Urinary kallidinogenase for the treatment of cerebral arterial stenosis

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Urinary kallidinogenase for the treatment of cerebral arterial stenosis

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Author(s): Liandong Zhao ¹ ^, ² , Ying Zhao ² , Qi Wan ¹ , Haijun Zhang ³

Publication date (Electronic): 13 October 2015

Journal: Drug Design, Development and Therapy

Publisher: Dove Medical Press

Keywords: urinary kallidinogenase, arterial stenosis, Alzheimer’s disease, Aβ1-40, Aβ1-42

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Abstract

Aim

Urinary kallidinogenase (UK) has shown promise in improving cerebral perfusion. This study aimed to examine how UK affects cognitive status and serum levels of amyloid betas (Aβs) 1-40 and 1-42 in patients with cerebral arterial stenosis.

Methods

Ninety patients with cerebral arterial stenosis were enrolled, of whom 45 patients received UK + conventional treatment (UK group), and 45 patients received conventional treatment alone as control group. Cognitive status and Aβ1-40 and Aβ1-42 serum levels were determined before treatment and at 4 weeks and 8 weeks after treatment.

Results

At 4 weeks after treatment, cognitive status in patients treated with UK clearly improved accompanied by Aβ1-40 serum levels decreasing while there was no change of Aβ1-42. Cognitive status in patients receiving UK continued to improve, Aβ1-40 serum levels declined further as well as Aβ1-42 serum levels began to decrease dramatically at 8 weeks after treatment.

Conclusion

UK could improve cognitive status and decrease both Aβ1-40 and Aβ1-42 serum levels to prevent ischemic cerebral injury, which represents a good option for patients with cerebral arterial stenosis.

Most cited references 22

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Neuroinflammation in Alzheimer’s disease

Fengjin Zhang, Linlan Jiang (2015)

Amyloid-β plaques and neurofibrillary tangles are the main neuropathological hallmarks in Alzheimer’s disease (AD), the most common cause of dementia in the elderly. However, it has become increasingly apparent that neuroinflammation plays a significant role in the pathophysiology of AD. This review summarizes the current status of neuroinflammation research related to AD, focusing on the connections between neuroinflammation and some inflammation factors in AD. Among these connections, we discuss the dysfunctional blood–brain barrier and alterations in the functional responses of microglia and astrocytes in this process. In addition, we summarize and discuss the role of intracellular signaling pathways involved in inflammatory responses in astrocytes and microglia, including the mitogen-activated protein kinase pathways, nuclear factor-kappa B cascade, and peroxisome proliferator–activated receptor-gamma transcription factors. Finally, the dysregulation of the control and release of pro- and anti-inflammatory cytokines and classic AD pathology (amyloid plaques and neurofibrillary tangles) in AD is also reviewed.

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Circle of willis atherosclerosis is a risk factor for sporadic Alzheimer's disease.

Walter Kalback, Alex E. Roher, Dean Luehrs … (2003)

We conducted a quantitative investigation of brain arterial atherosclerotic damage and its relationship to sporadic Alzheimer's disease (AD). Fifty-four consecutive autopsy cases, 32 AD and 22 nondemented control subjects, were examined to establish the degree of arterial stenosis. Vessel external and lumenal area measurements were taken from 3-mm arterial cross-sections to calculate a stenosis index. AD patient circle of Willis arteries possessed a significant degree of stenosis as a consequence of multiple and severe atherosclerotic lesions. These lesions were significantly more severe in AD cases than in age-matched controls (P<0.0001), and the number of stenoses and the index of occlusion (R=0.67; P<0.00001) were positively correlated. In addition, the index of stenosis significantly correlated with the following measures of AD neuropathological lesions: total plaque score, neuritic plaque score, neurofibrillary tangle score, Braak stage score, and white matter rarefaction score. Our study reveals an association between severe circle of Willis atherosclerosis and sporadic AD that should be considered a risk factor for this dementia. These observations strongly suggest that atherosclerosis-induced brain hypoperfusion contributes to the clinical and pathological manifestations of AD.

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Cerebral hemodynamics and vascular risk factors: setting the stage for Alzheimer's disease.

C La Vecchia (2011)

Considerable information is currently available from neuroimaging, pathological, and population-based prospective studies showing that vascular risk factors are independently associated with an increased risk of Alzheimer's disease (AD). Many of these studies indicate that vascular risk factors can predict the clinical development of cognitive dysfunction and AD onset. This review examines the role of cerebral hemodynamics and vasoactive molecules that contribute to the regulation of cerebral perfusion and how three common vascular risk factors to AD, namely, hypertension, diabetes type 2, and atherosclerosis, can alter cerebral blood flow (CBF) regulation and generate perfusion pressure deficits. It is proposed that these vascular risk factors (and presumably other vascular risk factors) initiate chronic brain hypoperfusion that ultimately impair signaling from neurons, astrocytes, and endothelial cells to vascular smooth muscle controlling vessel diameter. Impaired signaling involving vascular pathways in the elderly can attenuate vessel tone and deregulate CBF. Noxious cerebral hemodynamic responses to vascular risk factors and chronic brain hypoperfusion are partly explained by Poiseuille's Law which states that miniscule changes in vessel diameter can have a dramatic effect on vessel resistance and on the rate of blood flow. Using Poiseuille's model, even minor narrowing of arteriolar diameter can lead to major reductions in CBF and in suboptimal delivery of high energy nutrients to the brain, with lethal consequences to brain cells that participate in cognitive function. Regional brain cell loss sets the stage for age-related cognitive impairment and AD onset. Keeping cerebral hemodynamic homeostasis by careful management of vascular risk factors could be a decisive therapeutic target in the prevention of AD.

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Author and article information

Journal

Journal ID (nlm-ta): Drug Des Devel Ther

Journal ID (iso-abbrev): Drug Des Devel Ther

Journal ID (publisher-id): Drug Design, Development and Therapy

Title: Drug Design, Development and Therapy

Publisher: Dove Medical Press

ISSN (Electronic): 1177-8881

Publication date Collection: 2015

Publication date (Electronic): 13 October 2015

Volume: 9

Pages: 5595-5600

Affiliations

[1 ]Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China

[2 ]Department of Neurology, The Second People’s Hospital of Huai’an and The Affiliated Huai’an Hospital of Xuzhou Medical College, Huai’an, Jiangsu, People’s Republic of China

[3 ]Department of Oncology, Zhongda Hospital, Medical School, Southeast University, Nanjing, People’s Republic of China

Author notes

Correspondence: Qi Wan, Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, Guangzhou Road 300, Nanjing 210029, People’s Republic of China, Tel +86 25 8371 4511, Fax +86 25 8626 0332, Email wanqisry@ 123456sina.com

Haijun Zhang, Department of Oncology, Zhongda Hospital, Medical School, Southeast University, 87 Dingjiaqiao, Nanjing 210009, People’s Republic of China, Tel/fax +86 25 8327 5418, Email zhanghaijunseu@ 123456163.com

Article

Publisher ID: dddt-9-5595

DOI: 10.2147/DDDT.S93150

PMC ID: 4610775

SO-VID: c822614c-4df4-435b-bcd8-4a376db8e24a

License:

The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

Drug Design, Development and Therapy (submit here)

Urinary kallidinogenase for the treatment of cerebral arterial stenosis

Read this article at

Abstract

Aim

Methods

Results

Conclusion

Most cited references 22

Neuroinflammation in Alzheimer’s disease

Circle of willis atherosclerosis is a risk factor for sporadic Alzheimer's disease.

Cerebral hemodynamics and vascular risk factors: setting the stage for Alzheimer's disease.

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