ReviewActa neuropathologica2025
Multifactorial etiology of progressive supranuclear palsy (PSP): the genetic component.
Review in Acta neuropathologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
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Who cites it
5 citing papers in PubMed.
- Data-driven modelling of tau pathology reveals distinct progressive supranuclear palsy subtypes.Brain : a journal of neurology · 2026Article
- From clinical phenotypes to molecular precision: multimodal biomarkers for progressive supranuclear palsy.Frontiers in neuroscience · 2026Review
- Risk genes in progressive supranuclear palsy (PSP) affect integrity and function of microtubules.Frontiers in aging · 2026Review
- Increased tau-induced inflammatory responses are associated with a greater degree of atherosclerosis in progressive supranuclear palsy.Frontiers in aging neuroscience · 2025Article
- Characterisation of the function of a lncRNA containing SINE-VNTR-Alu 67 to regulate the genes at theExperimental biology and medicine (Maywood, N.J.) · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive supranuclear palsy (PSP) is mainly a sporadic disease. It has a multifactorial etiology and an interaction between environmental and genetic factors causes disease. While elucidation of environmental risks for PSP is still in its infancy, much has been learned about the genetic etiological component of PSP during the past few years. This article reviews genes that convey risk for PSP. All genes have been identified in association studies. Only those genes with the standard threshold for genome-wide significance of P < 5E-8 are covered. These genes include MAPT, KANSL1, PLEKHM1, STX6, MOBP, EIF2AK3, SLC01 A2, DUSP10, APOE, RUNX2, TRIM11, NFASC/CNTN2 and LRRK2. The physiologic function of these genes is described and their potential role in the etiology of PSP is discussed.
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Registered trials
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