ArticleAnnals of neurology2018
Variation at the TRIM11 locus modifies progressive supranuclear palsy phenotype.
Article in Annals of neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 49 citations in OpenAlex.
- Single-cell, spatial, and machine learning analyses identify ANKIB1 as an oligodendrocyte-anchored palmitoylation-associated candidate biomarker of Alzheimer's disease.Translational psychiatry · 2026Article
- Data-driven modelling of tau pathology reveals distinct progressive supranuclear palsy subtypes.Brain : a journal of neurology · 2026Article
- Dual targeting of the UPS and autophagy as a novel therapy for neurodegenerative proteinopathies.Frontiers in cellular neuroscience · 2026Review
- Identification of common variants influencing risk of the three-repeat tauopathy Pick's disease: a genome wide association study.medRxiv : the preprint server for health sciences · 2025Article
- Ubiquitination in the Nervous System: From Molecular Mechanisms to Disease Implications.Molecular neurobiology · 2025Review
- Multifactorial etiology of progressive supranuclear palsy (PSP): the genetic component.Acta neuropathologica · 2025Review
- A No-Brainer! The Therapeutic Potential of TRIM Proteins in Viral and Central Nervous System Diseases.Viruses · 2025Review
- Whole-genome sequencing analysis reveals new susceptibility loci and structural variants associated with progressive supranuclear palsy.Molecular neurodegeneration · 2024Article
- Whole-Genome Sequencing Analysis Reveals New Susceptibility Loci and Structural Variants Associated with Progressive Supranuclear Palsy.medRxiv : the preprint server for health sciences · 2024Article
- Tripartite Motif Protein Family in Central Nervous System Diseases.Cellular and molecular neurobiology · 2023Review
- TRIM11 protects against tauopathies and is down-regulated in Alzheimer's disease.Science (New York, N.Y.) · 2023Article
- Uncovering spatiotemporal patterns of atrophy in progressive supranuclear palsy using unsupervised machine learning.Brain communications · 2023Article
- It's a TRIM-endous view from the top: the varied roles of TRIpartite Motif proteins in brain development and disease.Frontiers in molecular neuroscience · 2023Review
- Protracted course progressive supranuclear palsy.European journal of neurology · 2022Article
- TRIM family proteins: roles in proteostasis and neurodegenerative diseases.Open biology · 2022Review
- Brain region-specific effects of nearly fixed sapiens-derived alleles.BMC genomic data · 2022Article
- Genetic and Epigenetic Constructs of Progressive Supranuclear Palsy.Annals of neurosciences · 2022Review
- Evolving concepts in progressive supranuclear palsy and other 4-repeat tauopathies.Nature reviews. Neurology · 2021Review
- Ondine's Curse in Frontotemporal Dementia with Parkinsonism Linked to Chromosome 17 Caused byMovement disorders clinical practice · 2021Article
- Tau-targeting antibody therapies: too late, wrong epitope or wrong target?Nature medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
23 authors at 11 institutions in 4 countries.
Funding
Abstract
objectiveThe basis for clinical variation related to underlying progressive supranuclear palsy (PSP) pathology is unknown. We performed a genome-wide association study (GWAS) to identify genetic determinants of PSP phenotype.
methodsTwo independent pathological and clinically diagnosed PSP cohorts were genotyped and phenotyped to create Richardson syndrome (RS) and non-RS groups. We carried out separate logistic regression GWASs to compare RS and non-RS groups and then combined datasets to carry out a whole cohort analysis (RS = 367, non-RS = 130). We validated our findings in a third cohort by referring to data from 100 deeply phenotyped cases from a recent GWAS. We assessed the expression/coexpression patterns of our identified genes and used our data to carry out gene-based association testing.
resultsOur lead single nucleotide polymorphism (SNP), rs564309, showed an association signal in both cohorts, reaching genome-wide significance in our whole cohort analysis (odds ratio = 5.5, 95% confidence interval = 3.2-10.0, p = 1.7 × 10
interpretationOur study suggests that the TRIM11 locus is a genetic modifier of PSP phenotype and potentially adds further evidence for the UPS having a key role in tau pathology, therefore representing a target for disease-modifying therapies. Ann Neurol 2018;84:485-496.
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.