ArticleEMBO molecular medicine2023
Active immunotherapy reduces NOTCH3 deposition in brain capillaries in a CADASIL mouse model.
Article in EMBO molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 27 citations in OpenAlex.
- Impairment of hippocampal gamma oscillations, mitochondria and neurovascular function in CADASIL.Brain : a journal of neurology · 2026Article
- 3D Vessels-on-Chip using isogenic hiPSC-derived VSMCs reveal NOTCH3-driven alterations in brain small vessel disease.Stem cell reports · 2026Article
- NOTCH3 CADASIL Variant Receptor Aggregation Requires NOTCH3 Wild-Type Receptors: Identification of Highly Selective Inhibitors That Block the Process.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Neuroinflammation and blood-brain barrier dysfunction in cerebral small vessel disease: mechanisms, biomarkers, and therapeutic implications.European journal of medical research · 2026Review
- Serum NOTCH3 Extracellular Domain in Patients With CADASIL.Neurology. Genetics · 2025Article
- Association Between Vascular NOTCH3 Aggregation and Disease Severity in a CADASIL Cohort - Implications for NOTCH3 Variant-Specific Disease Prediction.Annals of neurology · 2025Article
- The blood-brain barrier: a help and a hindrance.Brain : a journal of neurology · 2025Review
- The Pathobiology of Cerebrovascular Lesions in CADASIL Small Vessel Disease.Basic & clinical pharmacology & toxicology · 2025Review
- Inducing mononuclear cells of patients with CADASIL to construct a CSVD disease model.European journal of medical research · 2025Article
- NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL.CNS neuroscience & therapeutics · 2025Article
- CADASIL: A NOTCH3-associated cerebral small vessel disease.Journal of advanced research · 2024Review
- The N-acetylglucosaminyltransferase Radical fringe contributes to defects in JAG1-dependent turnover and signaling of NOTCH3 CADASIL mutants.The Journal of biological chemistry · 2024Article
- Association ofNeurology · 2024Article
- Article
- Analysis of the pathogenicity and pathological characteristics ofFrontiers in molecular neuroscience · 2024Article
- Progress in the Study of the Role and Mechanism of HTRA1 in Diseases Related to Vascular Abnormalities.International journal of general medicine · 2024Review
- Pathophysiology and probable etiology of cerebral small vessel disease in vascular dementia and Alzheimer's disease.Molecular neurodegeneration · 2023Review
- ER stress induced immunopathology involving complement in CADASIL: implications for therapeutics.Acta neuropathologica communications · 2023Article
- Active immunotherapy reduces NOTCH3 deposition in brain capillaries in a CADASIL mouse model.EMBO molecular medicine · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most common monogenic form of familial small vessel disease; no preventive or curative therapy is available. CADASIL is caused by mutations in the NOTCH3 gene, resulting in a mutated NOTCH3 receptor, with aggregation of the NOTCH3 extracellular domain (ECD) around vascular smooth muscle cells. In this study, we have developed a novel active immunization therapy specifically targeting CADASIL-like aggregated NOTCH3 ECD. Immunizing CADASIL TgN3R182C
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.