Pathological changes of the hippocampus and cognitive dysfunction following frontal lobe surgery in a rat model

Hem, Santiago; Albite, Romina; Loresi, Monica; Rasmussen, Jorge; Ajler, Pablo; Yampolsky, Claudio; Chabot, J; Gerszten, Peter C.; Goldschmidt, Ezequiel

doi:10.1007/s00701-016-2938-6

Cited by 14 publications

(11 citation statements)

References 46 publications

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“…Doublecortin (DCX), an immature neuronal marker, was used to detect the neurogenesis in dentate gyrus which plays a key role in spatial memory function (Hem et al, 2016 ). Hence, we also examined the possibility of POCD in aged mice might be related to a deficiency in dentate gyrus neurogenesis by DCX immunostaining.…”

Section: Resultsmentioning

confidence: 99%

Inhibiting RIPK1 Limits Neuroinflammation and Alleviates Postoperative Cognitive Impairments in D-Galactose-Induced Aged Mice

Duan

Wang

Chen

et al. 2018

Front. Behav. Neurosci.

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Neuroinflammation plays a critical role in the pathogenesis of postoperative cognitive dysfunction (POCD) of the elderly patients. Receptor-interacting protein kinase1 (RIPK1) is a key molecular switch modulating inflammation, apoptosis and necroptosis. Here, we investigated whether inhibiting RIPK1 by necrostatin-1 (Nec-1) could limit neuroinflammation and attenuate POCD in D-Galactose (D-Gal)-induced aged mice. The mice were subjected to anesthesia and partial hepatectomy, and necrostatin-1 was administered intraperitoneally 1 h prior to anesthesia and surgery. Cognitive function and movement were tested 24 h after surgery by open field, Barnes maze and puzzle box. The hippocampal tissues were collected to detect the following: neuroinflammation (Iba-1, IL-1α, IL-1β, TNF-α), Necroptosis (Propidium Iodide (PI) labeling, RIPK1, nuclear transcription factor kappa B (NF-κB) and neuroplasticity (doublecortin (DCX), NR2B, GluA1, GluA2). We found that anesthesia and surgery induced a significant deficit in spatial memory acquisition and impairment of executive function and memory to simple task in D-Galactose-induced aged mice. Inhibiting RIPK1 by necrostatin-1 strikingly mitigated cognitive impairment and alleviated postoperative amplified neuroinflammation, necroptosis and GluA1 loss in hippocampus. These suggest that targeting RIPK1 by necrostatin-1 may serve as a promising therapeutics for prevention of POCD in elderly patients.

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Section: Resultsmentioning

confidence: 99%

Inhibiting RIPK1 Limits Neuroinflammation and Alleviates Postoperative Cognitive Impairments in D-Galactose-Induced Aged Mice

Duan

Wang

Chen

et al. 2018

Front. Behav. Neurosci.

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“…(iii) These rearrangements in gray matter might be associated with compensation, which was influenced following multidomain cognitive impairments and AD-related CSF. Research interest is transforming to increasingly earlier diagnoses, since the origin of AD and the key to treatment probably lie in preventing progression to a fully-fledged disease (Hem et al, 2016;Slot et al, 2018). It should be noted that compensation in the structural network has been shown to be manifested earlier in AD-spectrum patients (Liu et al, 2020), and there is increasing interest in the study of structural network alterations to assess the progression in subjects who have a higher risk of AD (Sanchez-Benavides et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Brain Structural Network Compensation Is Associated With Cognitive Impairment and Alzheimer’s Disease Pathology

Sheng¹,

Chen²,

Shao³

et al. 2021

Front. Neurosci.

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BackgroundStructural network alterations in Alzheimer’s disease (AD) are related to worse cognitive impairment. The aim of this study was to quantify the alterations in gray matter associated with impaired cognition and their pathological biomarkers in AD-spectrum patients.MethodsWe extracted gray matter networks from 3D-T1 magnetic resonance imaging scans, and a graph theory analysis was used to explore alterations in the network metrics in 34 healthy controls, 70 mild cognitive impairment (MCI) patients, and 40 AD patients. Spearman correlation analysis was computed to investigate the relationships among network properties, neuropsychological performance, and cerebrospinal fluid pathological biomarkers (i.e., Aβ, t-tau, and p-tau) in these subjects.ResultsAD-spectrum individuals demonstrated higher nodal properties and edge properties associated with impaired memory function, and lower amyloid-β or higher tau levels than the controls. Furthermore, these compensations at the brain regional level in AD-spectrum patients were mainly in the medial temporal lobe; however, the compensation at the whole-brain network level gradually extended from the frontal lobe to become widely distributed throughout the cortex with the progression of AD.ConclusionThe findings provide insight into the alterations in the gray matter network related to impaired cognition and pathological biomarkers in the progression of AD. The possibility of compensation was detected in the structural networks in AD-spectrum patients; the compensatory patterns at regional and whole-brain levels were different and the clinical significance was highlighted.

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“…Therefore, BDNF has become an important biomarker of POCD ( Tian X.S. et al, 2015 ; Hem et al, 2016 ; Wu et al, 2016 ).…”

Section: Sevoflurane-inhalation Anesthesia and Pocdmentioning

confidence: 99%

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

Wang

Chen

Zhang

et al. 2021

Front. Aging Neurosci.

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Sevoflurane is one of the most widely used anesthetics for the induction and maintenance of general anesthesia in surgical patients. Sevoflurane treatment may increase the incidence of postoperative cognitive dysfunction (POCD), and patients with POCD exhibit lower cognitive abilities than before the operation. POCD affects the lives of patients and places an additional burden on patients and their families. Understanding the mechanism of sevoflurane-induced POCD may improve prevention and treatment of POCD. In this paper, we review the diagnosis of POCD, introduce animal models of POCD in clinical research, analyze the possible mechanisms of sevoflurane-induced POCD, and summarize advances in treatment for this condition.

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Pathological changes of the hippocampus and cognitive dysfunction following frontal lobe surgery in a rat model

Cited by 14 publications

References 46 publications

Inhibiting RIPK1 Limits Neuroinflammation and Alleviates Postoperative Cognitive Impairments in D-Galactose-Induced Aged Mice

Inhibiting RIPK1 Limits Neuroinflammation and Alleviates Postoperative Cognitive Impairments in D-Galactose-Induced Aged Mice

Brain Structural Network Compensation Is Associated With Cognitive Impairment and Alzheimer’s Disease Pathology

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

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