21 results on '"Domenga-Denier, Valérie"'
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2. Reducing Hypermuscularization of the Transitional Segment Between Arterioles and Capillaries Protects Against Spontaneous Intracerebral Hemorrhage
3. CADASIL brain vessels show a HTRA1 loss-of-function profile
4. Characterization of early white matter changes in CADASIL using microscopic diffusion imaging and relaxometry
5. Potassium channelopathy-like defect underlies early-stage cerebrovascular dysfunction in a genetic model of small vessel disease
6. Increased Notch3 Activity Mediates Pathological Changes in Structure of Cerebral Arteries
7. Reducing Timp3 or vitronectin ameliorates disease manifestations in CADASIL mice
8. Archetypal Arg169Cys Mutation in NOTCH3 Does Not Drive the Pathogenesis in Cerebral Autosomal Dominant Arteriopathy With Subcortical Infarcts and Leucoencephalopathy via a Loss-of-Function Mechanism
9. Characterisation of early ultrastructural changes in the cerebral white matter of CADASIL small vessel disease using high‐pressure freezing/freeze‐substitution
10. Abnormal recruitment of extracellular matrix proteins by excess Notch3ECD: a new pathomechanism in CADASIL
11. Blood brain barrier leakage is not a consistent feature of white matter lesions in CADASIL
12. Notch3ECD immunotherapy improves cerebrovascular responses in CADASIL mice
13. Notch3ECD immunotherapy improves cerebrovascular responses in CADASIL mice.
14. Severity of arterial defects in the retina correlates with the burden of intracerebral haemorrhage in COL4A1‐related stroke
15. Mechanistic insights into a TIMP3-sensitive pathway constitutively engaged in the regulation of cerebral hemodynamics
16. Author response: Mechanistic insights into a TIMP3-sensitive pathway constitutively engaged in the regulation of cerebral hemodynamics
17. Early white matter changes in CADASIL: evidence of segmental intramyelinic oedema in a pre-clinical mouse model
18. Transcriptome Analysis for Notch3 Target Genes Identifies Grip2 as a Novel Regulator of Myogenic Response in the Cerebrovasculature
19. Abnormal recruitment of extracellular matrix proteins by excess Notch3 ECD: a new pathomechanism in CADASIL.
20. Notch3 ECD immunotherapy improves cerebrovascular responses in CADASIL mice.
21. Abnormal recruitment of extracellular matrix proteins by excess Notch3 ECD: a new pathomechanism in CADASIL.
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