Trial reportNeurology2018
In vivo
Trial report in Neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 71 citations in OpenAlex.
- Investigating AD and non-AD [European journal of nuclear medicine and molecular imaging · 2026Article
- Tau pathology in epilepsy: emerging mechanisms and translational opportunities.Brain : a journal of neurology · 2026Review
- Distinct tau filament folds in human MAPT mutants P301L and P301T.Nature structural & molecular biology · 2025Article
- Tau filaments with the Alzheimer fold in human MAPT mutants V337M and R406W.Nature structural & molecular biology · 2025Article
- Plasma MTBR-tau243 biomarker identifies tau tangle pathology in Alzheimer's disease.Nature medicine · 2025Article
- Behavioral variant frontotemporal dementia (bvFTD): PET biomarker characterization of metabolism (18F-FDG), amyloid (11C-PIB) and tau (18F-AV1451) and its clinical correlate - analysis of a cohort from Argentina.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Tau degradation in Alzheimer's disease: Mechanisms and therapeutic opportunities.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Tau filaments with the Alzheimer fold in cases withbioRxiv : the preprint server for biology · 2024Article
- Synthesizing images of tau pathology from cross-modal neuroimaging using deep learning.Brain : a journal of neurology · 2024Article
- The MAPT p.E342K and p.R406W mutations are associated with progressive supranuclear palsy with atypical features.Parkinsonism & related disorders · 2024Article
- A review of the flortaucipir literature for positron emission tomography imaging of tau neurofibrillary tangles.Brain communications · 2024Review
- Assessing network degeneration and phenotypic heterogeneity in genetic frontotemporal lobar degeneration by decoding FDG-PET.NeuroImage. Clinical · 2024Article
- Leveraging Technology to Diagnose Alzheimer's Disease: A Systematic Review and Meta-Analysis.Healthcare (Basel, Switzerland) · 2023Review
- CSF MTBR-tau243 is a specific biomarker of tau tangle pathology in Alzheimer's disease.Nature medicine · 2023Article
- Frontotemporal Dementia, Where Do We Stand? A Narrative Review.International journal of molecular sciences · 2023Review
- Imaging of Tauopathies with PET Ligands: State of the Art and Future Outlook.Diagnostics (Basel, Switzerland) · 2023Review
- Patients carrying the mutation p.R406W in MAPT present with non-conforming phenotypic spectrum.Brain : a journal of neurology · 2023Article
- Brain PET Imaging: Frontotemporal Dementia.PET clinics · 2023Review
- Isoform-specific patterns of tau burden and neuronal degeneration in MAPT-associated frontotemporal lobar degeneration.Acta neuropathologica · 2022Article
- Optimum Differentiation of Frontotemporal Lobar Degeneration from Alzheimer Disease Achieved with Cross-Sectional Tau Positron Emission Tomography.Annals of neurology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo evaluate
methodsUsing a case-control study, we quantitatively and qualitatively compared tau PET scans in 10 symptomatic and 3 asymptomatic MAPT mutation carriers (n = 13, age range 42-67 years) with clinically normal (CN) participants (n = 241, age range 42-67 years) and an Alzheimer disease (AD) dementia cohort (n = 30, age range 52-67 years). Eight participants had
resultsTau PET signal was qualitatively and quantitatively different between participants with AD, CN participants, and
conclusionsTau PET shows higher magnitude of binding in
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.