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Tau Positron sentence examples within diffusion magnetic resonance

diffusion magnetic resonance

Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo.

Tau Deposition and Structural Connectivity Demonstrate Differential Association Patterns with Neurocognitive Tests

diffusion magnetic resonance

Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo.

Tau deposition and structural connectivity demonstrate differential association patterns with neurocognitive tests.

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Tau Positron sentence examples within magnetic resonance imaging

magnetic resonance imaging

We hypothesize that AD dementia can be categorized into subtypes based on multimodal imaging biomarkers such as magnetic resonance imaging (MRI), tau positron emission tomography (PET), and amyloid PET.

Topographical Heterogeneity of Alzheimer’s Disease Based on MR Imaging, Tau PET, and Amyloid PET

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Tau Positron sentence examples within tau positron emission

tau positron emission

Purpose Off-target binding in the skull and meninges is observed in some subjects undergoing tau positron emission tomography (PET) and could potentially differ between men and women.

Sex differences in off-target binding using tau positron emission tomography

tau positron emission

The purpose of this study was to correlate quantification of autoradiography signal using the novel next-generation tau positron emission tomography (PET) radiotracer [18F]PI-2620 with immunohistochemically determined tau-protein load in both formalin-fixed paraffin-embedded (FFPE) and frozen tissue samples of patients with Alzheimer's disease (AD) and Progressive Supranuclear Palsy (PSP).

Superiority of Formalin-Fixed Paraffin-Embedded Brain Tissue for in vitro Assessment of Progressive Supranuclear Palsy Tau Pathology With [18F]PI-2620

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10.1186/s13195-021-00776-w

Background β-amyloid (Aβ) and tau positron emission tomography (PET) detect the pathological changes that define Alzheimer’s disease (AD) in living people.

Detecting Alzheimer’s disease biomarkers with a brief tablet-based cognitive battery: sensitivity to Aβ and tau PET

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10.1002/dad2.12202

Amyloid and tau positron emission tomography (PET) scans were added at visit 2.

The Health & Aging Brain among Latino Elders (HABLE) study methods and participant characteristics

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10.1007/s12149-020-01566-4

Tau positron emission tomography (PET) might offer novel insights and be of great assistance in monitoring disease progression and supporting the differential diagnosis.

Radioactive synthesis of tau PET imaging agent 18F-AV-1451 and its role in monitoring the progression of Alzheimer’s disease and supporting differential diagnosis

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10.1001/jamaneurol.2021.1858

Importance Tau positron emission tomography (PET) tracers have proven useful for the differential diagnosis of dementia, but their utility for predicting cognitive change is unclear.

Accuracy of Tau Positron Emission Tomography as a Prognostic Marker in Preclinical and Prodromal Alzheimer Disease: A Head-to-Head Comparison Against Amyloid Positron Emission Tomography and Magnetic Resonance Imaging.

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10.1093/braincomms/fcab136

Recent ultrasensitive methods to measure plasma phosphorylated tau 181 (p-tau181) display strong correlations with tau positron emission tomography, p-tau181 in CSF, and tau pathology at autopsy.

Association of plasma P-tau181 with memory decline in non-demented adults

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10.1186/s13195-021-00876-7

Associations between tau positron emission tomography (PET) values and global and regional network measures were examined using linear regression models adjusted for age, sex, and total intracranial volume.

Tau-related grey matter network breakdown across the Alzheimer’s disease continuum

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10.1001/jamaneurol.2021.2293

Objective To conduct a head-to-head comparison of plasma p-tau181 and p-tau231 measured on the single-molecule array (Simoa) platform and p-tau181 and p-tau217 measured on the Meso Scale Discovery (MSD) platform on amyloid and tau positron emission tomography (PET) measures, neurodegeneration, vascular pathology, and cognitive outcomes.

Comparison of Plasma Phosphorylated Tau Species With Amyloid and Tau Positron Emission Tomography, Neurodegeneration, Vascular Pathology, and Cognitive Outcomes.

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10.1186/s13024-021-00430-x

We discuss how the new blood tests may be used in research and clinical practice, and what role they may play in relation to more established diagnostic tests, such as CSF biomarkers and amyloid and tau positron emission tomography, to facilitate the effective implementation of future disease-modifying therapies.

Moving fluid biomarkers for Alzheimer’s disease from research tools to routine clinical diagnostics

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10.1016/j.biopsych.2020.01.023

METHODS A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes.

Amyloid and Tau Pathology Associations With Personality Traits, Neuropsychiatric Symptoms, and Cognitive Lifestyle in the Preclinical Phases of Sporadic and Autosomal Dominant Alzheimer’s Disease

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10.1093/infdis/jiy663

Regional standardized uptake value ratios (SUVRs) for tau positron emission tomography (PET) were compared among 19 cognitively normal human immunodeficiency virus (HIV)-negative control individuals, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive individuals, and 17 cognitively impaired HIV-positive individuals.

Tau Positron Emission Tomography Binding Is Not Elevated in HIV-Infected Individuals.

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10.1001/jamaneurol.2019.4284

Amyloid and tau positron emission tomography scans were obtained in a subset of patients.

Association of Cognitive and Behavioral Features Between Adults With Tuberous Sclerosis and Frontotemporal Dementia.

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10.3760/CMA.J.ISSN.1673-4378.2019.04.024

We reviewed research advances on a variety of post-translational modifications of Tau, propagation mechanisms of Tau protein, neurological protection strategies targeting at Tau protein and Tau positron emission computed tomography (PET) imaging technology.

Advances in research of Tau protein leading to cognitive dysfunction

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10.3389/fnagi.2019.00208

In this study, 225 subjects with PHF-Tau Positron Emission Tomography (PET) images were divided into four groups based on whether they carried Apolipoprotein E ε4 (APOE 4) or abnormal cerebrospinal fluid Total-Tau (CSF T-Tau).

The Influence of Cerebrospinal Fluid Abnormalities and APOE 4 on PHF-Tau Protein: Evidence From Voxel Analysis and Graph Theory

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10.20944/preprints201909.0270.v1

The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD.

Reasons for Failed Trials of Disease-Modifying Treatments for Alzheimer Disease and Their Contribution in Recent Research

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10.1016/j.nicl.2019.102091

Background [18F]THK5351 is a tau positron emission tomography tracer that has shown promise in quantifying tau distribution in tauopathies such as Alzheimer's disease (AD) and progressive supranuclear palsy (PSP).

Rasagiline, a monoamine oxidase B inhibitor, reduces in vivo [18F]THK5351 uptake in progressive supranuclear palsy

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10.3390/biomedicines7040097

The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD.

Reasons for Failed Trials of Disease-Modifying Treatments for Alzheimer Disease and Their Contribution in Recent Research

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Tau Positron
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What is/are Tau Positron?

Tau Positron - Background β-amyloid (Aβ) and tau positron emission tomography (PET) detect the pathological changes that define Alzheimer’s disease (AD) in living people. [1] Amyloid and tau positron emission tomography (PET) scans were added at visit 2. [2] Tau positron emission tomography (PET) might offer novel insights and be of great assistance in monitoring disease progression and supporting the differential diagnosis. [3] Importance Tau positron emission tomography (PET) tracers have proven useful for the differential diagnosis of dementia, but their utility for predicting cognitive change is unclear. [4] Recent ultrasensitive methods to measure plasma phosphorylated tau 181 (p-tau181) display strong correlations with tau positron emission tomography, p-tau181 in CSF, and tau pathology at autopsy. [5] Associations between tau positron emission tomography (PET) values and global and regional network measures were examined using linear regression models adjusted for age, sex, and total intracranial volume. [6] Objective To conduct a head-to-head comparison of plasma p-tau181 and p-tau231 measured on the single-molecule array (Simoa) platform and p-tau181 and p-tau217 measured on the Meso Scale Discovery (MSD) platform on amyloid and tau positron emission tomography (PET) measures, neurodegeneration, vascular pathology, and cognitive outcomes. [7] We discuss how the new blood tests may be used in research and clinical practice, and what role they may play in relation to more established diagnostic tests, such as CSF biomarkers and amyloid and tau positron emission tomography, to facilitate the effective implementation of future disease-modifying therapies. [8] METHODS A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. [9] Regional standardized uptake value ratios (SUVRs) for tau positron emission tomography (PET) were compared among 19 cognitively normal human immunodeficiency virus (HIV)-negative control individuals, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive individuals, and 17 cognitively impaired HIV-positive individuals. [10] Amyloid and tau positron emission tomography scans were obtained in a subset of patients. [11] We reviewed research advances on a variety of post-translational modifications of Tau, propagation mechanisms of Tau protein, neurological protection strategies targeting at Tau protein and Tau positron emission computed tomography (PET) imaging technology. [12] In this study, 225 subjects with PHF-Tau Positron Emission Tomography (PET) images were divided into four groups based on whether they carried Apolipoprotein E ε4 (APOE 4) or abnormal cerebrospinal fluid Total-Tau (CSF T-Tau). [13] The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD. [14] Background [18F]THK5351 is a tau positron emission tomography tracer that has shown promise in quantifying tau distribution in tauopathies such as Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). [15] The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD. [16]

diffusion magnetic resonance

Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo. [1] Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo. [2] Recent advances in diffusion magnetic resonance imaging and the availability of tau positron emission tomography (PET) have made it possible to evaluate the association of tau and WM degeneration (tau-WM) in vivo. [3]

magnetic resonance imaging

We hypothesize that AD dementia can be categorized into subtypes based on multimodal imaging biomarkers such as magnetic resonance imaging (MRI), tau positron emission tomography (PET), and amyloid PET. [1]

tau positron emission

Purpose Off-target binding in the skull and meninges is observed in some subjects undergoing tau positron emission tomography (PET) and could potentially differ between men and women. [1] The purpose of this study was to correlate quantification of autoradiography signal using the novel next-generation tau positron emission tomography (PET) radiotracer [18F]PI-2620 with immunohistochemically determined tau-protein load in both formalin-fixed paraffin-embedded (FFPE) and frozen tissue samples of patients with Alzheimer's disease (AD) and Progressive Supranuclear Palsy (PSP). [2] Dear Editor, [F]PM-pyridinyl-butadienyl-benzothiazole 3 (PBB3), a propanol variant of the first tau positron emission tomography (PET) tracer, [C]PBB3, is reportedly a reliable tool for detecting tau fibrils in non-Alzheimer’s disease (AD) tauopathies [1]. [3] Background β-amyloid (Aβ) and tau positron emission tomography (PET) detect the pathological changes that define Alzheimer’s disease (AD) in living people. [4] Amyloid and tau positron emission tomography (PET) scans were added at visit 2. [5] Tau positron emission tomography (PET) might offer novel insights and be of great assistance in monitoring disease progression and supporting the differential diagnosis. [6] Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo. [7] Several tau positron emission tomography (PET) tracers have been developed and studied in Alzheimer’s disease (AD), but there is still a lack of 4R-tau specific tracers for non-AD tauopathies. [8] Background Tau positron emission tomography (PET) imaging can reveal the pathophysiology and neurodegeneration that occurs in Alzheimer’s disease (AD) in vivo. [9] METHODS Participants included 201 adults (mean age 53±8 years) who underwent 11C-Pittsburgh Compound B amyloid and 18F-Flortaucipir tau positron emission tomography (PET) imaging. [10] Recent advances in tau positron emission tomography tracers and diffusion magnetic resonance imaging allow the visualization of tau pathology and white-matter connectivity of the brain in vivo. [11] Importance Tau positron emission tomography (PET) tracers have proven useful for the differential diagnosis of dementia, but their utility for predicting cognitive change is unclear. [12] Recent ultrasensitive methods to measure plasma phosphorylated tau 181 (p-tau181) display strong correlations with tau positron emission tomography, p-tau181 in CSF, and tau pathology at autopsy. [13] Associations between tau positron emission tomography (PET) values and global and regional network measures were examined using linear regression models adjusted for age, sex, and total intracranial volume. [14] Objective To conduct a head-to-head comparison of plasma p-tau181 and p-tau231 measured on the single-molecule array (Simoa) platform and p-tau181 and p-tau217 measured on the Meso Scale Discovery (MSD) platform on amyloid and tau positron emission tomography (PET) measures, neurodegeneration, vascular pathology, and cognitive outcomes. [15] This study aims to determine whether comparable target regions of interest (ROIs) and cut-offs can be used across [18F]flortaucipir, [18F]RO948, and [18F]MK6240 tau positron emission tomography (PET) tracers for differential diagnosis of Alzheimer’s disease (AD) dementia vs either cognitively unimpaired (CU) individuals or non-AD neurodegenerative diseases. [16] Recent advances in diffusion magnetic resonance imaging and the availability of tau positron emission tomography (PET) have made it possible to evaluate the association of tau and WM degeneration (tau-WM) in vivo. [17] We discuss how the new blood tests may be used in research and clinical practice, and what role they may play in relation to more established diagnostic tests, such as CSF biomarkers and amyloid and tau positron emission tomography, to facilitate the effective implementation of future disease-modifying therapies. [18] For each subject, we infer three personalized parameters, the tau misfolding rate, the tau transport coefficient, and the tau-induced atrophy rate from four consecutive annual tau positron emission tomography scans and structural magnetic resonance images. [19] METHODS A total of 115 older adults with a parental or multiple-sibling family history of sporadic AD (PREVENT-AD [PRe-symptomatic EValuation of Experimental or Novel Treatments for AD] cohort) underwent amyloid and tau positron emission tomography and answered several questionnaires related to behavioral attributes. [20] [F-18]-MK-6240, a novel tau positron emission tomography (PET) tracer recently discovered for the in vivo detection of neurofibrillary tangles, has the potential to improve diagnostic accuracy in the detection of Alzheimer disease. [21] We hypothesize that AD dementia can be categorized into subtypes based on multimodal imaging biomarkers such as magnetic resonance imaging (MRI), tau positron emission tomography (PET), and amyloid PET. [22] O5-01-01 HEAD-TO-HEAD IN VIVO COMPARISON OF TAU POSITRON EMISSION TOMOGRAPHY LIGANDS FFLORTAUCIPIR AND F-RO948 Ruben Smith, Michael Sch€oll, Tomas Ohlsson, Jonas J€ogi, Olof Strandberg, Oskar Hansson, Clinical Memory ResearchUnit, Lund University, Malm€o, Sweden; Sk ane University Hospital, Lund, Sweden; Lund University, Malm€o, Sweden; Wallenberg Centre for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden; University College London, London, United Kingdom; Memory Clinic, Sk ane University Hospital, Lund, Sweden; ClinicalMemory ResearchUnit, Department of Clinical Sciences, Malm€o, Lund University, Lund, Sweden. [23] Regional standardized uptake value ratios (SUVRs) for tau positron emission tomography (PET) were compared among 19 cognitively normal human immunodeficiency virus (HIV)-negative control individuals, 20 HIV-negative patients with symptomatic Alzheimer disease, 15 cognitively normal HIV-positive individuals, and 17 cognitively impaired HIV-positive individuals. [24] BackgroundThe tau positron emission tomography (PET) ligand 18F-flortaucipir binds to paired helical filaments of tau in aging and Alzheimer’s disease (AD), but its utility in detecting tau aggregates in frontotemporal dementia (FTD) is uncertain. [25] Amyloid and tau positron emission tomography scans were obtained in a subset of patients. [26] METHOD Using 18F-AV-1451 tau positron emission tomography (PET), voxel-wise two-sample t-tests were performed between AD patients with obvious visuospatial dysfunction (VS-AD) and cognitively normal subjects, AD patients with little-to-no visuospatial dysfunction (non VS-AD) and cognitively normal subjects, respectively. [27] We reviewed research advances on a variety of post-translational modifications of Tau, propagation mechanisms of Tau protein, neurological protection strategies targeting at Tau protein and Tau positron emission computed tomography (PET) imaging technology. [28] Meaning Amyloid positron emission tomography is useful to detect early Alzheimer pathology; repeated tau positron emission tomography is useful to track disease progression. [29] The first cohort (TRIAD) comprised cognitively normal elderly participants (n = 124), participants with MCI (n = 50), and participants with Alzheimer disease (n = 50) who underwent tau positron emission tomography (PET) with fluorine 18-labeled MK6240 and amyloid-β PET with [18F]AZD4694. [30] In this study, 225 subjects with PHF-Tau Positron Emission Tomography (PET) images were divided into four groups based on whether they carried Apolipoprotein E ε4 (APOE 4) or abnormal cerebrospinal fluid Total-Tau (CSF T-Tau). [31] The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD. [32] Background [18F]THK5351 is a tau positron emission tomography tracer that has shown promise in quantifying tau distribution in tauopathies such as Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). [33] 1 Tau positron emission tomography (PET) may enhance in vivo diagnosis and testing of tau-based therapies in FTD, however, few tau ligands have been validated in FTD. [34] The application of amyloid, tau, and neurodegeneration biomarkers, including new biomarkers—such as Tau positron emission tomography, neurofilament light chain (blood and Cerebrospinal fluid (CSF) biomarker of axonal degeneration) and neurogranin (CSF biomarker of synaptic functioning)—to clinical trials allows more precise staging of AD. [35]