dl-3-正丁基邻苯二甲酸与α-突触核蛋白抗体的纳米线递送增强了情绪应激帕金森病的神经保护作用。

International review of neurobiology Pub Date : 2023-01-01 Epub Date: 2023-07-20 DOI:10.1016/bs.irn.2023.06.005
Lianyuan Feng, Aruna Sharma, Zhenguo Wang, Dafin F Muresanu, Z Ryan Tian, José Vicente Lafuente, Anca D Buzoianu, Ala Nozari, Cong Li, Ziquiang Zhang, Chen Lin, Hongyun Huang, Igor Manzhulo, Lars Wiklund, Hari Shanker Sharma
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引用次数: 0

摘要

压力是生活中最严重的后果之一,会导致多种慢性疾病和神经退行性变。最近的研究表明,情绪压力和其他类型的焦虑和抑郁会对帕金森氏症症状产生不利影响。然而,压力如何影响帕金森氏症的细节仍不清楚。众所周知,创伤性脑损伤、中风、糖尿病、创伤后应激障碍会改变疾病的沉淀、进展和持续性。然而,压力可能影响帕金森氏症的研究还不为人所知。本研究在模型实验中检验了固定应激对帕金森病大脑病理的影响。在之前的报告中,我们发现轻度创伤性脑损伤会加剧帕金森病的脑病理,单独或与间充质干细胞一起纳米递送dl-3-正丁基邻苯二甲酸可显著减轻帕金森病的大脑病理。在本章中,我们讨论了压力在加重帕金森病病理中的作用,并且dl-3-正丁基邻苯二甲酸与α-突触核蛋白单克隆抗体(ASNC)的纳米线递送能够诱导显著的神经保护作用。讨论了dl-3-正丁基邻苯二甲酸和ASNC诱导神经保护的可能机制和合适的临床治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nanowired delivery of dl-3-n-butylphthalide with antibodies to alpha synuclein potentiated neuroprotection in Parkinson's disease with emotional stress.

Stress is one of the most serious consequences of life leading to several chronic diseases and neurodegeneration. Recent studies show that emotional stress and other kinds of anxiety and depression adversely affects Parkinson's disease symptoms. However, the details of how stress affects Parkinson's disease is still not well known. Traumatic brain injury, stroke, diabetes, post-traumatic stress disorders are well known to modify the disease precipitation, progression and persistence. However, show stress could influence Parkinson's disease is still not well known. The present investigation we examine the role of immobilization stress influencing Parkinson's disease brain pathology in model experiments. In ore previous report we found that mild traumatic brain injury exacerbate Parkinson's disease brain pathology and nanodelivery of dl-3-n-butylphthalide either alone or together with mesenchymal stem cells significantly attenuated Parkinson's disease brain pathology. In this chapter we discuss the role of stress in exacerbating Parkinson's disease pathology and nanowired delivery of dl-3-n-butylphthalide together with monoclonal antibodies to alpha synuclein (ASNC) is able to induce significant neuroprotection. The possible mechanisms of dl-3-n-butylphthalide and ASNC induced neuroprotection and suitable clinical therapeutic strategy is discussed.

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