ReviewNature reviews. Neurology2012
Advances in understanding the molecular basis of frontotemporal dementia.
Review in Nature reviews. Neurology, 2012. 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 233 papers, 5 of them syntheses that pooled it.
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
233 citing papers in PubMed, 5 syntheses or guidelines pooled it, 410 citations in OpenAlex.
- Tracking disease progression in familial and sporadic frontotemporal lobar degeneration: Recent findings from ARTFL and LEFFTDS.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020Pooled it
- Meta-analysis of Genetic Modifiers Reveals Candidate Dysregulated Pathways in Amyotrophic Lateral Sclerosis.Neuroscience · 2019Pooled it
- TDP-43 as a potential biomarker for amyotrophic lateral sclerosis: a systematic review and meta-analysis.BMC neurology · 2018Pooled it
- Morphometric MRI as a diagnostic biomarker of frontotemporal dementia: A systematic review to determine clinical applicability.NeuroImage. Clinical · 2018Pooled it
- Pooled it
- Phase 2 study of palmitoylethanolamide combined with luteoline in frontotemporal dementia patients.Brain communications · 2025Trial
- An acetylated Tau-174 CSF biomarker discriminates between TDP-43 and tau pathology in patients with frontotemporal lobar degeneration.Nature medicine · 2026Article
- Clinical Clues to the Diagnostic Yield of Genetic Testing in Adults With Late-Onset Behavioral Change.Neurology. Genetics · 2026Article
- Frontotemporal dementia: Clinical aspects, genetics, and neuropathology of a family with a C9ORF72 expansion in Argentina.Brain pathology (Zurich, Switzerland) · 2026Article
- Mitochondria and Lipid Defects in Hereditary Progranulin-Related Frontotemporal Dementia.Cells · 2026Article
- Dysregulated neuronal mRNA transport and translation in FTD/ALS.NPJ dementia · 2026Review
- Associations of local white matter geometry with network efficiency, macrostructural abnormalities, and clinical severity in behavioural variant frontotemporal dementia.Brain communications · 2026Article
- Shared Neuroinflammatory Mechanisms Across Dementia Types: An Integrative Review.International journal of molecular sciences · 2025Review
- Patient-derived induced pluripotent stem cells with a C9orf72 expansion as a model to study frontotemporal dementia pathologies.Molecular biology of the cell · 2025Article
- Integrative proteomic analysis provides novel therapeutic insights for etiological subtypes of diabetes.Diabetes, obesity & metabolism · 2025Article
- Quantifying brain atrophy in Frontotemporal Dementia: a head-to-head comparison of neuroimaging techniques.medRxiv : the preprint server for health sciences · 2025Article
- Review
- The mechanisms underlying TDP-43-associated neurodegeneration in Alzheimer's disease and related dementias.Molecular psychiatry · 2025Review
- The Evolving Role of FDG-PET in Behavioral Variant Frontotemporal Dementia: Current Applications and Future Opportunities.International journal of molecular sciences · 2025Review
- Crystal structures of distinct parallel and antiparallel DNA G-quadruplexes reveal structural polymorphism in C9orf72 G4C2 repeats.Nucleic acids research · 2025Article
173 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Frontotemporal dementia (FTD) is a clinical syndrome with a heterogeneous molecular basis. Until recently, the underlying cause was known in only a minority of cases that were associated with abnormalities of the tau protein or gene. In 2006, however, mutations in the progranulin gene were discovered as another important cause of familial FTD. That same year, TAR DNA-binding protein 43 (TDP-43) was identified as the pathological protein in the most common subtypes of FTD and amyotrophic lateral sclerosis (ALS). Since then, substantial efforts have been made to understand the functions and regulation of progranulin and TDP-43, as well as their roles in neurodegeneration. More recently, other DNA/RNA binding proteins (FET family proteins) have been identified as the pathological proteins in most of the remaining cases of FTD. In 2011, abnormal expansion of a hexanucleotide repeat in the gene C9orf72 was found to be the most common genetic cause of both FTD and ALS. All common FTD-causing genes have seemingly now been discovered and the main pathological proteins identified. In this Review, we highlight recent advances in understanding the molecular aspects of FTD, which will provide the basis for improved patient care through the development of more-targeted diagnostic tests and therapies.
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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.