ArticleNature aging2025
Large-scale network analysis of the cerebrospinal fluid proteome identifies molecular signatures of frontotemporal lobar degeneration.
Article in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed.
- Distinct proteomic CSF profiles in genetic frontotemporal lobar degeneration.Brain : a journal of neurology · 2026Article
- Article
- Plasma Proteomic Changes in GRN and C9orf72 Frontotemporal Dementia.European journal of neurology · 2026Article
- Plasma proteomics link menopause timing to brain aging and dementia risk.Research square · 2026Article
- Plasma proteomics link menopause timing to brain aging and dementia risk.medRxiv : the preprint server for health sciences · 2026Article
- Decoding Dementia Mechanisms: Identification of Key Oligodendrocyte- Associated Genes through Integrative Bioinformatics and Machine Learning.Current topics in medicinal chemistry · 2026Article
- TDP-43 Regulates Rab4 Levels to Support Synaptic Vesicle Recycling and Neuromuscular Connectivity inInternational journal of molecular sciences · 2025Article
- Design considerations for C9orf72 disease prevention trials.Brain : a journal of neurology · 2025Review
- Cell autonomous microglia defects in a stem cell model of frontotemporal dementia tau.Molecular psychiatry · 2025Article
- Large-scale CSF proteome profiling identifies biomarkers for accurate diagnosis of frontotemporal dementia.Molecular neurodegeneration · 2025Article
- Shared and disease-specific pathways in frontotemporal dementia and Alzheimer's and Parkinson's diseases.Nature medicine · 2025Article
- Protein-based Diagnosis and Analysis of Co-pathologies Across Neurodegenerative Diseases: Large-Scale AI-Boosted CSF and Plasma Classification.Research square · 2025Article
- Protein-based Diagnosis and Analysis of Co-pathologies Across Neurodegenerative Diseases: Large-Scale AI-Boosted CSF and Plasma Classification.medRxiv : the preprint server for health sciences · 2025Article
- Benchmarking the AI-based diagnostic potential of plasma proteomics for neurodegenerative disease in 17,170 people.medRxiv : the preprint server for health sciences · 2025Article
- Opposing role of phagocytic receptors MERTK and AXL in Progranulin deficient FTD.Communications biology · 2025Article
- FTLD-associated proteomic signatures uncovered.Nature reviews. Neurology · 2025Article
- Brain aging rejuvenation factors in adults with genetic and sporadic neurodegenerative disease.Brain communications · 2025Article
- Cell autonomous microglia defects in a stem cell model of frontotemporal dementia.medRxiv : the preprint server for health sciences · 2024Article
Corrections and comments
- Erratum issued
- Update of
Authors and funding
72 authors.
Funding
Abstract
The pathophysiological mechanisms driving disease progression of frontotemporal lobar degeneration (FTLD) and corresponding biomarkers are not fully understood. Here we leveraged aptamer-based proteomics (>4,000 proteins) to identify dysregulated communities of co-expressed cerebrospinal fluid proteins in 116 adults carrying autosomal dominant FTLD mutations (C9orf72, GRN and MAPT) compared with 39 non-carrier controls. Network analysis identified 31 protein co-expression modules. Proteomic signatures of genetic FTLD clinical severity included increased abundance of RNA splicing (particularly in C9orf72 and GRN) and extracellular matrix (particularly in MAPT) modules, as well as decreased abundance of synaptic/neuronal and autophagy modules. The generalizability of genetic FTLD proteomic signatures was tested and confirmed in independent cohorts of (1) sporadic progressive supranuclear palsy-Richardson syndrome and (2) frontotemporal dementia spectrum clinical syndromes. Network-based proteomics hold promise for identifying replicable molecular pathways in adults living with FTLD. 'Hub' proteins driving co-expression of affected modules warrant further attention as candidate biomarkers and therapeutic targets.
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.