ArticleActa neuropathologica communications2022
Evidence of cerebellar TDP-43 loss of function in FTLD-TDP.
Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 26 citations in OpenAlex.
- The UNC13A cryptic exon associates with cognitive impairment in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- TDP-43 dysfunction facilitates the pathological conversion of tau.Molecular neurodegeneration · 2026Article
- Statins and genetic inhibition of the mevalonate pathway activate an ATF3-STMN2 regenerative program.bioRxiv : the preprint server for biology · 2026Article
- A neurotoxic cryptic peptide arising from TDP-43-dependent cryptic splicing of PKN1.Nature communications · 2026Article
- A Putative Role for the BCL2 Family of Proteins in the Pathophysiology of ALS.CNS & neurological disorders drug targets · 2026Article
- Quantitative Profiling of Nanoscopic Protein Aggregates Reveals Specific Fingerprint of TDP-43-Positive Assemblies in Motor Neuron Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Methylome analysis of FTLD patients with TDP-43 pathology identifies epigenetic signatures specific to pathological subtypes.Molecular neurodegeneration · 2025Article
- Neurological soft signs in neurodegenerative dementias: Results of the DemeNSS study.PCN reports : psychiatry and clinical neurosciences · 2025Article
- Multi-region brain transcriptomic analysis of amyotrophic lateral sclerosis reveals widespread RNA alterations and substantial cerebellum involvement.Molecular neurodegeneration · 2025Article
- TDP-43 Cryptic RNAs in Perry Syndrome: Differences across Brain Regions and TDP-43 Proteinopathies.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- NovelOpen biology · 2024Article
- Abundant transcriptomic alterations in the human cerebellum of patients with a C9orf72 repeat expansion.Acta neuropathologica · 2024Article
- RNA aptamer reveals nuclear TDP-43 pathology is an early aggregation event that coincides with STMN-2 cryptic splicing and precedes clinical manifestation in ALS.Acta neuropathologica · 2024Article
- TDP-43-regulated cryptic RNAs accumulate in Alzheimer's disease brains.Molecular neurodegeneration · 2023Article
- Clusters of co-abundant proteins in the brain cortex associated with fronto-temporal lobar degeneration.Alzheimer's research & therapy · 2023Article
- TDP-43 and NEAT long non-coding RNA: Roles in neurodegenerative disease.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 4 institutions in 1 country.
Funding
Abstract
Frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP) is a neurodegenerative disease primarily affecting the frontal and/or temporal cortices. However, a growing body of evidence suggests that the cerebellum contributes to biochemical, cognitive, and behavioral changes in FTLD-TDP. To evaluate cerebellar TDP-43 expression and function in FTLD-TDP, we analyzed TDP-43 protein levels and the splicing of a TDP-43 target, STMN2, in the cerebellum of 95 FTLD-TDP cases and 25 non-neurological disease controls. Soluble TDP-43 was decreased in the cerebellum of FTLD-TDP cases but a concomitant increase in insoluble TDP-43 was not seen. Truncated STMN2 transcripts, an indicator of TDP-43 dysfunction, were elevated in the cerebellum of FTLD-TDP cases and inversely associated with TDP-43 levels. Additionally, lower cerebellar TDP-43 associated with a younger age at disease onset. We provide evidence of TDP-43 loss of function in the cerebellum in FTLD-TDP, supporting further investigation into this understudied brain region.
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.