Impact of age-related neuroglial cell responses on hippocampal deterioration.

Impact of age-related neuroglial cell responses on hippocampal deterioration.
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DOI:
10.3389/fnagi.2015.00057
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发表时间:
2015
影响因子:
4.8
通讯作者:
Stewart MG
Stewart MG
中科院分区:
医学2区
文献类型:
--
作者:
Ojo JO;Rezaie P;Gabbott PL;Stewart MG

文献摘要

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衰老是发生散发性年龄相关性神经退行性疾病的最大风险因素之一,神经炎症是这种疾病表型的共同特征。在免疫豁免的脑中,介导神经炎症反应的神经胶质细胞受到中枢神经系统(CNS)微环境中生理因素的影响。这些生理因素包括但不限于涉及细胞粘附分子、神经元电活动以及神经递质和神经调质作用的细胞间通讯。然而,尽管神经胶质细胞活性的这种动态控制,在健康的老年大脑中,在海马体中明显观察到的潜在神经炎性反应存在改变,典型的是星形胶质细胞/小胶质细胞活化和促炎细胞因子产生和信号传导增加。这些变化可能在没有任何明显并发病理的情况下发生,然而,它们通常与大脑或认知功能的恶化相关。在这篇综述中,我们研究了两个重要的现象,首先是与年龄相关的脑退化(重点是海马功能)和潜在的神经胶质细胞反应之间的关系,其次是后者如何影响海马内的分子和细胞过程,使其容易受到与年龄相关的认知能力下降。
Aging is one of the greatest risk factors for the development of sporadic age-related neurodegenerative diseases and neuroinflammation is a common feature of this disease phenotype. In the immunoprivileged brain, neuroglial cells, which mediate neuroinflammatory responses, are influenced by the physiological factors in the microenvironment of the central nervous system (CNS). These physiological factors include but are not limited to cell-to-cell communication involving cell adhesion molecules, neuronal electrical activity and neurotransmitter and neuromodulator action. However, despite this dynamic control of neuroglial activity, in the healthy aged brain there is an alteration in the underlying neuroinflammatory response notably seen in the hippocampus, typified by astrocyte/microglia activation and increased pro-inflammatory cytokine production and signaling. These changes may occur without any overt concurrent pathology, however, they typically correlate with deteriorations in hippocamapal or cognitive function. In this review we examine two important phenomenons, firstly the relationship between age-related brain deterioration (focusing on hippocampal function) and underlying neuroglial response(s), and secondly how the latter affects molecular and cellular processes within the hippocampus that makes it vulnerable to age-related cognitive decline.