Search for dissertations about: "CADASIL"
Showing result 1 - 5 of 7 swedish dissertations containing the word CADASIL.
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1. Vascular Dysfunction in Stroke and CADASIL
Abstract : Cerebrovascular disease (CVD) is strongly linked to hypertension and generally occurs later in life than coronary artery disease (CAD). Three quarters of the patients with symptomatic CVD are above 65 years of age. The risk factors are the same for CVD and CAD, but the relative importance of the vascular risk factors differs greatly. READ MORE
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2. Microangiopathies of the human brain b immunohistochemical studies on extracellular matrix components in arterial vessels and endothelin
Abstract : Microangiopathies may cause ischemic brain lesions and are of fundamental importance in vascular dementia. Risk factors include high age, hypertension, diabetes and Alzheimer's disease. READ MORE
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3. CADASIL : a pure model for studying cerebral small vessel disease
Abstract : Cerebral autosomal dominant arteriopathy with subcortical infarct and leukoencephalopathy (CADASIL) is caused by a mutation on the NOTCH3 gene. The pathological driver behind this disease is the loss of vascular smooth muscle cells (VSMCs) in small blood vessels and subsequent fibrotic thickening of the vessel, causing stenosis. READ MORE
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4. Unraveling the role of NOTCH3 dysfunction in disease and for therapy development : a focus on CADASIL
Abstract : The Notch signaling pathway, including the Notch3 receptor, is involved in many pivotal contexts of cell signaling and cell fate determination processes during development and in adulthood. Different mutations in the NOTCH3 receptor, which is highly expressed in vascular smooth muscle cells (VSMC), are associated with various diseases, including developmental disorders, several forms of cancer, and vascular dementia. READ MORE
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5. Molecular diversity in the Notch receptor family
Abstract : We have studied the Notch family of transmembrane receptors, which play a crucial role in cell fate determination. The Notch signalling pathway represents a conserved mechanism to mediate signalling between adjacent, equivalent cells and to direct them to adopt different cell fates. READ MORE