Alzheimer`s disease (AD) posses a massive burden, but therapeutic options are currently limited to treatments that alleviate symptoms, without altering the disease progression. The paucity of therapeutic options is demanding a thorough re-examination of the pathophysiology of AD. Recent research has ...
Alzheimer`s disease (AD) posses a massive burden, but therapeutic options are currently limited to treatments that alleviate symptoms, without altering the disease progression. The paucity of therapeutic options is demanding a thorough re-examination of the pathophysiology of AD. Recent research has implicated a strong involvement of the vasculature in the pathogenesis of the disease. Pathological studies, imaging studies as well as studies with mouse models of AD have provided evidence for impaired neurovascular regulation of cerebral blood flow, aberrations in vascular morphology and density. Since the brain critical depends on the continuous supply of oxygen and nutrients, vascular deficits can constitute important causes of neurodegeneration and cognitive decline. Moreover, cerebral amyloid angiopathy induces changes in the proteolytic microenvironment with impairment of blood–brain barrier integrity, the occurrence of cerebral microbleeds and intracerebral hemorrhage. This in turn can cause dementia or aggravate existing cognitive deficits. Moreover, epidemiological studies have shown that risk factors for cardiovascular diseases like diabetes, hypertension and physical inactivity are also putative risk factors for AD, indicating that they share pathogenic mechanisms. Also, AD and vascular dementia often co-exist in patients with dementia, making a clear distinction between the two conditions elusive. Hence, approaches are needed which address the vascular aspects of AD and study the pathomechanism of the disease not only for neurons, but also integrate all cell types of the neurovascular unit including endothelial cells, perictyes, smooth muscle cells and astrocytes.
This Research Topic will discuss the vascular aspects of AD and the therapeutic opportunities relating to these vascular deficits. Topics may include but are not limited to:
• Association between cerebrovascular disease and AD
• Vascular dementia
• Microvessel pathology
• mechanisms of cerebrovascular dysfunction
• Blood-brain barrier impairment
• Cerebral hypoperfusion and ischemia
• Cerebral microbleeds, hemorrhages
• Hypertension, atherosclerosis, diabetes
• Imaging and novel diagnostics
• Animal models with vascular pathology/animal models of vascular dementia.
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