Relevant bibliographies by topics / P-tau181

Academic literature on the topic 'P-tau181'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "P-tau181"

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Xia, Chenyu, and Qiang Ma. "The Levels of Amyloid β-Protein and P181 in Peripheral Blood of Patients with Alzheimer’s Disease Combined with Helicobacter pylori Infection and Their Clinical Significance." Computational and Mathematical Methods in Medicine 2021 (December 20, 2021): 1–6. http://dx.doi.org/10.1155/2021/7135399.

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Objective. To analyze the levels of amyloid β-protein and P181 in peripheral blood of patients with Alzheimer’s disease combined with Helicobacter pylori infection and their clinical significance. Method. From January 2019 to June 2020, 59 patients were enrolled in this experiment including the AD group with 27 patients and the normal control group with 32 patients. The patients were divided into two groups: Alzheimer’s disease (AD) group ( n = 27 ) and control group ( n = 32 ), collecting the general data of patients, analyzing the diagnostic specificity and sensitivity of serum p-tau181 and Aβ42 and their influence on prognosis, and comparing the serum Aβ42 and p-tau181 concentrations for different HP infection degrees. Result. Single diagnostic sensitivity of Aβ42, p-tau181, and Aβ42 combined p-tau181 was 0.863, 0.854, and 0.972, respectively, and their specificity was 0.048, 0.206, and 0.305, respectively. Compared with the single diagnosis of serum Aβ42 and p-tau181, the combined diagnosis has higher sensitivity and specificity ( P < 0.05 ); age, years of education, serum Aβ42, and p-tau181 are factors affecting the prognosis of patients with Alzheimer’s disease combined with Helicobacter pylori infection; the concentration of Aβ42 in the control group was higher than that in the AD group, there was a statistical difference in the Aβ42 concentration between the two groups ( P < 0.05 ), and there was no statistical difference in the concentration of p-tau181 between the two groups ( P > 0.05 ); the HP positive infection rate of the AD group and the control group was 63.0% and 35.7%, respectively. The HP negative infection rate of the AD group and the control group was 37.0% and 64.3%, respectively. Compared with the control group, the positive rate of HP in the AD group was higher, and the difference was statistically significant ( P < 0.05 ); compared with HP-negative patients, HP-positive patients had a higher Aβ42 concentration, and the difference was statistically significant ( P < 0.05 ). The concentration of p-tau181 in the two groups was not statistically significant ( P > 0.05 ); Aβ42 gradually increases with increasing HP infection degree, and there are significant differences in serum Aβ42 levels between different degrees of infection. However, the level of serum p-tau181 does not change significantly with the increase of infection. Conclusion. There are significant alterations in the expression levels of Aβ42 and p-tau181 in peripheral blood of AD patients, and the levels of Aβ42 are related to HP infection; Aβ42 and p-tau181 are potential biomarkers for AD diagnosis and treatment.
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Benussi, Alberto, Thomas K. Karikari, Nicholas Ashton, Stefano Gazzina, Enrico Premi, Luisa Benussi, Roberta Ghidoni, et al. "Diagnostic and prognostic value of serum NfL and p-Tau181 in frontotemporal lobar degeneration." Journal of Neurology, Neurosurgery & Psychiatry 91, no. 9 (July 1, 2020): 960–67. http://dx.doi.org/10.1136/jnnp-2020-323487.

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ObjectiveTo assess the diagnostic and prognostic value of serum neurofilament light (NfL) and serum phospho-Tau181 (p-Tau181) in a large cohort of patients with frontotemporal lobar degeneration (FTLD).MethodsIn this retrospective study, performed on 417 participants, we analysed serum NfL and p-Tau181 concentrations with an ultrasensitive single molecule array (Simoa) approach. We assessed the diagnostic values of serum biomarkers in the differential diagnosis between FTLD, Alzheimer’s disease (AD) and healthy ageing; their role as markers of disease severity assessing the correlation with clinical variables, cross-sectional brain imaging and neurophysiological data; their role as prognostic markers, considering their ability to predict survival probability in FTLD.ResultsWe observed significantly higher levels of serum NfL in patients with FTLD syndromes, compared with healthy controls, and lower levels of p-Tau181 compared with patients with AD. Serum NfL concentrations showed a high accuracy in discriminating between FTLD and healthy controls (area under the curve (AUC): 0.86, p<0.001), while serum p-Tau181 showed high accuracy in differentiating FTLD from patients with AD (AUC: 0.93, p<0.001). In FTLD, serum NfL levels correlated with measures of cognitive function, disease severity and behavioural disturbances and were associated with frontotemporal atrophy and indirect measures of GABAergic deficit. Moreover, serum NfL concentrations were identified as the best predictors of survival probability.ConclusionsThe assessment of serum NfL and p-Tau181 may provide a comprehensive view of FTLD, aiding in the differential diagnosis, in staging disease severity and in defining survival probability.
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Salami, Alireza, Rolf Adolfsson, Micael Andersson, Kaj Blennow, Anders Lundquist, Annelie Nordin Adolfsson, Michael Schöll, Henrik Zetterberg, and Lars Nyberg. "Association of APOE ɛ4 and Plasma p-tau181 with Preclinical Alzheimer’s Disease and Longitudinal Change in Hippocampus Function." Journal of Alzheimer's Disease 85, no. 3 (February 1, 2022): 1309–20. http://dx.doi.org/10.3233/jad-210673.

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Background: The Apolipoprotein E (APOE) ɛ4 allele has been linked to increased tau phosphorylation and tangle formation. APOE ɛ4 carriers with elevated tau might be at the higher risk for Alzheimer’s disease (AD) progression. Previous studies showed that tau pathology begins early in areas of the medial temporal lobe. Similarly, APOE ɛ4 carriers showed altered hippocampal functional integrity. However, it remains unknown whether the influence of elevated tau accumulation on hippocampal functional changes would be more pronounced for APOE ɛ4 carriers. Objective: We related ɛ4 carriage to levels of plasma phosphorylated tau (p-tau181) up to 15 years prior to AD onset. Furthermore, elevated p-tau181 was explored in relation to longitudinal changes in hippocampal function and connectivity. Methods: Plasma p-tau181 was analyzed in 142 clinically defined AD cases and 126 matched controls. The longitudinal analysis involved 87 non-demented individuals (from population-based study) with two waves of plasma samples and three waves of functional magnetic resonance imaging during rest and memory encoding. Results: Increased p-tau181 was observed for both ɛ4 carriers and non-carriers close to AD onset, but exclusively for ɛ4 carriers in the early preclinical groups (7- and 13-years pre-AD). In ɛ4 carriers, longitudinal p-tau181 increase was paralleled by elevated local hippocampal connectivity at rest and subsequent reduction of hippocampus encoding-related activity. Conclusion: Our findings support an association of APOE ɛ4 and p-tau181 with preclinical AD and hippocampus functioning.
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Trelle, Alexandra N., Valerie A. Carr, Edward N. Wilson, Michelle S. Swarovski, Madison P. Hunt, Tyler N. Toueg, Tammy T. Tran, et al. "Association of CSF Biomarkers With Hippocampal-Dependent Memory in Preclinical Alzheimer Disease." Neurology 96, no. 10 (January 6, 2021): e1470-e1481. http://dx.doi.org/10.1212/wnl.0000000000011477.

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ObjectiveTo determine whether memory tasks with demonstrated sensitivity to hippocampal function can detect variance related to preclinical Alzheimer disease (AD) biomarkers, we examined associations between performance in 3 memory tasks and CSF β-amyloid (Aβ)42/Aβ40 and phosopho-tau181 (p-tau181) in cognitively unimpaired older adults (CU).MethodsCU enrolled in the Stanford Aging and Memory Study (n = 153; age 68.78 ± 5.81 years; 94 female) completed a lumbar puncture and memory assessments. CSF Aβ42, Aβ40, and p-tau181 were measured with the automated Lumipulse G system in a single-batch analysis. Episodic memory was assayed using a standardized delayed recall composite, paired associate (word–picture) cued recall, and a mnemonic discrimination task that involves discrimination between studied “target” objects, novel “foil” objects, and perceptually similar “lure” objects. Analyses examined cross-sectional relationships among memory performance, age, and CSF measures, controlling for sex and education.ResultsAge and lower Aβ42/Aβ40 were independently associated with elevated p-tau181. Age, Aβ42/Aβ40, and p-tau181 were each associated with (1) poorer associative memory and (2) diminished improvement in mnemonic discrimination performance across levels of decreased task difficulty (i.e., target–lure similarity). P-tau mediated the effect of Aβ42/Aβ40 on memory. Relationships between CSF proteins and delayed recall were similar but nonsignificant. CSF Aβ42 was not significantly associated with p-tau181 or memory.ConclusionsTests designed to tax hippocampal function are sensitive to subtle individual differences in memory among CU and correlate with early AD-associated biomarker changes in CSF. These tests may offer utility for identifying CU with preclinical AD pathology.
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Li, Ge, Cynthia L. Mayer, Daniel Morelli, Steven P. Millard, Wendy H. Raskind, Eric C. Petrie, Monique Cherrier, Anne M. Fagan, Murray A. Raskind, and Elaine R. Peskind. "Effect of simvastatin on CSF Alzheimer disease biomarkers in cognitively normal adults." Neurology 89, no. 12 (August 18, 2017): 1251–55. http://dx.doi.org/10.1212/wnl.0000000000004392.

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Objective:To examine potential disease-modifying effects of statin drugs, we conducted a 12-month randomized, placebo-controlled clinical trial of simvastatin in cognitively normal adults using change in CSF Alzheimer disease biomarkers as primary outcome measure.Methods:Participants were 45–64 years old and statin-naive with normal cognition and normal or mildly elevated cholesterol. Forty-six participants completed the 1-year study per protocol (25 in the simvastatin and 21 in the placebo group). Simvastatin was titrated to 40 mg/d. CSF Aβ42, total tau, and p-tau181 were measured at baseline and after 12 months of treatment using the INNO-BIA AlzBio3 assay. We used analysis of covariance to assess differences in biomarker change from baseline between treatment groups, adjusting for age, sex, and APOE ε4 status.Results:Changes from baseline did not differ significantly between treatment groups for any CSF biomarker, with p values of 0.53, 0.36, and 0.25 for CSF Aβ42, total tau, and p-tau181, respectively. There was no significant modifying effect of sex, APOE ε4, or baseline high-density lipoprotein or triglycerides on treatment group for any of the biomarkers (all p > 0.18). However, a significant interaction between treatment group and baseline low-density lipoprotein (LDL) was observed for p-tau181 (p = 0.003), where greater decreases from baseline in CSF p-tau181 concentrations were associated with higher baseline LDL level for the simvastatin group.Conclusions:Simvastatin-related reductions in CSF p-tau181 concentrations may be modulated by LDL cholesterol. The potential disease-modifying effects of simvastatin on CSF phospho-tau should be further investigated in persons with hypercholesterolemia.
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Maarouf, Chera L., Thomas G. Beach, Charles H. Adler, Michael Malek-Ahmadi, Tyler A. Kokjohn, Brittany N. Dugger, Douglas G. Walker, et al. "Quantitative Appraisal of Ventricular Cerebrospinal Fluid Biomarkers in Neuropathologically Diagnosed Parkinson's Disease Cases Lacking Alzheimer's Disease Pathology." Biomarker Insights 8 (January 2013): BMI.S11422. http://dx.doi.org/10.4137/bmi.s11422.

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Identifying biomarkers that distinguish Parkinson's disease (PD) from normal control (NC) individuals has the potential to increase diagnostic sensitivity for the detection of early-stage PD. A previous proteomic study identified potential biomarkers in postmortem ventricular cerebrospinal fluid (V-CSF) from neuropathologically diagnosed PD subjects lacking Alzheimer's disease (AD) neuropathology. In the present study, we assessed these biomarkers as well as p-tau181, Aβ42, and S100B by ELISA in PD (n = 43) and NC (n = 49) cases. The p-tau181/Aβ42 ratio and ApoA-1 showed statistically significant differences between groups. Multiple regression analysis demonstrated that p-tau181/Aβ42 had a significant odds ratio: OR = 1.42 (95% confidence interval [CI], 1.12–1.84), P = 0.006. Among the molecules investigated, intriguing correlations were observed that require further investigation. Our results suggest coexistent AD CSF biomarkers within the PD group notwithstanding that it was selected to minimize AD neuropathological lesions.
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Arcaro, Marina, Chiara Fenoglio, Maria Serpente, Andrea Arighi, Giorgio G. Fumagalli, Luca Sacchi, Stefano Floro, et al. "A Novel Automated Chemiluminescence Method for Detecting Cerebrospinal Fluid Amyloid-Beta 1-42 and 1-40, Total Tau and Phosphorylated-Tau: Implications for Improving Diagnostic Performance in Alzheimer’s Disease." Biomedicines 10, no. 10 (October 21, 2022): 2667. http://dx.doi.org/10.3390/biomedicines10102667.

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Recently, a fully automated instrument for the detection of the Cerebrospinal Fluid (CSF) biomarker for Alzheimer’s disease (AD) (low concentration of Amyloid-beta 42 (Aβ42), high concentration of total tau (T-tau) and Phosphorylated-tau (P-tau181)), has been implemented, namely CLEIA. We conducted a comparative analysis between ELISA and CLEIA methods in order to evaluate the analytical precision and the diagnostic performance of the novel CLEIA system on 111 CSF samples. Results confirmed a robust correlation between ELISA and CLEIA methods, with an improvement of the accuracy with the new CLEIA methodology in the detection of the single biomarkers and in their ratio values. For Aβ42 regression analysis with Passing–Bablok showed a Pearson correlation coefficient r = 0.867 (0.8120; 0.907% 95% CI p < 0.0001), T-tau analysis: r = 0.968 (0.954; 0.978% 95% CI p < 0.0001) and P-tau181: r = 0.946 (0.922; 0.962 5% 95% CI p < 0.0001). The overall ROC AUC comparison between ROC in ELISA and ROC in CLEIA confirmed a more accurate ROC AUC with the new automatic method: T-tau AUC ELISA = 0.94 (95% CI 0.89; 0.99 p < 0.0001) vs. AUC CLEIA = 0.95 (95% CI 0.89; 1.00 p < 0.0001), and P-tau181 AUC ELISA = 0.91 (95% CI 0.85; 0.98 p < 0.0001) vs. AUC CLEIA = 0.98 (95% CI 0.95; 1.00 p < 0.0001). The performance of the new CLEIA method in automation is comparable and, for tau and P-tau181, even better, as compared with standard ELISA. Hopefully, in the future, automation could be useful in clinical diagnosis and also in the context of clinical studies.
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Ewers, Michael, Nicolai Franzmeier, Marc Suárez-Calvet, Estrella Morenas-Rodriguez, Miguel Angel Araque Caballero, Gernot Kleinberger, Laura Piccio, et al. "Increased soluble TREM2 in cerebrospinal fluid is associated with reduced cognitive and clinical decline in Alzheimer’s disease." Science Translational Medicine 11, no. 507 (August 28, 2019): eaav6221. http://dx.doi.org/10.1126/scitranslmed.aav6221.

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Loss of function of TREM2, a key receptor selectively expressed by microglia in the brain, contributes to the development of Alzheimer’s disease (AD). We therefore examined whether soluble TREM2 (sTREM2) concentrations in cerebrospinal fluid (CSF) were associated with reduced rates of cognitive decline and clinical progression in subjects with AD or mild cognitive impairment (MCI). We measured sTREM2 in CSF samples from 385 elderly subjects, including cognitively normal controls, individuals with MCI, and subjects with AD dementia (follow-up period: mean, 4 years; range 1.5 to 11.5 years). In subjects with AD defined by evidence of CSF Aβ1–42 (amyloid β-peptide 1 to 42; A+) and CSF p-tau181 (tau phosphorylated on amino acid residue 181; T+), higher sTREM2 concentrations in CSF at baseline were associated with attenuated decline in memory and cognition. When analyzed in clinical subgroups, an association between higher CSF sTREM2 concentrations and subsequent reduced memory decline was consistently observed in individuals with MCI or AD dementia, who were positive for CSF Aβ1–42 and CSF p-tau181 (A+T+). Regarding clinical progression, a higher ratio of CSF sTREM2 to CSF p-tau181 concentrations predicted slower conversion from cognitively normal to symptomatic stages or from MCI to AD dementia in the subjects who were positive for CSF Aβ1–42 and CSF p-tau181. These results suggest that sTREM2 is associated with attenuated cognitive and clinical decline, a finding with important implications for future clinical trials targeting the innate immune response in AD.
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Santangelo, Roberto, Alessandro Dell'Edera, Arianna Sala, Giordano Cecchetti, Federico Masserini, Francesca Caso, Patrizia Pinto, et al. "The CSF p-tau181/Aβ42 Ratio Offers a Good Accuracy “In Vivo” in the Differential Diagnosis of Alzheimer’s Dementia." Current Alzheimer Research 16, no. 7 (September 4, 2019): 587–95. http://dx.doi.org/10.2174/1567205016666190725150836.

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Background: The incoming disease-modifying therapies against Alzheimer’s disease (AD) require reliable diagnostic markers to correctly enroll patients all over the world. CSF AD biomarkers, namely amyloid-β 42 (Aβ42), total tau (t-tau), and tau phosphorylated at threonine 181 (p-tau181), showed good diagnostic accuracy in detecting AD pathology, but their real usefulness in daily clinical practice is still a matter of debate. Therefore, further validation in complex clinical settings, that is patients with different types of dementia, is needed to uphold their future worldwide adoption. Methods: We measured CSF AD biomarkers’ concentrations in a sample of 526 patients with a clinical diagnosis of dementia (277 with AD and 249 with Other Type of Dementia, OTD). Brain FDG-PET was also considered in a subsample of 54 patients with a mismatch between the clinical diagnosis and the CSF findings. Results: A p-tau181/Aβ42 ratio higher than 0.13 showed the best diagnostic performance in differentiating AD from OTD (86% accuracy index, 74% sensitivity, 81% specificity). In cases with a mismatch between clinical diagnosis and CSF findings, brain FDG-PET partially agreed with the p-tau181/Aβ42 ratio, thus determining an increase in CSF accuracy. Conclusions: The p-tau181/Aβ42 ratio alone might reliably detect AD pathology in heterogeneous samples of patients suffering from different types of dementia. It might constitute a simple, cost-effective and reproducible in vivo proxy of AD suitable to be adopted worldwide not only in daily clinical practice but also in future experimental trials, to avoid the enrolment of misdiagnosed AD patients.
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Meyer, Pierre‐François, Nicholas J. Ashton, Thomas K. Karikari, Cherie Strikwerda‐Brown, Theresa Köbe, Julie Gonneaud, Alexa Pichet Binette, et al. "Plasma p‐tau231, p‐tau181, PET Biomarkers, and Cognitive Change in Older Adults." Annals of Neurology 91, no. 4 (February 18, 2022): 548–60. http://dx.doi.org/10.1002/ana.26308.

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Conference papers on the topic "P-tau181"

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Souza, João Pedro Ferrari, Wagner Brum, Lucas Hauschild, Lucas Da Ros, Pâmela Lukasewicz Ferreira, Bruna Bellaver, Douglas Leffa, et al. "ASSOCIATION OF VASCULAR RISK AND ALZHEIMER’S DISEASE PATHOLOGY WITH NEURODEGENERATION AND COGNITIVE DECLINE." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda024.

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Background: It is not fully understood how vascular risk factors (VRFs) are associated with Alzheimer’s disease (AD) pathology to promote neurodegeneration and cognitive decline. Objective: Investigate whether VRF burden synergistically interacts with AD pathology to accelerate neurodegeneration and cognitive decline in cognitively unimpaired (CU) individuals. Methods: We assessed 503 CU participants from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database. Individuals were dichotomized as having an elevated VRF burden if ≥ 2 VRFs (V+) and as presenting biological AD if CSF p-tau181 ≥ 24 pg/mL and CSF Aβ1-42 ≤ 976.6 pg/mL [(AT)+]. Neurodegeneration was assessed with plasma neurofilament light (NfL) and cognition with the modified version of the Preclinical Alzheimer’s Cognitive Composite. Results: Linear mixed-effects models demonstrated that an elevated VRF burden interacted with AD pathology to promote higher rates of neurodegeneration (β=5.68, p=.005) and cognitive decline (β=- 0.43, p=.019). Survival analysis demonstrated that only (AT)+V+ individuals had a significantly greater risk of clinical progression to cognitive impairment (adjusted Hazard Ratio=3.5, p <.001). Conclusion: Our results suggest that VRF burden and AD pathology synergistically lead to neurodegeneration and cognitive decline, favoring the onset of cognitive impairment. These findings support that the clinical evaluation of VRF burden might improve the clinical assessment especially of subjects at higher risk for developing cognitive impairment.
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Reports on the topic "P-tau181"

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Ma, Yunxing, Julia Brettschneider, and Joanna Collingwood. A systematic review and meta-analysis of cerebrospinal fluid amyloid and tau levels in patients progressing from Mild Cognitive Impairment to Alzheimer’s Disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0020.

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Review question / Objective: Reported levels of amyloid-beta and tau in human cerebrospinal fluid (CSF) are evaluated to discover if these biochemical markers can predict the transition from Mild Cognitive Impairment (MCI) to Alzheimer’s disease (AD). A systematic review and quantitative meta-analyses are performed to test relationships between three potential biomarkers in CSF (Aβ(1-42), T-tau, and P-tau181) and the evolution of AD in longitudinal evaluations of levels relative to baseline, using prior-published experimental data. The primary focus of the analysis is on the period describing the transition of a patient from MCI to AD, where it is critical to discover the main biomarker characteristics that differentiate patient outcomes for those who have a stable form of MCI, and those who progress to a confirmed diagnosis of AD. A secondary purpose of the review was to examine the status of iron in CSF as a function of disease status.
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