首页> 美国卫生研究院文献>Journal of Exercise Rehabilitation >Treadmill exercise improves motor coordination through ameliorating Purkinje cell loss in amyloid beta23-35-induced Alzheimer’s disease rats
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Treadmill exercise improves motor coordination through ameliorating Purkinje cell loss in amyloid beta23-35-induced Alzheimer’s disease rats

机译:跑步机运动可改善淀粉样蛋白β23-35诱发的阿尔茨海默氏病大鼠的浦肯野细胞损失从而改善运动协调性

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摘要

Alzheimer’s disease (AD) is a most common age-related neurodegenerative disease. AD is characterized by a progressive loss of neurons causing cognitive dysfunction. The cerebellum is closely associated with integration of movement, including motor coordination, control, and equilibrium. In the present study, we evaluated the effect of tread-mill exercise on the survival of Purkinje neurons in relation with reactive astrocyte in the cerebellum using Aβ25–35–induced AD rats. AD was induced by a bilateral intracerebroventricular (ICV) injection of Aβ25–35. The rats in the exercise groups were forced to run on a motorized treadmill for 30 min once a day for 4 weeks, starting 2 days after Aβ25–35 injection. In the present results, ICV injection of Aβ25–35 deteriorated motor coordination and balance. The number of calbindin-positive cells in the cerebellar vermis was decreased and glial fibrillary acidic protein (GFAP) expression in the cerebellar vermis was increased in the Aβ25–35-induced AD rats. Treadmill exercise improved motor coordination and balance. Treadmill exercise increased the number of Purkinje neurons and suppressed GFAP expression in the cerebellar vermis. The present study demonstrated that treadmill exercises alleviated dysfunction of motor coordination and balance by reduction of Purkinje cell loss through suppressing reactive astrocytes in the cerebellum of AD rats. The present study provides the possibility that treadmill exercise might be an important therapeutic strategy for the symptom improvement of AD patients.
机译:阿尔茨海默氏病(AD)是最常见的年龄相关性神经退行性疾病。 AD的特征在于神经元的逐渐丧失引起认知功能障碍。小脑与运动的整合密切相关,包括运动协调,控制和平衡。在本研究中,我们使用Aβ25–35诱导的AD大鼠评估了跑步机运动对小反应性星形胶质细胞相关的Purkinje神经元存活的影响。 AD是由双侧脑室内(ICV)注射Aβ25-35诱导的。运动组的大鼠被迫在Aβ25–35注射后2天开始,每天在电动跑步机上跑步30分钟,持续4周。在目前的结果中,ICV注射Aβ25-35会降低运动协调性和平衡性。在Aβ25-35诱发的AD大鼠中,小脑ver中的钙结合蛋白阳性细胞数量减少,小脑ver中的胶质纤维酸性蛋白(GFAP)表达增加。跑步机锻炼可改善运动协调性和平衡性。跑步机运动可增加小脑ver部浦肯野神经元的数量,并抑制GFAP表达。本研究表明,跑步机运动通过抑制AD大鼠小脑中的反应性星形胶质细胞,通过减少Purkinje细胞丢失来减轻运动协调和平衡功能障碍。本研究提供了跑步机运动可能是改善AD患者症状的重要治疗策略的可能性。

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