Alzheimerʼs Disease

Schliebs, Reinhard

doi:10.1007/978-3-642-30574-0_51

Cited by 2 publications

(5 citation statements)

References 244 publications

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“…Abundant evidence has already been reported on frequent occurrence of vascular changes in AD patients (for review, see Schliebs, 2013). The cerebrovascular abnormalities including thickening of the microvascular basement membranes, decreased luminal diameter, and microvascular degeneration, in particular in the temporal‐parietal cortex, have frequently been observed in AD patients (for review, see Nicolakakis and Hamel, 2011) and ultimately cause impaired cerebral perfusion (Kara et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

“…The cerebrovascular abnormalities including thickening of the microvascular basement membranes, decreased luminal diameter, and microvascular degeneration, in particular in the temporal‐parietal cortex, have frequently been observed in AD patients (for review, see Nicolakakis and Hamel, 2011) and ultimately cause impaired cerebral perfusion (Kara et al, 2012). Already more than twenty years ago, a casual relationship between vascular mechanism and development of sporadic AD has been hypothesized (De la Torre and Mussivand, 1993; for reviews, see Isingrini et al, 2009; Schliebs, 2013). The deposition of Aβ in the wall of cerebral blood vessels termed as cerebral amyloid angiopathy (CAA) provokes the cerebrovascular abnormality in AD (for review, see Schliebs, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…Already more than twenty years ago, a casual relationship between vascular mechanism and development of sporadic AD has been hypothesized (De la Torre and Mussivand, 1993; for reviews, see Isingrini et al, 2009; Schliebs, 2013). The deposition of Aβ in the wall of cerebral blood vessels termed as cerebral amyloid angiopathy (CAA) provokes the cerebrovascular abnormality in AD (for review, see Schliebs, 2013). Besides, in vivo and in vitro studies described Aβ as inhibitor of angiogenesis (Paris et al, 2004a,b).…”

Section: Introductionmentioning

confidence: 99%

“…One of the key angiogenic factors, vascular endothelial growth factor (VEGF), a highly conserved heparin-binding protein, was originally found in vascular endothelial cells. It is able to induce vascular endothelial cell proliferation, migration and vasopermeability in many types of tissue (for review, see Schliebs, 2013). As it has already been revealed, VEGF also exerts tropic and protective actions on neurons (for review, see Rosenstein and Krum, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…Alzheimer's disease (AD) is a progressive neurodegenerative disease and is the leading cause of age related, irreversible dementia. The AD is characterized by the extracellular deposition of senile plaques mainly formed of beta amyloid (Aβ), intracellular neurofibrilary tangles and neuronal loss (for reviews, see Schliebs, 2013; Schliebs and Arendt, 2011).…”

Section: Introductionmentioning

confidence: 99%

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Expression of vascular endothelial growth factor (VEGF) mRNA, VEGF receptor 2 (Flk‐1) mRNA, and of VEGF co‐receptor neuropilin (Nrp)‐1 mRNA in brain tissue of aging Tg2576 mice by in situ hybridization

Muche¹,

Bigl

Arendt

et al. 2015

Intl J of Devlp Neuroscience

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Vascular endothelial growth factor (VEGF) has been characterized as a heparin binding angiogenic growth factor displaying high specificity for endothelial cells. It is profoundly accumulated and co-localized with amyloid beta (Aβ) plaques in the brain of Alzheimer's disease patients. In order to examine the effect of Aβ plaques on the expression level of VEGF mRNA and its receptors, brain tissue of both transgenic Tg2576 and wild type mice at ages ranging from 13 to 22 months was subjected to in situ hybridization followed by densitometric assessment using computer-assisted image analysis. Strong expression of VEGF mRNA, fetal liver kinase (Flk)-1 mRNA, and neuropilin (Nrp)-1 mRNA in the piriform, entorhinal, somatosensory, frontal cortex and hippocampal formation of both transgenic and non-transgenic mice brain was detected. Developmentally, only expression of VEGF mRNA was increased with age in the entorhinal, and somatosensory cortex of wild type mice. In 20-month-old transgenic Tg2576 mice, up-regulation of VEGF mRNA, Flk-1 mRNA, and Nrp-1 mRNA transcripts was observed in the entorhinal cortex compared to age-matched wild type mice. Our data suggest up-regulation of VEGF mRNA, Flk-1 mRNA and Nrp-1 mRNA, at least in the entorhinal cortex at ages when Aβ deposition in Tg2576 is typically increasing.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Expression of vascular endothelial growth factor (VEGF) mRNA, VEGF receptor 2 (Flk‐1) mRNA, and of VEGF co‐receptor neuropilin (Nrp)‐1 mRNA in brain tissue of aging Tg2576 mice by in situ hybridization

Muche¹,

Bigl

Arendt

et al. 2015

Intl J of Devlp Neuroscience

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Hypoxic stress, brain vascular system, and β-amyloid: A primary cell culture study

Muche

Bürger

Arendt

et al. 2013

Nutritional Neuroscience

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This study stresses the hypothesis whether hypoxic events contribute to formation and deposition of β-amyloid (Aβ) in cerebral blood vessels by affecting the processing of endothelial amyloid precursor protein (APP). Therefore, cerebral endothelial cells (ECs) derived from transgenic Tg2576 mouse brain, were subjected to short periods of hypoxic stress, followed by assessment of formation and secretion of APP cleavage products sAPPα, sAPPβ, and Aβ as well as the expression of endothelial APP. Hypoxic stress of EC leads to enhanced secretion of sAPPβ into the culture medium as compared to normoxic controls, which is accompanied by increased APP expression, induction of vascular endothelial growth factor (VEGF) synthesis, nitric oxide production, and differential changes in endothelial p42/44 (ERK1/2) expression. The hypoxia-mediated up-regulation of p42/44 at a particular time of incubation was accompanied by a corresponding down-regulation of the phosphorylated form of p42/44. To reveal any role of hypoxia-induced VEGF in endothelial APP processing, ECs were exposed by VEGF. VEGF hardly affected the amount of sAPPβ and Aβ(1-40) secreted into the culture medium, whereas the suppression of the VEGF receptor action by SU-5416 resulted in decreased release of sAPPβ and Aβ(1-40) in comparison to control incubations, suggesting a role of VEGF in controlling the activity of γ-secretase, presumably via the VEGF receptor-associated tyrosine kinase. The data suggest that hypoxic stress represents a mayor risk factor in causing Aβ deposition in the brain vascular system by favoring the amyloidogenic route of endothelial APP processing. The hypoxic-stress-induced changes in β-secretase activity are presumably mediated by altering the phosphorylation status of p42/44, whereas the stress-induced up-regulation of VEGF appears to play a counteracting role by maintaining the balance of physiological APP processing.

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Alzheimerʼs Disease

Cited by 2 publications

References 244 publications

Expression of vascular endothelial growth factor (VEGF) mRNA, VEGF receptor 2 (Flk‐1) mRNA, and of VEGF co‐receptor neuropilin (Nrp)‐1 mRNA in brain tissue of aging Tg2576 mice by in situ hybridization

Expression of vascular endothelial growth factor (VEGF) mRNA, VEGF receptor 2 (Flk‐1) mRNA, and of VEGF co‐receptor neuropilin (Nrp)‐1 mRNA in brain tissue of aging Tg2576 mice by in situ hybridization

Hypoxic stress, brain vascular system, and β-amyloid: A primary cell culture study

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