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1.
帕金森病是人类常见的神经退行性疾病之一,其病理机制复杂,病因目前仍不清楚。近年来,帕金森病进程中免疫炎性反应引起人们的关注,小胶质细胞的激活以及炎性因子的高表达参与了帕金森病的发生、发展过程。因此,建立合适的帕金森病动物模型有助于更好地阐明其发病机制和筛选有效的治疗药物。脂多糖诱导的神经炎症可以复制一些帕金森病的病理特征。本文综述了脂多糖致帕金森病动物模型,并分析评价其特点和适用性。  相似文献   

2.
葡萄膜炎是临床常见的眼科疾病,易复发及致盲,我国约有5%~20%的法定盲是由葡萄膜炎引起,葡萄膜炎致病因素较为复杂,其中自身免疫反应是最重要的病因之一.免疫抑制剂是临床治疗葡萄膜炎的最常用药物,以激素最为常见.由于该病的发病机制尚未明确,因此需要建立合适的动物模型加以研究.内毒素诱导的葡萄膜炎(EIU)动物模型是目前研究葡萄膜炎发病机制和药物治疗的重要模型.本文就EIU模型的机制与疾病表现结合临床药物治疗与基础实验用药,对动物模型葡萄膜炎进行相关综述.  相似文献   

3.
帕金森病是一种常见的神经退行性疾病,利用脊椎动物模型和组织培养系统可对神经退行性疾病病理进行有价值的研究,但帕金森病及其治疗药物的病理、药理分子机制研究尚待深入.本文阐述如何利用线虫的遗传学和神经生物学特点对帕金森病及治疗药物进行研究和评价.  相似文献   

4.
主动脉瘤是常见的心血管疾病, 发病率逐年攀升, 目前无有效的药物预防和控制疾病进展, 手术是唯一的治疗方式, 但手术的风险较高, 并发症也较多, 因此, 深入研究主动脉瘤的发生机制并针对机制开发防治主动脉瘤的药物具有重要的意义, 稳定且能够模拟主动脉瘤发病进程的精准动物模型是主动脉瘤基础与临床转化研究的基本保障。目前主动脉瘤的建模方法较多, 各有特色, 本文就主动脉瘤动物模型的建立方法、优缺点及其应用进行综述。  相似文献   

5.
帕金森病是老年人常见的神经系统慢性进行性疾病,严重影响病人的健康和生活质量.本文对已上市和正在进行临床试验的十多个抗帕金森病药物的作用机制、疗效、给药剂量方案、毒副作用等作一综述.  相似文献   

6.
慢性非细菌性前列腺炎是泌尿科的常见疾病之一,症状复杂,病程迁延,严重影响患者的生活质量.慢性非细菌性前列腺炎发病机制目前尚不确定,制备理想的慢性非细菌性前列腺炎动物模型对研究其发病机制和治疗药物具有重要的现实意义.本文就慢性非细菌性前列腺炎的动物模型的最新研究进展作简要综述,并对各种模型的特点进行评析.  相似文献   

7.
帕金森病的药物治疗   总被引:3,自引:0,他引:3  
杨颖琳  史美甫 《中国药业》2005,14(12):19-22
目的:介绍帕金森病近年来的药物治疗进展.方法:对帕金森病治疗药物的种类、用法、不良反应及各自的优缺点进行总结.结果:目前最有效的药物是左旋多巴/卡比多巴,此外尚有多巴胺激动剂(包括麦角胺类及非麦角胺类)、儿茶酚-O-甲基转移酶抑制剂、单胺氧化酶B抑制剂、抗胆碱能药物及其他药物等,所有药物均有一定的不良反应.结论:现有药物治疗仅可明显改善症状,延缓疾病发展,但均不能有效治愈帕金森病.  相似文献   

8.
肠易激综合征发病机理迄今仍不明确,治疗尚无特效药物.选择一种客观、公认、具有良好重现性的动物模型是研究IBS病理生理、发病机制、药物治疗的基础,然而目前尚无统一公认的IBS动物模型.本文对目前国内外相关动物模型的制备方法、造模机理、优缺点进行综述,以期对IBS动物模型的研究及应用提供参考和借鉴.  相似文献   

9.
孙泓  蒲小平 《中国新药杂志》2007,16(22):1844-1848
胆石病是一种发生在胆囊和胆管的常见病、多发病,涉及一系列复杂的细胞及分子机制,如何制作和选择与人类胆石病相似的动物模型,不仅是深入研究胆石病发病机制的重要基础,也是筛选防治胆石病药物的有效手段。现概述目前常用的胆石病动物模型,并介绍胆石病药物靶点与治疗药物的研究进展。  相似文献   

10.
帕金森病的药物治疗   总被引:3,自引:0,他引:3  
帕金森病作为中老年人常见的神经系统变性病,对老年人健康生活影响极大,目前尚无治愈方法,仍需依靠药物控制症状,改善患者生活质量。本文对帕金森病药物治疗的各种常用药物、主要研究进展及药物治疗原则做一介绍。  相似文献   

11.
Studies have implicated methamphetamine exposure as a contributor to the development of Parkinson’s disease. There is a significant degree of striatal dopamine depletion produced by methamphetamine, which makes the toxin useful in the creation of an animal model of Parkinson’s disease. Parkinson’s disease is a progressive neurodegenerative disorder associated with selective degeneration of nigrostriatal dopaminergic neurons. The immediate need is to understand the substances that increase the risk for this debilitating disorder as well as these substances’ neurodegenerative mechanisms. Currently, various approaches are being taken to develop a novel and cost-effective anti-Parkinson’s drug with minimal adverse effects and the added benefit of a neuroprotective effect to facilitate and improve the care of patients with Parkinson’s disease. A methamphetamine-treated animal model for Parkinson’s disease can help to further the understanding of the neurodegenerative processes that target the nigrostriatal system. Studies on widely used drugs of abuse, which are also dopaminergic toxicants, may aid in understanding the etiology, pathophysiology and progression of the disease process and increase awareness of the risks involved in such drug abuse. In addition, this review evaluates the possible neuroprotective mechanisms of certain drugs against methamphetamine-induced toxicity.  相似文献   

12.
An important conceptual development to avoid the occurrence of motor dyskinesias in Parkinson’s disease is continuous dopaminergic stimulation. Studies in animal models and humans suggest that continuous dopaminergic stimulation could be achieved by the infusions of different dopamine agonists or levodopa, and may significantly reduce the risk of dyskinesias associated with treatment strategies utilising pulsatile treatment options. However, so far, these techniques have either necessitated frequent intake of oral therapy or invasive parenteral treatment. The rotigotine transdermal delivery system represents a significant development that allows a constant delivery of a non-ergot dopamine agonist using a once-daily regimen, achieving steady plasma levels. Clinical trials demonstrate the efficacy of rotigotine in early and advanced Parkinson’s disease, with important implications for treatment of non-motor symptoms of Parkinson’s disease.  相似文献   

13.
Oxidative stress is a ubiquitously observed hallmark of neurodegenerative disorders. Neuronal cell dysfunction and cell death due to oxidative stress may causally contribute to the pathogenesis of progressive neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, as well as acute syndromes of neurodegeneration, such as ischaemic and haemorrhagic stroke. Neuroprotective antioxidants are considered a promising approach to slowing the progression and limiting the extent of neuronal cell loss in these disorders. The clinical evidence demonstrating that antioxidant compounds can act as protective drugs in neurodegenerative disease, however, is still relatively scarce. In the following review, the available data from clinical, animal and cell biological studies regarding the role of antioxidant neuroprotection in progressive neurodegenerative disease will be summarised, focussing particularly on Alzheimer’s disease, Parkinson’s disease, Huntington’s disease and amyotrophic lateral sclerosis. The general complications in developing potent neuroprotective antioxidant drugs directed against these long-term degenerative conditions will also be discussed. The major challenges for drug development are the slow kinetics of disease progression, the unsolved mechanistic questions concerning the final causalities of cell death, the necessity to attain an effective permeation of the blood–brain barrier and the need to reduce the high concentrations currently required to evoke protective effects in cellular and animal model systems. Finally, an outlook as to which direction antioxidant drug development and clinical practice may be leading to in the near future will be provided.  相似文献   

14.
This was a small (~ 50 people) focused meeting on neurodegenerative disorders, with most of the speakers being from biotechnology or major pharmaceutical companies. The meeting covered a range of topics including introductions to Alzheimer’s disease and Parkinson’s disease, examples of targeting particular receptors/pathways, animal models and preclinical studies, clinical trial design and the use of biomarkers and imaging modalities. The major focus in the Alzheimer’s disease area was finding symptomatic treatments that are superior to acetylcholinesterase inhibitors and the extensive efforts that are ongoing to develop disease-modifying therapies. In terms of Parkinson’s disease there are now several reports examining the effects of dopamine agonists versus 3,4-dihydroxyphenylalanine on disease progression, and ongoing work with growth factors (e.g., glial cell line-derived neurotrophic factor) and mixed lineage/c-Jun N-terminal kinase inhibitors, such as CEP-1347. Small molecules that enhance endogenous signalling and repair pathways were also discussed.  相似文献   

15.
Introduction: Parkinson’s disease is a progressive neurodegenerative disease that affects millions of elderly individuals worldwide. Despite intensive efforts dedicated to find a better treatment, the pathogenesis of Parkinson’s Disease remains unknown. In search for a better therapy for the disease, several new in vivo and in vitro models of Parkinson´s disease have been developed in recent times.

Areas covered: The authors provide an outline of the various traditional models of Parkinson´s disease and address those that have been recently generated. They also discuss the utility of these models for the identification of drugs of potential therapeutic value for Parkinson´s Disease patients. From the cell based models and the well-known toxin-based animal models, to the recent genetic models and the increasingly used non-mammalian models, every model is worthwhile in the search for a better Parkinson´s Disease therapy.

Expert opinion: Almost 60 years after its discovery, levodopa is still the gold standard treatment for Parkinson's Disease patients. It seems unlikely that a single model can fully recapitulate the complexity of Parkinson's Disease in the same way it appears improbable that a unique treatment could relieve both the motor and non-motor symptoms of Parkinson's Disease altogether. Therefore treatment will probably require a combination of therapies.  相似文献   


16.
The risk of Parkinson’s disease is reduced by cigarette smoking, which raises some unanswered questions. Nicotine, a major component of tobacco smoke, could exert either nonreceptor-mediated biological effects or, more importantly, act on the different subtypes of nicotinic brain receptors, in particular those associated with the nigrostriatal dopaminergic pathway. There is now robust experimental evidence for a neuroprotective effect of nicotine upon dopaminergic neurons. By contrast, in animal models of Parkinson’s disease, nicotine alone has slight or no motor effects. However, nicotine may modulate dopamine transmission and has clear motor effects when associated with L-DOPA, reducing L-DOPA-induced dyskinesias. Clinical trials have yielded inconclusive results thus far and are hampered by different designs and small cohorts. Ongoing studies address either symptomatic motor or nonmotor symptoms, or neuroprotection. There is still no agreement on the daily dosage of nicotine or the method of administration. Together, these data suggest that nicotine or nicotinic receptor drugs have therapeutic potential for Parkinson’s disease, although the specific treatment regimens remain to be determined.  相似文献   

17.
Parkinson’s disease affects more than 1% of individuals older than 60 years of age. The gold standard of its symptomatic treatment is levodopa therapy, which in time leads to motor fluctuations and dyskinesia due to noncontinuous receptor stimulation. Dopamine agonists and monoamine oxidase-B inhibitors are recommended as initial therapy, but they are less effective in the advanced stages of the disease. Treatment should be individualized for the patient, dependent on the stage, with attention to nonmotor symptoms. No effective neuroprotective therapy for Parkinson’s disease is yet available, and there is currently substantial interest in the development of new nondopaminergic agents. Analogs of kynurenic acid and inhibitors of the enzymes involved in the synthesis of quinolinic acid may exert a neuroprotective effect.  相似文献   

18.
Parkinson’s disease (PD) is a debilitating neurodegenerative condition that is characterised by a progressive loss of dopaminergic neurones of the substantia nigra pars compacta (SNpc) and the presence of α-synuclein cytoplasmic inclusions (Lewy bodies). Cardinal symptoms include tremor, bradykinesia, and rigidity, although cognitive and autonomic disturbances are not uncommon. Pharmacological treatment targeting the dopaminergic network is relatively effective at ameliorating these symptoms, especially in the early stages of the disease, but none of these therapies are curative and they generate their own problems. As dopaminergic neuronal death in PD occurs in a gradual manner, it is amenable to treatments that can either protect remaining dopaminergic neurones or prevent death of those neurones that have begun to die. Use of neurotrophic factors is a potential candidate, as various factors have been shown to increase dopaminergic neuronal survival in culture and promote survival and axonal growth in animal models of PD. Glial cell line-derived neurotrophic factor (GDNF) is currently the most effective substance that has been intensively studied and shown to have a specific ‘dopaminotrophic’ effect. This review will therefore focus on studies that have investigated GDNF and discuss the potential for neurotrophic factor treatment in PD.  相似文献   

19.
Apoptosis is a form of physiological or programmed cell death. It has been speculated that this process might account for the death of selective neuronal populations in certain progressive neurodegenerative disorders, including Alzheimer’s disease (AD) and Parkinson’s disease (PD) and some circumstantial evidence to support this view has been forthcoming. Increased understanding of the molecular pathophysiology of neuronal apoptosis may therefore present significant new therapeutic targets, to slow or halt neurodegeneration. This article reviews patents from the last five years which claim the use of apoptotic modulators in neurodegenerative disease. Although there are a significant number of claims, very few are buttressed with strong experimental evidence; this is usually from cell culture studies, rather than animal models of neurodegenerative disease; only a single human clinical study was identified. Thus, although treatment of neurodegenerative disease by means of manipulating apoptosis is an area of much activity and holds promise for the future, clinical application of current patents is unlikely in the near future. Extant medications may conceivably exert some of their action through effects on apoptosis.  相似文献   

20.
Bee venom (BV), also known as apitoxin, is widely used in traditional oriental medicine to treat immune-related diseases. Recent studies suggest that BV could be beneficial for the treatment of neurodegenerative diseases. Parkinson’s disease (PD) is the second most common neurodegenerative disease next to Alzheimer’s disease, and PD pathologies are closely associated with neuroinflammation. Previous studies have suggested the neuroprotective effects of BV in animal models of PD are due to the modulation of inflammation. However, the molecular mechanisms responsible for the anti-neuroinflammatory effect of BV have not been elucidated in astrocytes. Here, the authors investigated the neuroprotective effects of BV and pramipexole (PPX; a positive control) in a subchronic MPTP-induced murine PD model. Both BV and PPX prevented MPTP-induced impairments in motor performance and reduced dopaminergic neuron loss, and furthermore, these neuroprotective effects of BV and PPX were found to be associated with reduced astroglial activation in vivo PD model. However, in MPP+ treated primary cultured astrocytes, BV modulated astrocyte activation, whereas PPX did not, indicating that the neuroprotective effects of PPX were not mediated by neuroinflammation. These findings suggest that BV should be considered a potential therapeutic or preventive agent for PD and other neuroinflammatory associated disorders.  相似文献   

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