Molecular pathogenesis of subarachnoid haemorrhage
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Molecular pathogenesis of subarachnoid haemorrhage. Baiping Zhang, Kaare Gugleholm, Lorna B. Day, Shu Ye, Roy O. Weller, Ian N.M. Day 5 November 2002. Pathogenesis and the stages involved in the formation of saccular aneurysm Cellular and molecular architecture of the vessel wall

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Molecular pathogenesis of subarachnoid haemorrhage

Molecular pathogenesis of subarachnoid haemorrhage

Baiping Zhang, Kaare Gugleholm, Lorna B. Day, Shu Ye, Roy O. Weller, Ian N.M. Day

5 November 2002


  • Pathogenesis and the stages involved in the formation of saccular aneurysm

  • Cellular and molecular architecture of the vessel wall

  • Molecular pathology

    • PKD1 gene and polycystin

    • COL3A1 and type III collagen

    • Fibrillin-1

    • Collagen IV and other basement membrane constituents

    • Alpha1-Antitrypsin (protease inhibitor)

  • Future focus


Subarachnoid haemorrhage sah
Subarachnoid haemorrhage (SAH) saccular aneurysm

  • Condition caused by the escape of blood from a cerebral artery into the subarachnoid space along the surface of the brain.

http://instruct.uwo.ca/anatomy/530/SagSin.gif


Pritchard, Foulkes, Lang, & Neil-Dwyer. 2001


Schematic overview of contributory factors to subarachnoid haemorrhage
Schematic overview of contributory factors to subarachnoid haemorrhage

B. Zhang et al./ The International Journal of Biochemistry & Cell Biology 35 (2003) 1341-1360


Commonest sites for saccular aneurysms
Commonest sites for Saccular Aneurysms haemorrhage

B. Zhang et al./ The International Journal of Biochemistry & Cell Biology 35 (2003) 1341-1360



Etiology involved in the formation of saccular aneurysms
Etiology involved in the formation of saccular aneurysms Cell Biology 35 (2003) 1341-1360

  • Majority of aneurysms occur between the ages of 40 and 70

    • Ageing effects on the arteries

  • Increased incidence of saccular aneurysms in families with

    • Polycystic kidney disease

    • Fibromuscular dysplasia

    • Moyamoya disease

    • Marfan Syndrome

    • EDS type IV


Pkd1 gene and polycystin
PKD1 gene and polycystin Cell Biology 35 (2003) 1341-1360

  • Adult polycystic kidney disease is an autosomal dominant disorder in which renal cysts form, leading to progressive loss of glomerular filtration and subsequently to renal failure and end-stage renal disease.

  • PKD1 gene causing (PKD)

    • Encodes for a protein named polycystin

  • Polycystin - participates in protein-protein and protein-carbohydrate interactions in the extracellular matrix

adpkd.cimr.cam.ac.uk/ buttons/pkd1_hs_350.gif


Col3a1 and type iii collagen
COL3A1 and type III collagen Cell Biology 35 (2003) 1341-1360

  • Ehlers-Danlos Syndrome Vascular Type

    • Arterial rupture risk

    • Thin transparent skin

    • Early bruising

    • Joint laxity

    • Ligament weakness

    • Bowel rupture

  • (EDS type IV)

    • Defective collagen III synthesis

    • Vascular expression on COL3A1


Collagen iv and other basement membrane constituents
Collagen IV and other basement membrane constituents Cell Biology 35 (2003) 1341-1360

  • Collagen IV defects cause Alport’s syndrome.

  • Alports syndrome characterized sensorineural hearing loss and haematuria.

    • Its is therefore plausible new hypothesis that defects in the basement membrane as well as defects in the elastic and medial layer may predispose intracranial aneurysms


Protease inhibitor alpha1 antitrypsin
Protease inhibitor (alpha1-Antitrypsin) Cell Biology 35 (2003) 1341-1360

  • Most abundant and potent natural inhibitor of elastase.

  • Alpha1-Antitrypsin activity has been claimed to be reduced in both intracranial and abdominal aortic aneurysm.


Future focus
Future focus Cell Biology 35 (2003) 1341-1360


Fibrillin 1 and fbn1
Fibrillin-1 and FBN1 Cell Biology 35 (2003) 1341-1360

  • Marfan syndrome is an autosomal dominant heritable disorder of connective tissue with prominent manifestations affecting the skeletal, ocular and cardiovascular systems.

  • Progressive dilation of the aortic root and aortic dissection and rupture are frequent, and mitral and aotic valve insufficiency may also occur early.

    • Caused by mutations in FBN1 gene encoding fibrilin-1

      • Mutations of this gene also cause type I fibrillinopathies


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