ReviewJournal of molecular neuroscience : MN2011
Novel types of frontotemporal lobar degeneration: beyond tau and TDP-43.
Review in Journal of molecular neuroscience : MN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 39 citations in OpenAlex.
- Pathomorphological Diagnostic Criteria for Focal Cortical Dysplasias and Other Common Epileptogenic Lesions-Review of the Literature.Diagnostics (Basel, Switzerland) · 2023Review
- Pharmacotherapy for Frontotemporal Dementia.CNS drugs · 2021Review
- The Role of White Matter Dysfunction and Leukoencephalopathy/Leukodystrophy Genes in the Aetiology of Frontotemporal Dementias: Implications for Novel Approaches to Therapeutics.International journal of molecular sciences · 2021Review
- Relevance of biomarkers across different neurodegenerative diseases.Alzheimer's research & therapy · 2020Review
- Extended FTLD pedigree segregating a Belgian GRN-null mutation: neuropathological heterogeneity in one family.Alzheimer's research & therapy · 2018Review
- Acetylation-induced TDP-43 pathology is suppressed by an HSF1-dependent chaperone program.Nature communications · 2017Article
- Progranulin deficiency induces overactivation of WNT5A expression via TNF-α/NF-κB pathway in peripheral cells from frontotemporal dementia-linked granulin mutation carriers.Journal of psychiatry & neuroscience : JPN · 2016Article
- Tau-Centric Targets and Drugs in Clinical Development for the Treatment of Alzheimer's Disease.BioMed research international · 2016Review
- Progranulin Deficiency Reduces CDK4/6/pRb Activation and Survival of Human Neuroblastoma SH-SY5Y Cells.Molecular neurobiology · 2015Article
- Different Brain Regions are Infected with Fungi in Alzheimer's Disease.Scientific reports · 2015Article
- Amyotrophic lateral sclerosis: an update on recent genetic insights.Journal of neurology · 2013Review
- Cerebrospinal fluid neurofilament light chain protein levels in subtypes of frontotemporal dementia.BMC neurology · 2013Article
- The genetics and neuropathology of frontotemporal lobar degeneration.Acta neuropathologica · 2012Review
- Clinico-pathological correlations of the most common neurodegenerative dementias.Frontiers in neurology · 2012Article
- Astrocytes carrying the superoxide dismutase 1 (SOD1G93A) mutation induce wild-type motor neuron degeneration in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Neuropathology of frontotemporal lobar degeneration: a review.Dementia & neuropsychologiaReview
- Clinical neuropathology practice guide 5-2013: markers of neuronal maturation.Clinical neuropathologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 4 countries.
Funding
Abstract
Most cases of frontotemporal lobar degeneration (FTLD) are characterized by the abnormal accumulation of either the microtubule-associated protein tau or the transactive response DNA-binding protein with M(r) 43 kDa, TDP-43 (FTLD-tau and FTLD-TDP, respectively). However, there remain ∼10% of cases, composed of a heterogenous collection of uncommon disorders, for which the molecular basis remains uncertain. In this review, we describe the characteristic genetic, clinical, and pathological features of the major tau/TDP-negative FTLD subtypes, with focus on recent advances in our understanding of their molecular basis. This includes the discovery that the pathological changes in atypical FTLD with ubiquitinated inclusions, neuronal intermediate filament inclusion disease, and basophilic inclusion body disease are immunoreactive for the fused in sarcoma (FUS) protein, resulting in the creation of a new molecular subgroup (FTLD-FUS), and studies clarifying the functional consequences of pathogenic CHMP2B mutations.
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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.