中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (9): 1349-1355.doi: 10.4103/1673-5374.165208

• 综述:脑损伤修复保护与再生 •    下一篇

脑卒中转化道路上的绊脚石:因为没有考虑合并症?

  

  • 收稿日期:2015-07-09 出版日期:2015-09-28 发布日期:2015-09-28

Neuroinflammation and comorbidities are frequently ignored factors in CNS pathology

Raluca Elena Sandu2, Ana Maria Buga1, 2, Adriana Uzoni1, 3, Eugen Bogdan Petcu4, Aurel Popa-Wagner1, 2   

  1. 1 Department of Psychiatry, University of Medicine Rostock, Germany
    2 Center of Clinical and Experimental Research, University of Medicine and Pharmacy Craiova, Romania
    3 Biochemistry Department, University of Medicine and Pharmacy “Victor Babes” Timisoara, Romania
    4 Griffith University School of Medicine, Regenerative Medicine Centre, Brisbane, Australia
  • Received:2015-07-09 Online:2015-09-28 Published:2015-09-28
  • Contact: Aurel Popa-Wagner, M.D., Ph.D.,aurel.popa-wagner@med.uni-rostock.de.
  • Supported by:

    Dr. Raluca Elena Sandu was supported by a POSDRU grant no. 159/1.5/S/136893 grant: “Strategic partnership for the increase of the scientific research quality in medical universities through the award of doctoral and postdoctoral fellowships–DocMed.Net_2.0”.

摘要:

所有临床前成功的实验性脑卒中的药物干预方法均未能成功转化到临床应用中。导致这种情况的部分原因可以用人类疾病的复杂性和异质性来解释,而另外一种原因是与疾病相关的合并症会使神经保护药物在临床实践中疗效大幅降低。对于脑卒中,仍未被完全揭示清楚的病理生理学的一个重要方面是神经炎症。在当前条件下,轻微的但具有持续性的神经炎症对疾病的影响日益明显,例如神经炎症是脑小血管疾病的病理原因之一。此外,逐渐加快的老化和其他一些高发危险因素,如肥胖、高血压、糖尿病和动脉粥样硬化等也是促进慢性神经炎症的“帮凶”。这些都可能会加剧各种病理组织变化,并造成一些后续的脑卒中并发症,如老年痴呆症、抑郁症和神经退行性疾病,进而形成病理的恶性循环。然而,最近的数据表明,炎症过程可能与多种神经退行性途径密切相关。这篇综述文章阐述了老化、合并症和神经炎症之间的关系,此种关联会加重脑血管疾病结果,总结了脑卒中事件后并发症的发展,包括抑郁症和神经退行性疾病。

Abstract:

Virtually all drug interventions that have been successful pre-clinically in experimental stroke have failed to prove their efficacy in a clinical setting. This could be partly explained by the complexity and heterogeneity of human diseases as well as the associated co-morbidities which may render neuroprotective drugs less efficacious in clinical practice. One aspect of crucial importance in the physiopathology of stroke which is not completely understood is neuroinflammation. At the present time, it is becoming evident that subtle, but continuous neuroinflammation can provide the ground for disorders such as cerebral small vessel disease. Moreover, advanced aging and a number of highly prevalent risk factors such as obesity, hypertension, diabetes and atherosclerosis could act as “silent contributors” promoting a chronic proinflammatory state. This could aggravate the outcome of various pathological entities and can contribute to a number of subsequent post-stroke complications such as dementia, depression and neurodegeneration creating a pathological vicious cycle. Moreover, recent data suggests that the inflammatory process might be closely linked with multiple neurodegenerative pathways related to depression. In addition, pro-inflammatory cytokines could play a central role in the pathophysiology of both depression and dementia.

Key words: aging, stroke, neuroinflammation, comorbidities, depression, dementia