Dysregulated neuronal–microglial cross-talk during aging, stress and inflammation

Communication between neurons and microglia is essential for maintaining homeostasis in the central nervous system (CNS) during both physiological and inflammatory conditions. While microglial activation is necessary and beneficial in response to injury or disease, excessive or prolonged activation...

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Bibliographic Details
Published in:Experimental neurology 2012-01, Vol.233 (1), p.40-48
Main Authors: Jurgens, Heidi A., Johnson, Rodney W.
Format: Article
Language:English
Subjects:
Aging
Animals
Brain
Cell Communication - physiology
Cytokines
Cytokines - metabolism
Humans
Inflammation
Inflammation - pathology
Microglia
Microglia - physiology
Neurons - physiology
Stress
Stress, Psychological - pathology
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Summary:Communication between neurons and microglia is essential for maintaining homeostasis in the central nervous system (CNS) during both physiological and inflammatory conditions. While microglial activation is necessary and beneficial in response to injury or disease, excessive or prolonged activation can have deleterious effects on brain function and behavior. To prevent inflammation-associated damage, microglia reactivity is actively modulated by neurons in the healthy brain. Age or stress-induced disruption of normal neuronal–microglial communication could lead to an aberrant central immune response when additional stressors are applied. Recent work suggests that both aging and stress shift the CNS microenvironment to a pro-inflammatory state characterized by increased microglial reactivity and a reduction in anti-inflammatory and immunoregulatory factors. This review will discuss how heightened neuroinflammation associated with aging and stress may be compounded by the concomitant loss of neuronally derived factors that control microglial activation, leaving the brain vulnerable to excessive inflammation and neurobehavioral complications upon subsequent immune challenge. ▶ The interaction of neurons and microglia is essential in maintaining CNS homeostasis. ▶ Aging and stress lead to heightened neuroinflammation and increased microglial reactivity. ▶ Neuronal control of microglial activation is disrupted by aging, stress and inflammation. ▶ Loss of neuronal-microglial communication has deleterious consequences for brain and behavior.
ISSN:0014-4886
1090-2430
DOI:10.1016/j.expneurol.2010.11.014