cerebral amyloid angiopathy/hypoxia

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Hypoxia and reoxygenation of brain microvascular smooth muscle cells in vitro: cellular responses and expression of cerebral amyloid angiopathy-associated proteins.

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Hypoxia is known to cause complex cascades of physiological, biochemical, and morphological changes in the brain. Cerebral microvascular smooth muscle cell (MV-SMC) damage may occur following hypoxic conditions and lead to SMC dysfunction. However, little is known about the exact cellular and

Non-CAA angiopathies and their possible interactions with cerebral amyloid angiopathy.

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Cerebral amyloid angiopathy (CAA) is one of the two most common cerebral arteriopathies seen in the brains of elderly patients. The other is arteriosclerosis (AS), historically considered a consequence of chronic hypertension and also described as lipohyalinosis (LH), a clinicopathologic association

Angiopoietin like-4 as a novel vascular mediator in capillary cerebral amyloid angiopathy.

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Increasing evidence suggests that vascular dysfunction in the brain is associated with early stages of Alzheimer's disease. Amyloid-β deposition in the microvasculature of the brain, a process referred to as capillary cerebral amyloid angiopathy (capillary CAA), propagates vascular remodelling,

ABCG2 is upregulated in Alzheimer's brain with cerebral amyloid angiopathy and may act as a gatekeeper at the blood-brain barrier for Abeta(1-40) peptides.

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Alzheimer's disease (AD) is characterized by accumulation and deposition of Abeta peptides in the brain. Abeta deposition in cerebrovessels occurs in many AD patients and results in cerebral amyloid angiopathy (AD/CAA). Since Abeta can be transported across blood-brain barrier (BBB), aberrant Abeta

Effects of anoxia and hypoxia on amyloid precursor protein processing in cerebral microvascular smooth muscle cells.

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Cerebral amyloid angiopathy (CAA) is characterized by the degeneration of cerebral microvascular smooth muscle cells (MV-SMC) and the replacement of normal vessel wall components by beta-amyloid (Abeta) protein. Little is known regarding the mechanisms of SMC degeneration in CAA. The effects of

Hypoxia and GABA shunt activation in the pathogenesis of Alzheimer's disease.

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We have previously observed that the conversion of mild cognitive impairment to definitive Alzheimer's disease (AD) is associated with a significant increase in the serum level of 2,4-dihydroxybutyrate (2,4-DHBA). The metabolic generation of 2,4-DHBA is linked to the activation of the γ-aminobutyric

Vascular change of hippocampal capillary is associated with vascular change of retinal capillary in aging.

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Vascular deficiency, such as deleterious change of endothelial cells, becomes the prominent feature of hippocampal microvessels during the processes of aging in rodents and it seems to be associated with deficiency of intellectual behavior in aged subjects. The hippocampal microvessels and

Smooth muscle cells and the pathogenesis of cerebral microvascular disease ("angiomyopathies").

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Many forms of human cerebral microvascular disease result from abnormal proliferation and/or degeneration of smooth muscle cells (SMC) in the vessel wall of arteries and arterioles. Human cerebral microvessel-derived smooth muscle cells (MV-SMC) in culture can be used to study the pathogenesis of

Modeling cerebrovascular pathophysiology in amyloid-β metabolism using neural-crest-derived smooth muscle cells.

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There is growing recognition of cerebrovascular contributions to neurodegenerative diseases. In the walls of cerebral arteries, amyloid-beta (Aβ) accumulation is evident in a majority of aged people and patients with cerebral amyloid angiopathy. Here, we leverage human pluripotent stem cells to

Chronic cerebral hypoperfusion alters amyloid-β transport related proteins in the cortical blood vessels of Alzheimer's disease model mouse.

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Abnormal accumulation of amyloid-β (Aβ) peptide defines progression of Alzheimer's disease (AD) pathology in brain. Here, we investigated expressive changes of two main Aβ transport receptors low-density lipoprotein receptor related protein-1 (LRP1) and receptor for advanced glycation end products

Is Vasomotion in Cerebral Arteries Impaired in Alzheimer's Disease?

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A substantial body of evidence supports the hypothesis of a vascular component in the pathogenesis of Alzheimer's disease (AD). Cerebral hypoperfusion and blood-brain barrier dysfunction have been indicated as key elements of this pathway. Cerebral amyloid angiopathy (CAA) is a cerebrovascular

SRF and myocardin regulate LRP-mediated amyloid-beta clearance in brain vascular cells.

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Amyloid beta-peptide (Abeta) deposition in cerebral vessels contributes to cerebral amyloid angiopathy (CAA) in Alzheimer's disease (AD). Here, we report that in AD patients and two mouse models of AD, overexpression of serum response factor (SRF) and myocardin (MYOCD) in cerebral vascular smooth

Post-mortem assessment of hypoperfusion of cerebral cortex in Alzheimer's disease and vascular dementia.

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Perfusion is reduced in the cerebral neocortex in Alzheimer's disease. We have explored some of the mechanisms, by measurement of perfusion-sensitive and disease-related proteins in post-mortem tissue from Alzheimer's disease, vascular dementia and age-matched control brains. To distinguish

Cognitive impairment and cellular/vascular changes in the cerebral white matter.

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A possible relation between cerebral white-matter injury and dementia was intuitively attributed by Alzheimer to changes affecting the small penetrating vessels that supply the cerebral white matter. Several observations support the view that white-matter changes detectable by neuroimaging may

Potential predictors of hippocampal atrophy in Alzheimer's disease.

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The hippocampus is a vulnerable and plastic brain structure that is damaged by a variety of stimuli, e.g. hypoxia, hypoperfusion, hypoglycaemia, stress and seizures. Alzheimer's disease is a common and important disorder in which hippocampal atrophy is reported. Indeed, the available evidence

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