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1. Rare variants in ANO1, encoding a calcium-activated chloride channel, predispose to moyamoya disease.

2. Lysyl hydroxylase 3–mediated post-translational modifications are required for proper biosynthesis of collagen α1α1α2(IV)

4. Phenotype and imaging features associated with APP duplications

6. COL4A1/COL4A2 and inherited platelet disorder gene variants in fetuses showing intracranial hemorrhage.

7. Age-related loss of Notch3 underlies brain vascular contractility deficiencies, glymphatic dysfunction, and neurodegeneration in mice

8. An AluYa5 Insertion in the 3′UTR of COL4A1 and Cerebral Small Vessel Disease

10. Synopsis of Guidelines for the Clinical Management of Cerebral Cavernous Malformations: Consensus Recommendations Based on Systematic Literature Review by the Angioma Alliance Scientific Advisory Board Clinical Experts Panel

11. The pleiotropy associated with de novo variants in CHD4, CNOT3, and SETD5 extends to moyamoya angiopathy

13. Further refinement of COL4A1 and COL4A2 related cortical malformations

15. Age-related loss of Notch3 underlies brain vascular contractility deficiencies, glymphatic dysfunction, and neurodegeneration in mice

16. Estudios genéticos en pacientes y familias con sospecha de enfermedades neurovasculares hereditarias

17. Recalibrating vascular malformations and mechanotransduction by pharmacological intervention

19. Nontraumatic Pediatric Intracerebral Hemorrhage

23. Bi-allelic variants in the ESAM tight-junction gene cause a neurodevelopmental disorder associated with fetal intracranial hemorrhage

24. Genetic studies in patients and families suspected of hereditary neurovascular diseases

25. Biallelic NPR1 loss of function variants are responsible for neonatal systemic hypertension.

26. European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy Endorsed by Vascular European Reference Network (VASCERN)

27. sj-docx-2-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

28. sj-docx-3-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

29. Additional file 1 of Biallelic variants in NOS3 and GUCY1A3, the two major genes of the nitric oxide pathway, cause moyamoya cerebral angiopathy

30. sj-docx-4-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

31. Additional file 5 of Biallelic variants in NOS3 and GUCY1A3, the two major genes of the nitric oxide pathway, cause moyamoya cerebral angiopathy

32. sj-docx-1-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

33. sj-docx-5-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

34. sj-docx-6-eso-10.1177_23969873221144089 – Supplemental material for European Stroke Organisation (ESO) Guidelines on Moyamoya angiopathy: Endorsed by Vascular European Reference Network (VASCERN)

35. Additional file 2 of Biallelic variants in NOS3 and GUCY1A3, the two major genes of the nitric oxide pathway, cause moyamoya cerebral angiopathy

36. Additional file 3 of Biallelic variants in NOS3 and GUCY1A3, the two major genes of the nitric oxide pathway, cause moyamoya cerebral angiopathy

37. Additional file 4 of Biallelic variants in NOS3 and GUCY1A3, the two major genes of the nitric oxide pathway, cause moyamoya cerebral angiopathy

38. Phenotypic variability in 446 CADASIL patients: Impact of NOTCH3 gene mutation location in addition to the effects of age, sex and vascular risk factors

39. Elderly CADASIL patients with intact neurological status

40. Recalibrating vascular malformations and mechanotransduction by pharmacological intervention.

41. sj-pdf-1-jcb-10.1177_0271678X221126280 - Supplemental material for Phenotypic variability in 446 CADASIL patients: Impact of NOTCH3 gene mutation location in addition to the effects of age, sex and vascular risk factors

42. APOE [Latin Small Letter Open E]2 is associated with white matter hyperintensity volume in CADASIL

46. Adult-onset genetic leukoencephalopathies: A MRI pattern-based approach in a comprehensive study of 154 patients

48. Heterozygous HTRA1 nonsense or frameshift mutations are pathogenic

49. Genome-wide association study of intracranial aneurysms identifies 17 risk loci and genetic overlap with clinical risk factors

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