ReviewJournal of stroke2015
Genetics of cerebral small vessel disease.
Review in Journal of stroke, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 99 citations in OpenAlex.
- Rethinking Temporopolar White-Matter Hyperintensity in CADASIL: A Context-Dependent Biomarker.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Diagnostic Value and Clinical Significance of Temporopolar White-Matter Hyperintensities in CADASIL and Sporadic Small-Vessel Disease.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Association of imaging-defined brain age with disease severity and adverse outcomes in CADASIL.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Sex-Based Differences in Disease Burden and Phenotype in CADASIL: A Multicenter Study of 368 Korean Patients.Neurology. Genetics · 2026Article
- Early Onset, High Comorbidity Burden, and Regional Disparities of CADASIL: A Nationwide Cohort Study in South Korea.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Serum NOTCH3 Extracellular Domain in Patients With CADASIL.Neurology. Genetics · 2025Article
- Commissural Fiber Disruption Is Associated With Symptom Onset in Cerebral Autosomal-Dominant Arteriopathy With Subcortical Infarcts and Leukoencephalopathy.Journal of the American Heart Association · 2025Article
- Review
- Signaling pathways and molecular mechanisms involved in the onset and progression of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL); a focus on Notch3 signaling.The journal of headache and pain · 2025Review
- The Relationship Between Blood Omega-3 Levels and the Small Vessel Disease in Ischemic Stroke Patients: A Case-Control Study.Health science reports · 2025Article
- Endothelial cells as key players in cerebral small vessel disease.Nature reviews. Neuroscience · 2025Review
- CADASIL orFrontiers in neurology · 2025Review
- Emerging biomarkers and frontier therapies: unveiling the role of endothelial dysfunction in cerebral small vessel disease.Frontiers in neurology · 2025Review
- Multimodal neuroimaging ofFrontiers in neuroscience · 2025Article
- Impact of cerebral small vessel disease burden and drug level at admission on direct oral anticoagulant associated intracerebral hemorrhage.European stroke journal · 2024Article
- Impaired cerebral interstitial fluid dynamics in cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy.Brain communications · 2024Article
- Modeling of age-related neurological disease: utility of zebrafish.Frontiers in aging neuroscience · 2024Review
- Differential blood-based biomarkers of subcortical and deep brain small vessel disease.Therapeutic advances in neurological disorders · 2024Article
- Impaired intracellular CaScience signaling · 2023Article
- Blood-brain barrier leakage hotspots collocating with brain lesions due to sporadic and monogenic small vessel disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral small vessel disease (SVD) is an important cause of stroke and cognitive impairment among the elderly and is a more frequent cause of stroke in Asia than in the US or Europe. Although traditional risk factors such as hypertension or diabetes mellitus are important in the development of cerebral SVD, the exact pathogenesis is still uncertain. Both, twin and family history studies suggest heritability of sporadic cerebral SVD, while the candidate gene study and the genome-wide association study (GWAS) are mainly used in genetic research. Robust associations between the candidate genes and occurrence of various features of sporadic cerebral SVD, such as lacunar infarction, intracerebral hemorrhage, or white matter hyperintensities, have not yet been elucidated. GWAS, a relatively new technique, overcomes several shortcomings of previous genetic techniques, enabling the detection of several important genetic loci associated with cerebral SVD. In addition to the more common, sporadic cerebral SVD, several single-gene disorders causing cerebral SVD have been identified. The number of reported cases is increasing as the clinical features become clear and diagnostic examinations are more readily available. These include cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy, COL4A1-related cerebral SVD, autosomal dominant retinal vasculopathy with cerebral leukodystrophy, and Fabry disease. These rare single-gene disorders are expected to play a crucial role in our understanding of cerebral SVD pathogenesis by providing animal models for the identification of cellular, molecular, and biochemical changes underlying cerebral small vessel damage.
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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.