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Stability of Parkinson's Diseased Animal Models Induced by Neurotoxins; a Serious Drawback to Success of Parkinson's Disease Therapeutic Studies

机译:神经毒素诱导的帕金森病变动物模型的稳定性;帕金森病治疗研究成功的严重缺点

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Parkinson's Disease (PD) arises from the degeneration of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) [1]. PD is clinically incurable since its pathological mechanism is not completely distinct [2]. The clinical manifestations of PD consist of motor symptoms such as resting tremor, hypokinesia, rigidity, and postural instability [3]. However, other non-motor complications such as olfactory, gastrointestinal, thermoregulatory and genitourinary dysfunction, sleep disturbances, anxiety, fatigue and oral cavity problems have been reported [4-9]. To effectively understand the disease mechanism through which PD operates and solves the issue of PD incurability, many animal models in combination with neurotoxins have been developed to aid in investigating this neurological disease. The most widely used neurotoxins in PD experiments that have been extensively reviewed in literature include MPTP, 6-OHDA, paraquat, and rotenone [10-20]. Animal models are important tools used to investigate the mechanisms and pharmacological therapies of PD. In recent times, researchers engaged in both in vitro and in vivo studies on PD using animal models and new improved approaches such as the temporal and cell-specific expression of mutated genes in vertebrates have been developed [21]. According to many experts in the field, non-motor features remain under-recognized, under-researched, and thus, under-treated [22, 23]. In summary, the main disadvantage of the animal models of PD reported in the literature includes the difference of the neurotoxins metabolism between the animals and humans, the difference in the brain size and complication of brain functions between tested animals and humans, which limits the direct interpretation of the experimental results to the clinic [10, 24].
机译:帕金森病(PD)的出现多巴胺能神经细胞变性是临床上不可治愈的,因为其病态机制不完全不同的[2]。PD的临床表现包括马达静止震颤等症状,运动功能减退,刚性,姿势不稳定[3]。其他非机动车嗅觉等并发症,胃肠、体温调节和泌尿生殖器的障碍、睡眠障碍、焦虑、疲劳和口腔问题据报道[第4 - 9]。这种疾病PD的运作机制和解决PD不能矫正的问题,许多动物模型结合神经毒素开发了帮助调查呢神经系统疾病。神经毒素在PD实验注射广泛地查阅的文献包括MPTP药物,6-OHDA、百草枯和鱼藤酮(10 - 20)。模型是重要的工具用于调查的机制和药物治疗PD。在体外和体内研究PD使用动物模型和新的改进方法等突变的时间和特异性表达基因在脊椎动物发展[21]。根据许多专家在这个领域,非机动车功能保持病因,尚未明确,因此under-treated[22日23)。在文献中报告的PD动物模型包括神经毒素的区别动物和人类之间的代谢,在大脑中不同大小和并发症动物和测试之间的大脑功能人类,这限制了直接的诠释实验结果的诊所(10,24)。

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