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本文引用的文献

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Surveillance, phagocytosis, and inflammation: how never-resting microglia influence adult hippocampal neurogenesis.监测、吞噬作用和炎症:永不休息的小胶质细胞如何影响成年海马神经发生。
Neural Plast. 2014;2014:610343. doi: 10.1155/2014/610343. Epub 2014 Mar 19.
2
Relative importance of redox buffers GSH and NAD(P)H in age-related neurodegeneration and Alzheimer disease-like mouse neurons.氧化还原缓冲剂谷胱甘肽(GSH)和烟酰胺腺嘌呤二核苷酸(磷酸)(NAD(P)H)在与年龄相关的神经退行性变及阿尔茨海默病样小鼠神经元中的相对重要性。
Aging Cell. 2014 Aug;13(4):631-40. doi: 10.1111/acel.12216. Epub 2014 Mar 21.
3
Age-related changes in cognition and speech perception.与年龄相关的认知和言语感知变化。
Korean J Audiol. 2013 Sep;17(2):54-8. doi: 10.7874/kja.2013.17.2.54. Epub 2013 Sep 24.
4
Erythropoietin: powerful protection of ischemic and post-ischemic brain.促红细胞生成素:对缺血性和缺血后脑的强大保护作用。
Exp Biol Med (Maywood). 2014 Nov;239(11):1461-75. doi: 10.1177/1535370214523703. Epub 2014 Mar 4.
5
Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial.维生素 E 和美金刚对阿尔茨海默病功能衰退的影响:TEAM-AD VA 合作随机试验。
JAMA. 2014 Jan 1;311(1):33-44. doi: 10.1001/jama.2013.282834.
6
Heart disease and stroke statistics--2014 update: a report from the American Heart Association.《2014年心脏病和中风统计数据更新:美国心脏协会报告》
Circulation. 2014 Jan 21;129(3):e28-e292. doi: 10.1161/01.cir.0000441139.02102.80. Epub 2013 Dec 18.
7
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Neurobiol Aging. 2014 Jan;35(1):179-90. doi: 10.1016/j.neurobiolaging.2013.06.023. Epub 2013 Aug 15.
10
Mild therapeutic hypothermia is superior to controlled normothermia for the maintenance of blood pressure and cerebral oxygenation, prevention of organ damage and suppression of oxidative stress after cardiac arrest in a porcine model.轻度治疗性低温对于维持血压和脑氧合、预防器官损伤以及抑制猪模型心脏骤停后的氧化应激优于控制性正常体温。
J Transl Med. 2013 May 20;11:124. doi: 10.1186/1479-5876-11-124.

心脏骤停导致的神经元损伤:数分钟内衰老数年。

Neuronal injury from cardiac arrest: aging years in minutes.

作者信息

Cherry Brandon H, Sumien Nathalie, Mallet Robert T

机构信息

Department of Integrative Physiology and Anatomy, University of North Texas Health Science Center, 3500 Camp Bowie Blvd, Fort Worth, TX, 76107-2699, USA,

出版信息

Age (Dordr). 2014;36(4):9680. doi: 10.1007/s11357-014-9680-x. Epub 2014 Aug 8.

DOI:10.1007/s11357-014-9680-x
PMID:25104136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4150914/
Abstract

Cardiac arrest is a leading cause of death and permanent disability. Most victims succumb to the oxidative and inflammatory damage sustained during cardiac arrest/resuscitation, but even survivors typically battle long-term neurocognitive impairment. Although extensive research has delineated the complex mechanisms that culminate in neuronal damage and death, no effective treatments have been developed to interrupt these mechanisms. Of importance, many of these injury cascades are also active in the aging brain, where neurons and other cells are under persistent oxidative and inflammatory stress which eventually damages or kills the cells. In light of these similarities, it is reasonable to propose that the brain essentially ages the equivalent of several years within the few minutes taken to resuscitate a patient from cardiac arrest. Accordingly, cardiac arrest-resuscitation models may afford an opportunity to study the deleterious mechanisms underlying the aging process, on an accelerated time course. The aging and resuscitation fields both stand to gain pivotal insights from one another regarding the mechanisms of injury sustained during resuscitation from cardiac arrest and during aging. This synergism between the two fields could be harnessed to foster development of treatments to not only save lives but also to enhance the quality of life for the elderly.

摘要

心脏骤停是导致死亡和永久性残疾的主要原因。大多数受害者死于心脏骤停/复苏期间遭受的氧化和炎症损伤,但即使是幸存者通常也会长期与神经认知障碍作斗争。尽管广泛的研究已经阐明了最终导致神经元损伤和死亡的复杂机制,但尚未开发出有效的治疗方法来阻断这些机制。重要的是,许多这些损伤级联反应在衰老的大脑中也很活跃,在那里神经元和其他细胞处于持续的氧化和炎症应激之下,最终会损害或杀死细胞。鉴于这些相似之处,有理由提出,在从心脏骤停中复苏患者所需的几分钟内,大脑实际上老化了相当于几年的时间。因此,心脏骤停复苏模型可能提供一个机会,在加速的时间进程中研究衰老过程背后的有害机制。衰老和复苏领域都有望从彼此那里获得关于心脏骤停复苏期间和衰老期间所遭受损伤机制的关键见解。这两个领域之间的这种协同作用可以被利用来促进治疗方法的开发,不仅可以挽救生命,还可以提高老年人的生活质量。