ReviewCells2023
HnRNP Pathologies in Frontotemporal Lobar Degeneration.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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
8 citing papers in PubMed, 7 citations in OpenAlex.
- Widespread hnRNP K Mislocalisation Suggests Differential Neuronal Vulnerability in the Neurodegenerative and Ageing Human Brain.Neuropathology and applied neurobiology · 2026Article
- ENDOU-1-induced cytoplasmic HnRNPA3 recognizes m6A methylation on the upstream reading frame of human CHOP transcripts to achieve maximal CHOP translation.Cellular and molecular life sciences : CMLS · 2026Article
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- From development to disease: the neuronal role of hnRNPs through the lens ofFrontiers in cell and developmental biology · 2026Review
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- Elevated Levels of Active GSK3β in the Blood of Patients with Myotonic Dystrophy Type 1 Correlate with Muscle Weakness.International journal of molecular sciences · 2025Article
- Analysis of the splicing landscape of the frontal cortex in FTLD-TDP reveals subtype specific patterns and cryptic splicing.Acta neuropathologica · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frontotemporal dementia (FTD) is the second most common form of young-onset (<65 years) dementia. Clinically, it primarily manifests as a disorder of behavioural, executive, and/or language functions. Pathologically, frontotemporal lobar degeneration (FTLD) is the predominant cause of FTD. FTLD is a proteinopathy, and the main pathological proteins identified so far are tau, TAR DNA-binding protein 43 (TDP-43), and fused in sarcoma (FUS). As TDP-43 and FUS are members of the heterogeneous ribonucleic acid protein (hnRNP) family, many studies in recent years have expanded the research on the relationship between other hnRNPs and FTLD pathology. Indeed, these studies provide evidence for an association between hnRNP abnormalities and FTLD. In particular, several studies have shown that multiple hnRNPs may exhibit nuclear depletion and cytoplasmic mislocalisation within neurons in FTLD cases. However, due to the diversity and complex association of hnRNPs, most studies are still at the stage of histological discovery of different hnRNP abnormalities in FTLD. We herein review the latest studies relating hnRNPs to FTLD. Together, these studies outline an important role of multiple hnRNPs in the pathogenesis of FTLD and suggest that future research into FTLD should include the whole spectrum of this protein family.
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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.