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Construction and validation of risk prediction model for postoperative cognitive dysfunction in patients with weakened colorectal cancer

ABSTRACT: Interventions: Case series:N/A Primary outcome(s): Mini-Mental State Examination,MMSE;Montreal Cognitive Assessment, MoCA Study Design: Cohort study

DISEASE(S): Colorectal Cancer

PROVIDER: 85198 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Study on the effect and mechanism of percutaneous acupoint nerve electrical stimulation in postoperative cognitive dysfunction

Project description:Interventions: Group TEAS:percutaneous acupoint nerve electrical stimulation;Group CON:nothing Primary outcome(s): MMSE, Mini-mental State Examination;QoR-40, 40-Item Quality of Restoration;cortisol;noradrenaline;D-LAC;DAO Study Design: Parallel

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Effect of Esketamine combined with lumboquadrat nerve block on postoperative anxiety, depression and cognitive function in senile patients undergoing radical resection of colorectal cancer

Project description:Interventions: LP group:ropivacaine;ES group:ropivacaine+esketamine Primary outcome(s): Mini-mental State Examination (MMSE) Score;Hospital Anxiety and Depression Scale (HADS) Score Study Design: Parallel

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To observe the effect of individualized ventilation combined with auricular acupoint pressing needle on the quality of emergence from anesthesia and postoperative cognitive function of patients undergoing laparoscopic colorectal cancer surgery o

Project description:Interventions: Auricular acupoint pressing needle:Auricular acupoint pressing needle at the end of the operation;Control group:N/A Primary outcome(s): time to spontaneous respiration recovery ;time to extubation ;time to orientation ;RASS;Mini-mental State Examination(MMSE);heart rate (HR);mean arterial pressure (MAP);cerebral oxygen saturation(rSO2);optic nerve sheath diameter(ONSD);internal jugular vein valve function;time to emergence;Montreal Cognitive Assessment Scale (MOCA) Study Design: Parallel

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Discovering new peripheral plasma biomarkers to identify cognitive decline in type 2 diabetes

Project description:Type 2 diabetes mellitus (T2DM) is an independent risk factor of Alzheimer's disease (AD), thus, identifying who among the increasing T2DM populations may develop into AD is important for early intervention. By using TMT-labeling coupled high-throughput mass spectrometry, we conducted a comprehensive plasma proteomic analysis in none-T2DM people (Ctrl, n=30), and the age-/sex-matched T2DM patients with mild cognitive impairment (T2DM-MCI, n=30) or T2DM without MCI (T2DM-nMCI, n=25). The candidate biomarkers identified by proteomics and bioinformatics analyses were verified by ELISA, and their diagnostic capabilities were evaluated with machine learning. A total of 53 differentially expressed proteins (DEPs) were identified in T2DM-MCI compared with T2DM-nMCI patients. These DEPs were significantly enriched in multiple biological processes, such as amyloid neuropathies, CNS disorders, and metabolic acidosis. Among the DEPs, alpha-1-antitrypsin (SERPINA1), major viral protein (PRNP), valosin-containing protein (VCP) showed strong collection with AD high-risk genes APP, MAPT, APOE, PSEN1, and PSEN2. And the levels of PP2A cancer inhibitor (CIP2A), PRNP, corticotropin releasing factor binding protein (CRHBP) were significantly increased, while the level of VCP was decreased in T2DM-MCI patients compared with the T2DM-nMCI, and these changes were correlated with the mini-mental state examination (MMSE) score. Further machine learning data showed that increases of CIP2A, ratio of β-amyloid (rAβ42/40), and rGSK-3β(T/S9) (ratio of total to serine-9-phosphorylated glycogen synthase kinase-3β) had the greatest power to identify mild cognitive decline in T2DM patients.

2023-03-11 | PXD027870 | Pride

Identifying main functional pathways associated with cognitive resilience to Alzheimer ´s Disease

Project description:Understanding the mechanisms involved in cognitive resilience in Alzheimer’s disease (AD) represents a promising strategy to identify novel treatments for dementia in AD. Previous findings from our group revealed that the study of aged-Tg2576 cognitive resilient individuals is a suitable tool for this purpose. Here, by performing a transcriptomic analysis of the prefrontal cortex of demented and resilient Tg2576 mice, we have been able to hypothesize that pathways involved in inflammation, amyloid degradation, memory function and neurotransmission may be playing a role on cognitive resilience in AD. Intriguingly, the results obtained in this study are suggestive of a reduction of the influx of peripheral immune cells into the brain on cognitive resilient subjects. Indeed, Cd4 mRNA expression is significantly reduced on Tg2576 mice with cognitive resilience and interestingly, we have found a negative correlation between CD4 mRNA levels in the periphery and the score in the Mini-Mental State Exam of AD patients. All of this, highlights the importance of understanding the role of the immune system on the development of neurodegenerative diseases and points out to the infiltration of CD4+ cells in the brain as a key player of cognitive dysfunction in AD.

2023-09-19 | GSE180968 | GEO

Correlation between preoperative dyslipidemia and perioperative neurocognitive impairment in elderly patients with colorectal cancer

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Gene expression profile of single-cell level alterations in hippocampal tissue in a rat model of radiation-induced cognitive dysfunction

Project description:Radiotherapy is an important therapeutic option for the treatment of primary and metastatic brain tumors, and there is increasing concern about the side effects associated with it as survival time after treatment increases. By far, cognitive dysfunction is the most common radiation-induced central nervous system injury. Studies have shown that the hippocampus is involved in radiation-induced cognitive dysfunction. We constructed a model of radiation-induced cognitive dysfunction by irradiating the whole brain of one-month-old rats with 20 Gy, and analyzed the expression profiles in the hippocampus of rats with radiation-induced cognitive dysfunction using single-cell RNA sequencing (scRNA-seq).

2023-12-12 | GSE249426 | GEO

The reverse transcriptase inhibitor 3TC protects against age-related cognitive dysfunction

Project description:Aging is the primary risk factor for most neurodegenerative diseases, including Alzheimer's disease. Major hallmarks of brain aging include neuroinflammation/immune activation and reduced neuronal health/function. These processes contribute to cognitive dysfunction (a key risk factor for Alzheimer's disease), but their upstream causes are incompletely understood. Age-related increases in transposable element (TE) transcripts might contribute to reduced cognitive function with brain aging, as the reverse transcriptase inhibitor 3TC reduces inflammation in peripheral tissues and TE transcripts have been linked with tau pathology in Alzheimer's disease. However, the effects of 3TC on cognitive function with aging have not been investigated. Here, in support of a role for TE transcripts in brain aging/cognitive decline, we show that 3TC: (a) improves cognitive function and reduces neuroinflammation in old wild-type mice; (b) preserves neuronal health with aging in mice and Caenorhabditis elegans; and (c) enhances cognitive function in a mouse model of tauopathy. We also provide insight on potential underlying mechanisms, as well as evidence of translational relevance for these observations by showing that TE transcripts accumulate with brain aging in humans, and that these age-related increases intersect with those observed in Alzheimer's disease. Collectively, our results suggest that TE transcript accumulation during aging may contribute to cognitive decline and neurodegeneration, and that targeting these events with reverse transcriptase inhibitors like 3TC could be a viable therapeutic strategy.

2023-03-23 | GSE213848 | GEO

Rescuing over-activated microglia by acetaminophen treatment restores cognitive performance in the Dp(16) mouse model of Down Syndrome.

Project description:Microglia are the resident immune cells of the brain and have been implicated in mechanisms essential for cognitive functions. Down syndrome (DS), the most frequent cause of genetic intellectual disability, is caused by the presence of a supernumerary chromosome 21, which contains genes essential for the function of the immune system. Here, we investigated the presence of microglial alterations and their implication for cognitive impairment in the Dp(16) mouse model of DS. In the hippocampus of Dp(16) mice and individuals with DS, we found microglial morphology indicative of an activated state. Accordingly, we found increased levels of pro-inflammatory cytokines and altered interferon signaling in Dp(16) mice. In addition, Dp(16) mice showed decreased dendritic spine density and cognitive deficits. Remarkably, depletion of defective microglia by PLX3397 treatment or rescue of the microglia activated state by the commonly used anti-inflammatory drug acetaminophen fully rescued dendritic-spine density and cognitive deficits in Dp(16) mice. Our data suggest an involvement of microglia in the cognitive impairment of DS animals and identify a new therapeutic approach for the potential rescue of cognitive disabilities in individuals with DS.

2020-09-22 | PXD015113 | Pride

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