Home › Research › Topics › phosphorylated
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.
-
This large review pooled 113 studies (nearly 30,000 people) comparing different forms of blood phosphorylated tau for detecting Alzheimer's pathology. p-tau217 was clearly the best-performing marker, correctly identifying disease pathology about 88% of the time, outperforming other tau variants like p-tau181.
-
Tauopathies encompass a large majority of dementia diagnoses and are characterized by toxic neuronal or glial inclusions of the microtubule-associated protein tau.
-
Tau aggregation driven by microtubule-associated protein tau (MAPT) mutations is central to frontotemporal dementia pathology, yet no disease-modifying therapies effectively target mutant tau.
-
The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies.
-
A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed.
-
Plasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations.
-
We recently confirmed and extended these findings using recombinant TauOs generated from full-length human tau in the presence of arachidonic acid (Balducci et al., 2025; Figure 1).
-
Alzheimer's disease (AD), the most common cause of dementia, is characterized by the accumulation of amyloid-β (Aβ) in senile plaques and abnormally hyperphosphorylated tau proteins in neurofibrillary tangles.
-
WMH burden positively correlated to Neurofilament-Light (NfL) and pTau181.
-
Our results suggest that microstructural features derived from NODDI such as fISO might be useful adjunct markers to tau, which needs to be confirmed in longitudinal studies.
-
Understanding how plasma tau biomarkers are influenced by co-pathologies and comorbidities is crucial for their accurate implementation.
-
Tauopathies are neurodegenerative diseases characterized by pathological tau protein inclusions and dementia.
-
Our findings support a broader interpretation of TBK1-associated neurodegeneration and highlight the importance of multimodal diagnostic approaches that integrate molecular, genetic, imaging, and neuropathological tools.
-
39/100
Tauopathies are neurodegenerative disorders characterized by the abnormal accumulation and aggregation of hyperphosphorylated tau protein.
-
Lack of vitamin D is associated with cognitive decline and Alzheimer's disease.
-
Etalanetug presented an adequate safety and immunogenicity profile in healthy adults.
-
Researchers at the University of Pittsburgh developed a new plasma p-tau217 test (using a different antibody than existing commercial tests) and validated it in 363 people, including some with genetic early-onset Alzheimer's mutations and community-dwelling older adults.
-
This study included 887
-
Transactive response DNA-binding protein of 43 kDa (TDP-43) and tau proteins play critical roles in neurodegenerative diseases, particularly frontotemporal lobar degeneration (FTLD) and Alzheimer's disease (AD).
-
Intrinsic capacity (IC) is a recent key concept proposed by the World Health Organization (WHO) based on aspects of functional ability (both physical and mental) rather than the presence or absence of diseases, with a potential to predict several health outcomes.
-
39/100
Dementia encompasses a range of neurodegenerative diseases (NDDs) presenting with progressive decline in memory, cognition, language and ability to complete daily tasks.
-
All participants had heterozygous c.1184A > G, p.Asp395Gly in VCP.
-
Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions.
-
As a result of multiple phosphorylation, Tau undergoes early conformational changes involving the bending of the intact amino (N)-terminus over the third repeated domain, which in turn was evidenced by positive immunolabeling with the monoclonal antibody Alz-50 [2].
-
For all 3 analytes, less than 10% difference was observed between the concentrations measured on day 0 and after 14 days of transportation and refrigeration.
-
Neuronal dysfunction has been extensively studied as a central feature of neurodegenerative tauopathies.
-
Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years.
-
Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disorder in which tau neurofibrillary tangles are a pathological hallmark closely associated with cognitive dysfunction and neurodegeneration.
-
Plasma p-tau217 levels showed a significant increase across advancing AD stages, with all between-group comparisons remaining significant after false discovery rate adjustment ( p p = 0.002) and CSF p-tau181 (β = 3.2, 95% CI 1.4-5.0, p = 0.001).
-
This study aims to assess the evolution of cognitive performances over a 5-year follow-up period in community-dwelling older people with negative plasma p-tau181 levels and to determine whether frailty could discriminate between those who experience cognitive decline and those who do not, in the p-tau negative groups.
-
62/100
Plasma p-tau217 and p-tau217/Aβ42 concentrations demonstrated robust diagnostic performance in a heterogeneous clinical cohort; interpretation requires consideration of kidney function.
-
LLMD participants were more likely to be tau PET and Aβ PET positive than HCs.
-
This approach offers a sensitive method for identifying individuals at high risk for AD-related cognitive decline.
-
Tauopathies, including Alzheimer's disease and frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), are characterized by the aberrant aggregation of tau protein into neurofibrillary tangles.
-
Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning.
-
In DDI (n = 431), participants were classified as CN A-/T- (n = 169), A+/T- (CN = 26, MCI = 24), A+/T+ (CN = 40, MCI = 105), and A-/T+ (CN = 34, MCI = 33), with a mean age of 64.1 years and 55.9% female.
-
Tauopathies, including Alzheimer's disease (AD) and Frontotemporal Dementia (FTD), are histopathologically defined by the aggregation of hyperphosphorylated pathological tau (pTau) as neurofibrillary tangles in the brain.
-
Tau protein plays a pivotal role in maintaining neuronal structure and function through its regulation of microtubule stability and neuronal polarity.
-
We identified several significant sex-specific and sex-dimorphic differentially expressed genes in neurons, microglia, astrocytes and oligodendrocytes, including both cross-sectional changes and alterations from 7 months to 17 months of age.
-
Through analytical validation, this assay demonstrated robust performance across multiple lots, operators, and instruments and could be used as a tool for diagnosing AD.
-
Retrograde bias better predicted tau progression than anterograde bias, but our best-fitting biophysical models incorporate the mixed effects of both retrograde- and anterograde-directed spread, with notable tau-strain-specific differences.
-
Three progression clusters emerged in both cohorts: stable cognition, slow decline, and rapid decline-each including cases initially classified as CN or MCI.
-
BackgroundAlzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by cognitive deficit and pathological accumulation of amyloid-β (Aβ) and tau proteins.
-
Here we present the cases of two individuals with language and behavioral symptoms indicative of the early clinical manifestations of both Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD).
-
The 4R-like pattern was more prevalent and more strongly expressed (84.3%, mean score, 2.0 ± 1.1) in patients with a consensus diagnosis of PSP/CBD (joint diagnostic group of clinically likely 4R tauopathies) than in all other groups (11.6%, 0.26 ± 0.75, P < 0.0001).
-
(69.4% female) were aged 68.3 ± 5.1 years at their first PET scans.
-
We aim to compare the biological staging of Alzheimer Disease using two different tau PET tracers.
-
41/100
CSF BD‐tau shows potential as a biomarker of treatment effect in AD but not bvFTD.
-
Our results elucidate the characteristics and genetic associations of p‐tau217 in a population‐based setting.
-
Plasma p-tau212 might have utility for theragnostics, monitoring therapy efficacy, and as a target engagement biomarker in clinical trials both in sporadic and DSAD.
From across this tag
8 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 8. The same 8 appear here every time.
- A phenotypic screen for novel small molecules that correct tau‐mediated pathologies in human frontotemporal dementia neurons
- Interface between tauopathies and synucleinopathies: a tale of two proteins
- Comparative In Vitro and In Vivo Quantifications of Pathologic Tau Deposits and Their Association with Neurodegeneration in Tauopathy Mouse Models
- Diagnostic performance of MK and Flortaucipir tau PET for the biological staging of Alzheimer disease
- Tau Antibody Targeting Pathological Species Blocks Neuronal Uptake and Interneuron Propagation of Tau in Vitro
- A human iPSC model of Tauopathies engineered for 4R Tau isoform expression endogenously develops late‐stage neuronal Tau pathology
- Retarded axonal transport of R406W mutant tau in transgenic mice with a neurodegenerative tauopathy
- Inhibition of phospholipase A2 in rat brain decreases the levels of total Tau protein