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Review: cerebral microvascular pathology in ageing and neurodegeneration.

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TLDR
Cerebral microvascular pathology in ageing and neurodegeneration is a major concern in the field of neuropathology and Applied Neurobiology.
Abstract
This review of age-related brain microvascular pathologies focuses on topics studied by this laboratory, including anatomy of the blood supply, tortuous vessels, venous collagenosis, capillary remnants, vascular density and microembolic brain injury. Our studies feature thick sections, large blocks embedded in celloidin, and vascular staining by alkaline phosphatase. This permits study of the vascular network in three dimensions, and the differentiation of afferent from efferent vessels. Current evidence suggests that there is decreased vascular density in ageing, Alzheimer's disease and leukoaraiosis, and cerebrovascular dysfunction precedes and accompanies cognitive dysfunction and neurodegeneration. A decline in cerebrovascular angiogenesis may inhibit recovery from hypoxia-induced capillary loss. Cerebral blood flow is inhibited by tortuous arterioles and deposition of excessive collagen in veins and venules. Misery perfusion due to capillary loss appears to occur before cell loss in leukoaraiosis, and cerebral blood flow is also reduced in the normal-appearing white matter. Hypoperfusion occurs early in Alzheimer's disease, inducing white matter lesions and correlating with dementia. In vascular dementia, cholinergic reductions are correlated with cognitive impairment, and cholinesterase inhibitors have some benefit. Most lipid microemboli from cardiac surgery pass through the brain in a few days, but some remain for weeks. They can cause what appears to be a type of vascular dementia years after surgery. Donepezil has shown some benefit. Emboli, such as clots, cholesterol crystals and microspheres can be extruded through the walls of cerebral vessels, but there is no evidence yet that lipid emboli undergo such extravasation.

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Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders.

TL;DR: Mechanisms of BBB dysfunction in neurodegenerative disorders, notably Alzheimer's disease, are examined, and therapeutic opportunities relating to these neurovascular deficits are highlighted.
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The pathobiology of vascular dementia

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Neuropathogenesis of delirium: review of current etiologic theories and common pathways.

TL;DR: It is unlikely that any one of these theories is fully capable of explaining the etiology or phenomenologic manifestations of delirium but rather that two or more of these act together to lead to the biochemical derangement and, ultimately, to the complex cognitive and behavioral changes characteristic ofdelirium.
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Deficiency in mural vascular cells coincides with blood-brain barrier disruption in alzheimer’s disease

TL;DR: A decrease in mural vascular cells in AD is demonstrated, and it is shown that pericyte number and coverage in the cortex and hippocampus of AD subjects compared with neurologically intact controls are reduced, contributing to disrupted vascular barrier properties and resultant neuronal dysfunction during AD pathogenesis.
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White matter changes in Alzheimer's disease: a focus on myelin and oligodendrocytes.

TL;DR: It is concluded that white matter abnormalities, and in particular myelin and oligodendrocytes, could be mechanistically important in AD pathology and could be potential treatment targets.
References
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Molecular regulation of angiogenesis and lymphangiogenesis.

TL;DR: The angiogenic growth of blood vessels and lymphatic vessels coordinates several biological processes such as cell proliferation, guided migration, differentiation and cell–cell communication.
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Longitudinal assessment of neurocognitive function after coronary-artery bypass surgery.

TL;DR: In this article, the effect of perioperative decline on long-term cognitive function after coronary-artery bypass grafting (CABG) surgery was investigated in 261 patients who underwent CABG, and neurocognitive tests were performed preoperatively (at base line), before discharge, and six weeks, six months, and five years after the surgery.
Journal ArticleDOI

Basement membranes: structure, assembly and role in tumour angiogenesis

TL;DR: The basement membrane (BM) as mentioned in this paper is a specialized form of extracellular matrix (ECM) which mediates tissue compartmentalization and sends signals to epithelial cells about the external microenvironment.
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