ArticleActa neuropathologica2024
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.
Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Distinct cellular phenotypes of language and executive decline in amyotrophic lateral sclerosis.Cell · 2026Article
- TDP-43 proteinopathy as a biomarker and therapeutic target in amyotrophic lateral sclerosis.Biochemical Society transactions · 2026Review
- TDP-43: [GU]-ardian of the transcriptome.Molecular neurodegeneration · 2026Review
- TDP-43 pathology is linked to motor neuron loss and is independent of stress granulesbioRxiv : the preprint server for biology · 2026Article
- Preservation of miR-9-5p and miR-124-3p in ALS-resistant oculomotor neurons contrasts with their downregulation in vulnerable spinal motor neurons, irrespective of TDP-43 pathology.Acta neuropathologica · 2026Article
- Metabolic signatures of ferritin and TDP-43 co-pathology provide a mechanistic basis for stratified therapeutic approaches in ALS.bioRxiv : the preprint server for biology · 2026Article
- Neuronal TDP-43 regulates myelin formation via neurexin 1 mRNA stabilization.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Aberrant Splicing Signatures Underpin Oligodendrocyte Damage in ALS and Neuron Loss in FTD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Pathological TDP-43 filaments accumulate at synapses and cause synaptic dysfunction.bioRxiv : the preprint server for biology · 2026Article
- TDP-43 dysfunction leads to the accumulation of cryptic transposable element-derived exons, crypTEs, in iPSC derived neurons and ALS/FTD patient tissues.bioRxiv : the preprint server for biology · 2026Article
- Amygdala TDP-43 pathology is associated with behavioural dysfunction and ferritin accumulation in amyotrophic lateral sclerosis.Brain communications · 2026Article
- Computationally-designed aptamers targeting RAD51-BRCA2 interaction impair homologous recombination and induce synthetic lethality.Nature communications · 2025Article
- 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
- Skin TDP-43 pathology as a candidate biomarker for predicting amyotrophic lateral sclerosis decades prior to motor symptom onset.bioRxiv : the preprint server for biology · 2025Article
- Brain Iron as a Surrogate Biomarker of Pathological TDP-43 Identifies Brain Region-Specific Signatures in Ageing, Alzheimer's Disease and Amyotrophic Lateral Sclerosis.bioRxiv : the preprint server for biology · 2025Article
- Integrative assessment of RNA sequencing and in silico analysis to pinpoint mRNAs, lncRNAs, and circRNAs interactions with miRNAs underlying arsenic-induced neurotoxicity.BMC genomics · 2025Article
- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- Sporadic ALS induced pluripotent stem cell derived neurons reveal hallmarks of TDP-43 loss of function.Nature communications · 2025Article
- Large-scale RNA-Seq mining reveals ciclopirox olamine induces TDP-43 cryptic exons.Nature communications · 2025Article
- Long-read RNA sequencing unveils a novel cryptic exon in MNAT1 along with its full-length transcript structure in TDP-43 proteinopathy.Communications biology · 2025Article
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
Abstract
TDP-43 is an aggregation-prone protein which accumulates in the hallmark pathological inclusions of amyotrophic lateral sclerosis (ALS). However, the analysis of deeply phenotyped human post-mortem samples has shown that TDP-43 aggregation, revealed by standard antibody methods, correlates poorly with symptom manifestation. Recent identification of cryptic-splicing events, such as the detection of Stathmin-2 (STMN-2) cryptic exons, are providing evidence implicating TDP-43 loss-of-function as a potential driving pathomechanism but the temporal nature of TDP-43 loss and its relation to the disease process and clinical phenotype is not known. To address these outstanding questions, we used a novel RNA aptamer, TDP-43
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