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      Urinary kallidinogenase for the treatment of cerebral arterial stenosis

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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.

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          Most cited references 21

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

          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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              Severe carotid stenosis and impaired cerebral hemodynamics can influence cognitive deterioration.

              To evaluate whether severe carotid stenosis and related hemodynamics impairment may increase the risk of cognitive deterioration in asymptomatic subjects. A total of 210 subjects with unilateral asymptomatic severe carotid stenosis and 109 healthy controls were included and prospectively evaluated for a 36-month period. At entry, demographics, vascular risk profile, and pharmacologic treatments were defined. Cerebral hemodynamics was assessed by transcranial Doppler-based breath-holding index (BHI) test. Cognitive status was evaluated with the Mini-Mental State Examination (MMSE) at entry and at the end of the follow-up period. Cognitive deterioration was defined as a decrease in the MMSE score of 3 points or more during the overall follow-up period. Subjects with carotid stenosis showed an increased probability of developing cognitive deterioration compared with the group without stenosis (odds ratio [OR] 4.16 [95% confidence interval (CI) 1.89-9.11]; p < 0.001). The presence of an impaired BHI ipsilateral to the stenosis was associated with an increased incidence of reduction in cognitive performance (OR 14.66 [95% CI 7.51-28.59]; p < 0.001). Our findings show that the presence of a severe carotid stenosis influences cognitive deterioration over a 36-month period in asymptomatic subjects. An associated hemodynamic impairment significantly increases the risk. Evaluation of functional consequences of carotid stenosis may offer the opportunity to select a group with an increased risk of developing cognitive impairment from subjects with asymptomatic severe carotid stenosis.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2015
                13 October 2015
                : 9
                : 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
                dddt-9-5595
                10.2147/DDDT.S93150
                4610775
                © 2015 Zhao et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) 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.

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                Original Research

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