RNA-binding protein implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD).
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P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models.
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Primary age-related tauopathy (PART) is a β-amyloid-independent tauopathy, thought by some to be a distinct process from Alzheimer disease neuropathologic change (ADNC).
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Cognitively impaired patients with negative biomarkers of amyloidosis but with neurochemical evidence of Tau pathophysiology or neurodegeneration or both are classified as "suspected non-Alzheimer pathophysiology" (SNAP), according to the 2018 research framework for a biological definition of Alzheimer's disease (AD).
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Alzheimer disease (AD) is the leading cause of dementia globally and is defined by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles formed by the accumulation of phosphorylated tau (p-tau).
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Neurodegenerative diseases, including Alzheimer's Disease (AD), Parkinson's Disease (PD), Lewy Body Disease (LBD), and related dementias, represent a global health challenge, particularly in aging populations.
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HTT IAs carriers patients exhibited decreased survival after disease onset compared to non-carriers.
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Biomarkers to determine underlying frontotemporal lobar degeneration (FTLD) tau or TAR DNA-binding protein (TDP) pathology during life are needed to advance clinical trials targeting specific FTD pathologies.
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Soluble phosphorylated tau has become a key biomarker for Alzheimer's disease pathology, yet further mechanistic studies are needed beyond observational investigations to clarify the relationship between soluble p-tau species and intracellular tau pathology.
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To efficiently implement plasma and cerebrospinal fluid (CSF) biomarkers for staging and prognosis of Alzheimer disease (AD), we must understand their dynamics across disease progression.
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Tauopathies, such as Alzheimer's disease and frontotemporal dementia, are common neurodegenerative diseases characterized by misfolding, hyperphosphorylation, and aggregation of tau.
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The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders.
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Most common clinical diagnosis was PSP (41%) for PSP; unspecified FTD (36%) for CBD; AD for AGD (57%) and Other-4R groups (48%), without sex differences.
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Sowohl in der Tau- als auch in der Amyloid-PET-Bildgebung zeigte die Quantifizierung eine gute bis exzellente Vorhersage der visuellen Beurteilung (Tau: AUC=0,86, p<0,0001; Amyloid: AUC=0,99, p<0,0001).
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.
- Generalizability of tau and amyloid plasma biomarkers in Alzheimer's disease cohorts of diverse genetic ancestries
- Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer's disease pathology
- Plasma Phosphorylated Tau at Threonine 181 and Neuropsychiatric Symptoms in Preclinical and Prodromal Alzheimer Disease
- Co-occurrence of multiple pathologies in a case of frontotemporal dementia with TBK1 mutation: first in vivo detection of alpha-synuclein and tau co-pathology
- Concurrent Changes in Plasma Phosphorylated Tau 217, Tau PET, and Cognition in Preclinical Alzheimer Disease
- Diagnostic Accuracy of a Plasma Phosphorylated Tau 217 Immunoassay for Alzheimer Disease Pathology
- Colocalization of tau and alpha-synuclein epitopes in Lewy bodies
- Tau reduction prevents neuronal loss and reverses pathological tau deposition and seeding in mice with tauopathy
- Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury