ReviewThe journal of headache and pain2025
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.
Review in The journal of headache and pain, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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.
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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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Migraine is a risk factor for dementia: a systematic review and meta-analysis of cohort studies.The journal of headache and pain · 2025Pooled it
- NOTCH3 Mutations in CADASIL: a multicellular perspective on neurodegeneration.Cell communication and signaling : CCS · 2026Review
- Novel Mutation ofBalkan journal of medical genetics : BJMG · 2025Article
- Neuroimaging and Genetic Markers of Cerebral Small Vessel Disease and Cognitive Outcomes: A Systematic Review and Meta-Analysis (NEUROGEN-SVD Study).Diagnostics (Basel, Switzerland) · 2025Article
- CADASIL orFrontiers in neurology · 2025Review
- Differential presence of cerebral microbleeds in an amyloid mouse model compared with a CADASIL mouse model.Alzheimer's & dementia (New York, N. Y.)Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an autosomal-dominantly inherited cerebral small-vessel disease (SVD). CADASIL has diverse clinical features such as migraine with aura, dementia, and recurrent strokes, and is caused by a pathogenic mutation in the NOTCH3 gene which encodes a transmembrane receptor found in smooth muscle cells of small arteries and pericytes of brain capillaries. Pathogenic mutations alter the number of cysteine residues in the extracellular domain of NOTCH3, leading to the abnormal accumulation of granular osmiophilic material in the vessels of affected individuals. In addition, potential signaling pathways, such as transforming growth factor beta (TGF-β), may be involved in pathogenesis of the disease. This review aims to elucidate these mechanisms, particularly NOTCH3, in the context of CADASIL pathogenesis, providing insight into the role of NOTCH3 signaling and discussing the significance of these pathways for potential future therapeutic interventions in CADASIL patients.
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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 Socratic graph.