Exaggerated neuroinflammation and sickness behavior in aged mice after activation of the peripheral innate immune system

By J. P. Godbout, Jing Chen, J. Abraham, A. Richwine, B. Berg, Keith W. Kelley, Rodney W. Johnson. The FASEB Journal, 2005

790 citations recorded by the source corpus.

Subfields: Biological Psychiatry, Critical Care and Intensive Care Medicine, Neurology

View Paper: https://www.semanticscholar.org/paper/dc4a6b87496f53317072a60219159b98070aecd9

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In Biological Psychiatry

In Critical Care and Intensive Care Medicine

David J. Loane

In Neurology

Citations in the corpus

Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “Consistent with the observation that aged animals show primed microglial responses to secondary stimulation with LPS (Godbout et al., 2005), it has been shown that CD200 expression on neuronal dendrites decreases with age (Ojo et al., 2011) and glia prepared from CD2002/2 mice show heightened…”
Minocycline attenuates lipopolysaccharide (LPS)-induced neuroinflammation, sickness behavior, and anhedonia (2008, methodology): “Aged BALB/c mice (22–24 m) have an exaggerated neuroinflammatory response to LPS injection [10,13,14].”
Cytokine, Sickness Behavior, and Depression (2009, background): “This is shown to be the case in aged mice [58] and in obese mice [59].”
Role of Microglia in Neurotrauma (2010, positive): “NADPH oxidase is also thought to be a crucial component of microglial signaling, one that regulates the NF B pathway and proinflammatory gene expression in these cells.37,39 NADPH oxidase knockout results in attenuated proinflammatory production and reduced microglia-mediated neurotoxicity.37 With a”
Microglia derived from aging mice exhibit an altered inflammatory profile (2007, methodology): “Pro-inflammatory cytokines are chronically increased in the aging brain (Godbout et al., 2005), leading to en-”
Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, positive): “It has been proposed that microglia in the aged brain are ‘primed’ to respond more rapidly, produce more pronounced inflammatory responses and proliferate more vigorously than microglia in the young brain following TBI (Conde and Streit, 2006b; Godbout et al., 2005).”
Normal aging induces A1-like astrocyte reactivity (2018, background): “We observed by qPCR that LPS treatment induces an up-regulation of A1 reactive genes in astrocytes from the hippocampus, striatum, and cortex (Fig.”
Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration (2007, background): “, 2006) or aging and sentience (Godbout et al., 2005), microglia can become primed, where additional stimuli result in an exaggerated and prolonged pro-inflammatory response that enhances neuron damage.”
Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “More specifically, it was found in mice that aging was associated with increased markers of activated or primed microglia together with increased inflammation, and that, upon subsequent immune stimulation with LPS administered peripherally, primed microglial cells were responsible for the overproduc”
Early-Life Programming of Later-Life Brain and Behavior: A Critical Role for the Immune System (2009, background): “Supported in part by R01MH083698.”
β-Adrenergic Receptor Antagonism Prevents Anxiety-like Behavior and Microglial Reactivity Induced by Repeated Social Defeat (2011, methodology): “Primed or reactive microglia are increased with aging (Godbout et al., 2005), early life infection (Bilbo et al., 2005, 2008), neurodegenerative disease (Cunningham et al., 2005), and autoimmunity (Raivich and Banati, 2004).”