Suppr超能文献

肌酸的神经保护作用。

The neuroprotective role of creatine.

作者信息

Klein Autumn M, Ferrante Robert J

机构信息

Neurology Department, Brigham and Womens Hospital, Boston, MA 02115, USA; and Harvard Medical School, Boston, MA 02115, USA.

出版信息

Subcell Biochem. 2007;46:205-43. doi: 10.1007/978-1-4020-6486-9_11.

Abstract

Significant progress has been made in identifying neuroprotective agents and their translation to patients with neurological disorders. While the direct causative pathways of neurodegeneration remain unclear, they are under great clinical and experimental investigation. There are a number of interrelated pathogenic mechanisms triggering molecular events that lead to neuronal death. One putative mechanism reported to play a prominent role in the pathogenesis of neurological diseases is impaired energy metabolism. If reduced energy stores play a role in neuronal loss, then therapeutic strategies that buffer intracellular energy levels may prevent or impede the neurodegenerative process. Recent studies suggest that impaired energy production promotes neurological disease onset and progression. Sustained ATP levels are critical to cellular homeostasis and may have both direct and indirect influence on pathogenic mechanisms associated with neurological disorders. Creatine is a critical component in maintaining cellular energy homeostasis, and its administration has been reported to be neuroprotective in a wide number of both acute and chronic experimental models of neurological disease. In the context of this chapter, we will review the experimental evidence for creatine supplementation as a neurotherapeutic strategy in patients with neurological disorders, including Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Alzheimer's disease, as well as in ischemic stroke, brain and spinal cord trauma, and epilepsy.

摘要

在识别神经保护剂并将其应用于神经疾病患者方面已取得重大进展。虽然神经退行性变的直接致病途径仍不明确,但正在进行大量临床和实验研究。有许多相互关联的致病机制引发导致神经元死亡的分子事件。据报道,一种在神经疾病发病机制中起重要作用的假定机制是能量代谢受损。如果能量储备减少在神经元丢失中起作用,那么缓冲细胞内能量水平的治疗策略可能预防或阻碍神经退行性变过程。最近的研究表明,能量产生受损会促进神经疾病的发生和发展。持续的ATP水平对细胞稳态至关重要,可能对与神经疾病相关的致病机制产生直接和间接影响。肌酸是维持细胞能量稳态的关键成分,据报道,在多种急性和慢性神经疾病实验模型中,给予肌酸具有神经保护作用。在本章中,我们将综述补充肌酸作为神经治疗策略用于神经疾病患者(包括亨廷顿舞蹈病、帕金森病、肌萎缩侧索硬化症和阿尔茨海默病)以及缺血性中风患者、脑和脊髓创伤患者及癫痫患者的实验证据。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验