Angiogenic proteins are expressed by brain blood vessels in Alzheimer's disease

Thirumangalakudi, Lakshmi; Samany, Pezhman Ghatreh; Owoso, Akinkunle; Wiskar, Brandt; Grammas, Paula

doi:10.3233/jad-2006-10114

Cited by 103 publications

(80 citation statements)

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“…In AD, trans-endothelial trafficking of leukocytes from vascular compartment into the brain parenchyma involves MMPs, which remodel ECM and junctional components (White et al 2006). Expression of MMPs is regulated at transcriptional, translational, and post-translational levels with tissue inhibitor of metalloproteinase (TIMP) (Flex et al 2006;Thirumangalakudi et al 2006). MMP-9 and TIMPs are elevated in postmortem brain tissue of AD patients (Shibata et al 2005).…”

Section: Matrix Metalloproteinases In Ad Pathogenesis Under Oxidativementioning

confidence: 99%

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

2011

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Oxidative stress has been proposed to be an important factor in the pathogenesis of Alzheimer's disease (AD) and contributed to β-amyloid (Aβ) generation. Interaction between oxidative stress and neuro-inflammation leads to Aβ generation. AD is associated with an increase in blood-brain barrier (BBB) permeability due to tight junction involvement. Oxidative stress decreases the expression of low-density lipoprotein receptor-related protein 1 and up-regulates receptor for advanced glycation end products in BBB and increases the BBB permeability, which could potentially lead to increased deposition of Aβ within AD brain. Apoptosis takes place in the pathogenesis of AD, and oxidative stress contributes to apoptosis through both extrinsic pathway and intrinsic pathway. Oxidative stress-induced apoptosis may be a potential factor to Aβ generation. Aβ generation requires two sequential cleavages of APP, with the two proteolytic enzymes: β-secretase and γ-secretase. Oxidative damage up-regulates Aβ via inducing activity of β- and γ-secretases. In this review, we will focus on the mechanism and pathway that oxidative stress contributes to Aβ generation.

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Section: Matrix Metalloproteinases In Ad Pathogenesis Under Oxidativementioning

confidence: 99%

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

2011

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“…Elevated levels of Ang-2 and VEGF were found in cerebral blood vessels of AD patients, resulting in impaired BBB integrity. 103 While these factors normally promote angiogenesis, there is a no increased vascularity in AD, probably because of the anti-angiogenic properties of Ab. 103 A different study showed elevated serum levels of Ang-1 in AD patients.…”

Section: Angiopoietinsmentioning

confidence: 99%

“…103 While these factors normally promote angiogenesis, there is a no increased vascularity in AD, probably because of the anti-angiogenic properties of Ab. 103 A different study showed elevated serum levels of Ang-1 in AD patients. The cognitive performance of the subjects was evaluated using the mini-mental state examination and a correlation was found Table 2.…”

Section: Angiopoietinsmentioning

confidence: 99%

Morphogens and blood-brain barrier function in health and disease

Wevers

Vries

2015

Tissue Barriers

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“…Recent findings support its key role in cell adhesion in inflammatory processes and angiogenesis [8]. Therefore, it can be speculated that endocan may play a role in the pathogenesis of AD [4, 7, 8]. …”

Section: Introductionmentioning

confidence: 99%

“…Recent studies have supported accompanying cerebrovascular pathology in the pathogenesis of AD [1-3]. Cerebral hypoperfusion and angiogenic activation of the brain endothelium are supposed to play an important role in the deposition of amyloid plaques and in inflammatory processes, which causes neuronal death [4, 5]. In addition, supporting this knowledge, increased expression of angiogenic factors, like transforming growth factor-β (TGF-β) and VEGF, has been shown to be related to AD in some studies [2, 4, 6, 7].…”

Section: Introductionmentioning

confidence: 99%

Higher Serum Endocan Level Is Associated with Alzheimer Disease

Varan

Guner

Sümer

et al. 2017

Dement Geriatr Cogn Disord

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Background: The novel molecule endocan, which is released by endothelium and is regulated by proangiogenic and proinflammatory cytokines, may have a role in the pathophysiology of Alzheimer disease (AD). The aim of this study was to evaluate the relationship between serum endocan levels and AD. Methods: A total of 134 patients (47 AD, 42 amnestic mild cognitive impairment [aMCI], and 45 control patients) 65 years of age and older were recruited in this study. Cognitive status of the patients was evaluated by performing the Montreal Cognitive Assessment (MOCA) and the Mini-Mental State Examination (MMSE). Serum endocan levels were measured with an enzyme-linked immunosorbent assay kit. Results: Median serum endocan level was significantly higher in AD patients (380.1 ng/mL) than in both aMCI patients (247.7 ng/mL) and controls (277.6 ng/mL; p < 0.01). Serum endocan level had a weak but significant correlation with MMSE and MOCA scores (r = –0.219 and r = –0.232; p = 0.012 and p = 0.01, respectively). Serum endocan level was detected as a factor independently associated with AD. The cutoff serum level of endocan predicting AD was >288.94 ng/mL in receiver operating characteristic curve analysis (area under the curve 0.71, 95% CI 66.7–90.9, sensitivity 80.9%, specificity 59.8%; p < 0.01). Conclusion: Higher serum endocan levels may be associated with the pathogenesis of AD.

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Angiogenic proteins are expressed by brain blood vessels in Alzheimer's disease

Cited by 103 publications

References 0 publications

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

Oxidative Stress and β-Amyloid Protein in Alzheimer’s Disease

Morphogens and blood-brain barrier function in health and disease

Higher Serum Endocan Level Is Associated with Alzheimer Disease

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