NEUROINFLAMMATION IN THE NORMAL AGING HIPPOCAMPUS

被引：245

作者：

Barrientos, R. M. ^{[1
]}

Kitt, M. M. ^{[1
]}

Watkins, L. R. ^{[1
]}

Maier, S. F. ^{[1
]}

机构：

[1] Univ Colorado, Dept Psychol & Neurosci, Ctr Neurosci, Boulder, CO 80309 USA

来源：

NEUROSCIENCE | 2015年 / 309卷

关键词：

normal aging; neuroinflammation; memory impairments; microglial priming; danger signals; neuroendocrine dysregulation; LONG-TERM POTENTIATION; TRAUMATIC BRAIN-INJURY; RAT DENTATE GYRUS; POSTOPERATIVE COGNITIVE DYSFUNCTION; CENTRAL-NERVOUS-SYSTEM; INTERLEUKIN-1 RECEPTOR ANTAGONIST; MESSENGER-RNA EXPRESSION; PERIPHERAL IMMUNE CHALLENGE; AGED MOUSE HIPPOCAMPUS; IMMEDIATE-EARLY GENE;

D O I：

10.1016/j.neuroscience.2015.03.007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 [神经生物学];

摘要：

A consequence of normal aging is a greater susceptibility to memory impairments following an immune challenge such as infection, surgery, or traumatic brain injury. The neuroinflammatory response, produced by these challenges results in increased and prolonged production of pro-inflammatory cytokines in the otherwise healthy aged brain. Here we discuss the mechanisms by which long-lasting elevations in pro-inflammatory cytokines in the hippocampus produce memory impairments. Sensitized microglia are a primary source of this exaggerated neuroinflammatory response and appear to be a hallmark of the normal aging brain. We review the current understanding of the causes and effects of normal aging-induced microglial sensitization, including dysregulations of the neuroendocrine system, potentiation of neuroinflammatory responses following an immune challenge, and the impairment of memories. We end with a discussion of therapeutic approaches to prevent these deleterious effects. (C) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

引用

页码：84 / 99

页数：16

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