Sleep and immune function: glial contributions and consequences of aging

Ingiosi, Ashley M; Opp, Mark R.; Krueger, James M.

doi:10.1016/j.conb.2013.02.003

Cited by 87 publications

(60 citation statements)

References 61 publications

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“…The increase in sleep behavior and attenuation of the post-acute inflammatory response appear contradictory. However, inflammation and, more recently, microglial activation have been implicated in sleep regulation (for review, see Ingiosi 60 ). It has been proposed that some drugs, such as methamphetamine, exert sleep regulatory effects through actions on microglia 61 .…”

Section: Discussionmentioning

confidence: 99%

Resolvins AT-D1 and E1 differentially impact functional outcome, post-traumatic sleep, and microglial activation following diffuse brain injury in the mouse

Harrison¹,

Rowe²,

Ellis³

et al. 2015

Brain, Behavior, and Immunity

102

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Traumatic brain injury (TBI) is induced by mechanical forces which initiate a cascade of secondary injury processes, including inflammation. Therapies which resolve the inflammatory response may promote neural repair without exacerbating the primary injury. Specific derivatives of omega-3 fatty acids loosely grouped as specialized pro-resolving lipid mediators (SPMs) and termed resolvins promote the active resolution of inflammation. In the current study, we investigate the effect of two resolvin molecules, RvE1 and AT-RvD1, on post-traumatic sleep and functional outcome following diffuse TBI through modulation of the inflammatory response. Adult, male C57BL/6 mice were injured using a midline fluid percussion injury (mFPI) model (6-10 min righting reflex time for brain-injured mice). Experimental groups included mFPI administered RvE1 (100ng daily), AT-RvD1 (100ng daily), or vehicle (sterile saline) and counterbalanced with uninjured sham mice. Resolvins or saline were administered daily for seven consecutive days beginning 3 days prior to TBI to evaluate proof-of-principle to improve outcome. Immediately following diffuse TBI, post-traumatic sleep was recorded for 24 hours post-injury. For days 1-7 post-injury, motor outcome was assessed by Rotarod. Cognitive function was measured at 6 days post-injury using Novel Object Recognition (NOR). At 7 days post-injury, microglial activation was quantified using immunohistochemistry for Iba-1. In the diffuse brain-injured mouse, AT-RvD1 treatment, but not RvE1, mitigated motor and cognitive deficits. RvE1 treatment significantly increased post-traumatic sleep in brain-injured mice compared to all other groups. RvE1 treated mice displayed a higher proportion of ramified microglia and lower proportion of activated rod microglia in the cortex compared to saline or AT-RvD1 treated brain-injured mice. Thus, RvE1 treatment modulated post-traumatic sleep and the inflammatory response to TBI, albeit independently of improvement in motor and cognitive outcome as seen in AT-RvD1-treated mice. This suggests AT-RvD1 may impart functional benefit through mechanisms other than resolution of inflammation alone.

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Section: Discussionmentioning

confidence: 99%

Resolvins AT-D1 and E1 differentially impact functional outcome, post-traumatic sleep, and microglial activation following diffuse brain injury in the mouse

Harrison¹,

Rowe²,

Ellis³

et al. 2015

Brain, Behavior, and Immunity

102

View full text Add to dashboard Cite

show abstract

“…Thus, it is likely that undisrupted sleep continuity, and/or undisturbed sleep architecture, is of great importance for the function of the endogenous descending pain modulatory systems, and potentially also for the action of exogenous analgesics. The complex effects of central cytokines, serotonin, and other neurotransmitters (e.g., acetylcholine, glutamate, and adenosine) on sleep regulation are beyond the scope of this review [20,22,103], but it is obvious that therapeutic modalities directed towards modulating these mediators are of high interest.…”

Section: Pathophysiologic Mechanisms Underlying the Connection Betweementioning

confidence: 99%

Polysomnographic characteristics in nonmalignant chronic pain populations: A review of controlled studies

Bjurström¹,

Irwin²

2016

Sleep Medicine Reviews

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Summary Sleep and pain are critical homeostatic systems that interact in a bidirectional manner. Complaints of sleep disturbance are ubiquitous among patients with chronic pain disorders, and conversely, patients with persistent insomnia symptoms commonly report suffering from chronic pain. Sleep deprivation paradigms demonstrate that partial or complete sleep loss induce hyperalgesia, possibly due to shared mechanistic pathways including neuroanatomic and molecular substrates. Further, chronic pain conditions and sleep disturbances are intertwined through comorbidities, which together cause detrimental psychological and physical consequences. This critical review examines 29 polysomnography studies to evaluate whether nonmalignant chronic pain patients, as compared to controls, show differences in objective measures of sleep continuity and sleep architecture. Whereas these controlled studies did not reveal a consistent pattern of objective sleep disturbances, alterations of sleep continuity were commonly reported. Alterations of sleep architecture such as increases in light sleep or decreases in slow-wave sleep were less commonly reported and findings were mixed and also inconsistent. Methodological flaws were identified, which complicated interpretation and limited conclusions; hence, recommendations for future research are suggested. Knowledge of abnormalities in the sleep process has implications for understanding the pathophysiology of chronic pain conditions, which might also direct the development of novel intervention strategies.

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“…Sleep has well-documented effects on the immune system, in that sleep and sleep loss modulate optimal immune function, and certain cytokines and other immune modulators enhance or suppress sleep [86–88]. Glial, and particularly microglial, dysfunction has been described in aging and AD (reviewed in [89,90]). Perhaps not coincidentally, active and passive immunotherapy presents a promising approach to AD prevention and treatment (reviewed in [91]).…”

Section: Possible Mechanisms?mentioning

confidence: 99%

The sleep–wake Cycle and Alzheimer’s Disease: What do We know?

Lim

Gerstner

Holtzman

2014

Neurodegener. Dis. Manag.

131

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SUMMARY Sleep–wake disturbances are a highly prevalent and often disabling feature of Alzheimer’s disease (AD). A cardinal feature of AD includes the formation of amyloid plaques, associated with the extracellular accumulation of the amyloid-β (Aβ) peptide. Evidence from animal and human studies suggests that Aβ pathology may disrupt the sleep–wake cycle, in that as Aβ accumulates, more sleep–wake fragmentation develops. Furthermore, recent research in animal and human studies suggests that the sleep–wake cycle itself may influence Alzheimer’s disease onset and progression. Chronic sleep deprivation increases amyloid plaque deposition, and sleep extension results in fewer plaques in experimental models. In this review geared towards the practicing clinician, we discuss possible mechanisms underlying the reciprocal relationship between the sleep–wake cycle and AD pathology and behavior, and present current approaches to therapy for sleep disorders in AD.

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Sleep and immune function: glial contributions and consequences of aging

Cited by 87 publications

References 61 publications

Resolvins AT-D1 and E1 differentially impact functional outcome, post-traumatic sleep, and microglial activation following diffuse brain injury in the mouse

Resolvins AT-D1 and E1 differentially impact functional outcome, post-traumatic sleep, and microglial activation following diffuse brain injury in the mouse

Polysomnographic characteristics in nonmalignant chronic pain populations: A review of controlled studies

The sleep–wake Cycle and Alzheimer’s Disease: What do We know?

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