ReviewNature reviews. Neurology2011
Corticobasal degeneration: a pathologically distinct 4R tauopathy.
Review in Nature reviews. Neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers, 7 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
117 citing papers in PubMed, 7 syntheses or guidelines pooled it, 235 citations in OpenAlex.
- Genetic correlates of corticobasal degeneration: a systematic review and meta-analysis.Journal of neurology · 2026Pooled it
- Tau PET imaging in progressive supranuclear palsy: a systematic review and meta-analysis.Journal of neurology · 2023Pooled it
- Pooled it
- Cerebrospinal Fluid Biomarkers in Multiple System Atrophy Relative to Parkinson's Disease: A Meta-Analysis.Behavioural neurology · 2021Pooled it
- Similarities and Differences in the Pattern of Tau Hyperphosphorylation in Physiological and Pathological Conditions: Impacts on the Elaboration of Therapies to Prevent Tau Pathology.Frontiers in neurology · 2020Pooled it
- [Tauopathies : From molecule to therapy].Der Nervenarzt · 2018Pooled it
- A systematic review of lessons learned from PET molecular imaging research in atypical parkinsonism.European journal of nuclear medicine and molecular imaging · 2016Pooled it
- Aβ1-15/16 as a potential diagnostic marker in neurodegenerative diseases.Neuromolecular medicine · 2013Trial
- Structural compression and entorhinal vulnerability: Linking tentorial adjacency to tau burden and dementia progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Integrating Metabolic, Perfusion, and Microstructural Parameters for Quantitative Neuroimaging in Rare Neurodegenerative Diseases: A Hybrid PET/MRI Approach.Diagnostics (Basel, Switzerland) · 2026Article
- Autophagy-Neuroinflammation Axis in Neurodegenerative Diseases: Mechanisms and Therapeutic Potential.Cells · 2026Review
- A critical appraisal of the link between apolipoprotein E and Tau.Current opinion in neurology · 2026Review
- Post-translational modifications as a regulatory code for tau function in health and disease.Frontiers in dementia · 2026Review
- Tau protein: Physiological functions and multifaceted roles in neurodegenerative and psychiatric disorders.Genomic psychiatry : advancing science from genes to society · 2025Article
- N-Amino Peptide-Graphene Quantum Dot Loaded Small Extracellular Vesicles for Targeted Therapy of Tauopathies.Advanced nanobiomed research · 2025Article
- Understanding Tau pathology: Insights from animal models.Zoological research · 2025Review
- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- Differences in the soluble and insoluble proteome between primary tauopathies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The Role of Tau in Neuronal Function and Neurodegeneration.Neurology international · 2025Review
- Probe-dependent Proximity Profiling (ProPPr) Uncovers Similarities and Differences in Phospho-Tau-Associated Proteomes Between Tauopathies.Molecular neurodegeneration · 2025Article
57 more citing papers are in PubMed but not listed here.
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 3 institutions in 1 country.
Funding
Abstract
Corticobasal degeneration (CBD) is a rare, progressive neurodegenerative disorder with onset in the 5(th) to 7(th) decade of life. It is associated with heterogeneous motor, sensory, behavioral and cognitive symptoms, which make its diagnosis difficult in a living patient. The etiology of CBD is unknown; however, neuropathological and genetic evidence supports a pathogenetic role for microtubule-associated protein tau. CBD pathology is characterized by circumscribed cortical atrophy with spongiosis and ballooned neurons; the distribution of these changes dictates the patient's clinical presentation. Neuronal and glial tau pathology is extensive in gray and white matter of the cortex, basal ganglia, diencephalon and rostral brainstem. Abnormal tau accumulation within astrocytes forms pathognomonic astrocytic plaques. The classic clinical presentation, termed corticobasal syndrome (CBS), comprises asymmetric progressive rigidity and apraxia with limb dystonia and myoclonus. CBS also occurs in conjunction with other diseases, including Alzheimer disease and progressive supranuclear palsy. Moreover, the pathology of CBD is associated with clinical presentations other than CBS, including Richardson syndrome, behavioral variant frontotemporal dementia, primary progressive aphasia and posterior cortical syndrome. Progress in biomarker development to differentiate CBD from other disorders has been slow, but is essential in improving diagnosis and in development of disease-modifying therapies.
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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.