Postoperative cognitive deficits and neuroinflammation in the hippocampus triggered by surgical trauma are exacerbated in aged rats

Cao, Xun; Ma, Hong; Wang, Junke; Liu, Fang; Wu, Bingyang; Tian, Ayong; Wang, Lingling; Tan, Wen-Fei

doi:10.1016/j.pnpbp.2010.07.027

Cited by 157 publications

(142 citation statements)

References 39 publications

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“…Postoperative cognitive dysfunction (POCD) is characterized by the progressive deterioration of intellectual/cognitive function following both cardiac and major noncardiac surgery [1, 2]. The International Study of POCD estimated the overall incidence of POCD at 25.8% at 1 week and 9.9% after 3 months [1].…”

Section: Introductionmentioning

confidence: 99%

“…Mounting evidence indicates that POCD is associated with surgery-induced neuroinflammatory processes, which may influence neuronal function either directly or through modulation of intraneuronal pathways [5-7]. High levels of neuroinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α play a pivotal role in surgery-induced cognitive deficits [2, 8]. Inhibition of central proinflammatory cytokine signaling restores neuronal function and reverses cognitive deficits induced by chronic neuroinflammation [9].…”

Section: Introductionmentioning

confidence: 99%

“…Additionally, Rosczyk et al have demonstrated that locomotor activity is not depressed in either adult or aged mice following sham operation (minor abdominal surgery), which reveals that the decrease in locomotion is not due to minor surgical procedures [20]. It is likely that a more “major” surgery (partial hepatectomy) would induce a state of neuroinflammation that could result in sickness behavior [2, 7, 21-25]. …”

Section: Introductionmentioning

confidence: 99%

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Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

Jiang

et al. 2018

Cell Physiol Biochem

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Background/Aims: TREM2 plays a crucial role in modulating microglial function through interaction with DAP12, the adapter for TREM2. Emerging evidence has demonstrated that TREM2 could suppress neuroinflammatory responses by repression of microglia-mediated cytokine production. This study investigated the potential role of TREM2 in surgery-induced cognitive deficits and neuroinflammatory responses in wild-type (WT) and APPswe/PS1dE9 mice. Methods: Adult APPswe/PS1dE9 transgenic male mice (a classic transgenic model of Alzheimer’s disease, 3 months old) and their age-matched WT mice received intracerebral lentiviral particles encoding the mouse TREM2 gene and then were subjected to partial hepatectomy at 1 month after the lentiviral particle injection. The behavioral changes were evaluated with an open-field test and Morris water maze test on postoperative days 3, 7, and 14. Hippocampal TREM2, DAP12, and interleukin (IL)-1β were measured at each time point. Ionized calcium-binding adapter molecule 1 (Iba-1), microglial M2 phenotype marker Arg1, synaptophysin, tau hyperphosphorylation (T396), and glycogen synthase kinase-3β (GSK-3β) were also examined in the hippocampus. Results: Surgical trauma induced an exacerbated cognitive impairment and enhanced hippocampal IL-1β expression in the transgenic mice on postoperative days 3 and 7. A corresponding decline in the levels of TREM2 was also found on postoperative days 3, 7, and 14. Overexpression of TREM2 downregulated the levels of IL-1β, ameliorated T396 expression, inhibited the activity of GSK-3β, and improved sickness behavior. Increased Arg1 expression and a high level of synaptophysin were also observed in the transgenic mice following TREM2 overexpression. Conclusion: The downregulation of TREM2 exacerbated surgery-induced cognitive deficits and exaggerated neuroinflammatory responses in this rodent model. Overexpression of TREM2 potentially attenuated these effects by decreasing the associated production of proinflammatory cytokines, inhibiting tau hyperphosphorylation, and enhancing synaptophysin expression.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

Jiang

et al. 2018

Cell Physiol Biochem

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“…In addition, the inflammatory response to hypoxia has been shown to contribute to the resulting renal tissue injury (13). Inflammation-associated factors include complement proteins and chemokines, including tumor necrosis factor-α (TNF-α), interferon (IFN)-γ, interleukin (IL)-1β and IL-6 (14). Inhibition of their production has been shown to attenuate I/R-induced tissue injury (15); in a previous study, catalpol protected mice against renal I/R injury by suppressing the phosphoinositide-3-kinase/Akt-endothelial nitric oxide synthase signaling pathway, as well as the expression of TNF-α, IL-1β, IL-6 and IL-10 (16).…”

Section: Introductionmentioning

confidence: 99%

Gypenoside attenuates renal ischemia/reperfusion injury in mice by inhibition of ERK signaling

Zhu

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Gynostemma pentaphyllum is a traditional Chinese medicine reported to possess a wide range of health benefits. As the major component of G. pentaphyllum, gypenoside (GP) displays various anti-inflammatory and anti-oxidant properties. However, it is unclear whether GP can protect against ischemia/reperfusion (I/R)-induced renal injury, and the underlying molecular mechanisms associated with this process remain unknown. In the present study, a renal

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“…The mechanism of the way in which surgery impairs cognition is not yet clear, but possibly stressinduced hormonal responses, inflammatory cascades, and circulatory, respiratory, and temperature instability due to surgery are involved. The role of surgery-induced inflammation in POCD is enhanced by age (26).…”

Section: Surgery Neuroinflammation and Admentioning

confidence: 99%

Alzheimer disease and anesthesia

Inan¹,

ŞATIRLAR²

2015

Turk J Med Sci

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Alzheimer disease (AD) is one of the most common neurodegenerative diseases and the most prevalent form of dementia. Some factors in the development of AD, age being the best-known one, have been suggested; however, no causes have been found yet. The pathophysiology of the disease is highly complex, current therapies are palliative, and a cure is still lacking. Adverse effects of anesthetics in the elderly have been reported since the 1950s; however, awareness of this old problem has recently gained importance again. Whether exposure to surgery and general anesthesia (GA) is associated with the development of AD has been questioned. As the population is aging, many elderly patients will need to be anesthetized, and maybe some were already anesthetized before they were diagnosed. Exposure to anesthetics has been demonstrated to promote pathogenesis of AD in both in vitro and in vivo studies. However, to date, there have not been any clinical trials to address a link between exposure to GA and the development of AD in humans. Therefore, before making any conclusions we need further studies, but we should be aware of the potential risks and take cautions with vulnerable elderly patients.

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Postoperative cognitive deficits and neuroinflammation in the hippocampus triggered by surgical trauma are exacerbated in aged rats

Cited by 157 publications

References 39 publications

Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

Upregulation of TREM2 Ameliorates Neuroinflammatory Responses and Improves Cognitive Deficits Triggered by Surgical Trauma in Appswe/PS1dE9 Mice

Gypenoside attenuates renal ischemia/reperfusion injury in mice by inhibition of ERK signaling

Alzheimer disease and anesthesia

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