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Critical Care (London, England) Dec 2019Memory gaps in intensive care unit (ICU) survivors are associated with psychiatric disorders. The ICU diaries improve the patient's factual memory of the ICU, but it is... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Memory gaps in intensive care unit (ICU) survivors are associated with psychiatric disorders. The ICU diaries improve the patient's factual memory of the ICU, but it is not clear if they reduce the incidence of psychiatric disorders in patients and relatives after hospital discharge. The aim of this study is to evaluate the literature on the effect of ICU diaries for patients admitted in ICU and their relatives.
METHODS
Two authors independently searched the online databases PubMed, OVID, Embase, EBSCO host, and PsycINFO from inception to July 2019. Studies were included if the intervention group (ICU diary) was compared with a group with no diaries and the sample was comprised patients ≥ 18 years old admitted in the ICU for more than 24 h and their relatives. Randomized clinical trials, observational studies, letter with original data, and abstracts were included, irrespective of the language. The search was not limited by any specific outcome. Review articles, commentaries, editorials, and studies without a control group were excluded. Structured tools were used to assess the methodological quality ("Risk Of Bias In Non-randomized Studies of Interventions (ROBINS-I)" for cohort studies and the "Cochrane Risk of Bias tool" for included RCTs and before/after studies). A random-effects model was employed considering the anticipated variability between the studies.
RESULTS
Seven hundred eighty-five titles were identified for screening. Two additional studies were selected after a reference search, and after a full-text review, a total of 12 studies were included. When pooling the results, ICU diary was associated with lower risk of depression (RR 0.41, 95% CI 0.23-0.75) and better quality of life (10.3 points higher in SF-36 general health score, 95% CI 0.79-19.8), without a decrease in anxiety or post-traumatic stress disorder (PTSD). For the relatives receiving an ICU diary, there was no difference in the incidence of PTSD, anxiety, or depression.
CONCLUSION AND RELEVANCE
This systematic review and meta-analysis supports the use of ICU diaries to reduce the risk of depression and preserve the quality of life of patients after ICU admission. ICU diaries do not seem to have any beneficial effect on the relatives of the patients.
TRIAL REGISTRATION
PROSPERO, CRD42019136639.
Topics: Critical Illness; Diaries as Topic; Family; Humans; Intensive Care Units; Memory Disorders; Outcome Assessment, Health Care; Patients; Stress Disorders, Post-Traumatic; Survivors
PubMed: 31842929
DOI: 10.1186/s13054-019-2678-0 -
Journal of Neuroinflammation Nov 2021Microglial polarization toward pro-inflammatory M1 phenotype are major contributors to the development of perioperative neurocognitive disorders (PNDs). Metabolic...
BACKGROUND
Microglial polarization toward pro-inflammatory M1 phenotype are major contributors to the development of perioperative neurocognitive disorders (PNDs). Metabolic reprogramming plays an important role in regulating microglial polarization. We therefore hypothesized that surgical trauma can activate microglial M1 polarization by metabolic reprogramming to induce hippocampal neuroinflammation and subsequent postoperative cognitive impairment.
METHODS
We used aged mice to establish a model of PNDs, and investigated whether surgical trauma induced metabolic reprograming in hippocampus using PET/CT and GC/TOF-MS based metabolomic analysis. We then determined the effect of the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) on hippocampal microglial M1 polarization, neuroinflammation, and cognitive function at 3 d after surgery.
RESULTS
We found that surgery group had less context-related freezing time than either control or anesthesia group (P < 0.05) without significant difference in tone-related freezing time (P > 0.05). The level of Iba-1 fluorescence intensity in hippocampus were significantly increased in surgery group than that in control group (P < 0.05) accompanied by activated morphological changes of microglia and increased expression of iNOS/CD86 (M1 marker) in enriched microglia from hippocampus (P < 0.05). PET/CT and metabolomics analysis indicated that surgical trauma provoked the metabolic reprogramming from oxidative phosphorylation to glycolysis in hippocampus. Inhibition of glycolysis by 2-DG significantly alleviated the surgical trauma induced increase of M1 (CD86CD206) phenotype in enriched microglia from hippocampus and up-regulation of pro-inflammatory mediators (IL-1β and IL-6) expression in hippocampus. Furthermore, glycolytic inhibition by 2-DG ameliorated the hippocampus dependent cognitive deficit caused by surgical trauma.
CONCLUSIONS
Metabolic reprogramming is crucial for regulating hippocampal microglial M1 polarization and neuroinflammation in PNDs. Manipulating microglial metabolism might provide a valuable therapeutic strategy for treating PNDs.
Topics: Aging; Anesthesia; Animals; Behavior, Animal; Cell Polarity; Cognitive Dysfunction; Glycolysis; Hippocampus; Male; Memory Disorders; Metabolomics; Mice; Mice, Inbred C57BL; Microglia; Neuroinflammatory Diseases; Postoperative Complications; Surgical Procedures, Operative; Wounds and Injuries
PubMed: 34774071
DOI: 10.1186/s12974-021-02318-5 -
Neuroscience Bulletin Aug 2021Alzheimer's disease (AD) is the most common neurodegenerative disorder and there is currently no cure. Neural circuit dysfunction is the fundamental mechanism underlying... (Review)
Review
Alzheimer's disease (AD) is the most common neurodegenerative disorder and there is currently no cure. Neural circuit dysfunction is the fundamental mechanism underlying the learning and memory deficits in patients with AD. Therefore, it is important to understand the structural features and mechanisms underlying the deregulated circuits during AD progression, by which new tools for intervention can be developed. Here, we briefly summarize the most recently established cutting-edge experimental approaches and key techniques that enable neural circuit tracing and manipulation of their activity. We also discuss the advantages and limitations of these approaches. Finally, we review the applications of these techniques in the discovery of circuit mechanisms underlying β-amyloid and tau pathologies during AD progression, and as well as the strategies for targeted AD treatments.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Humans; Memory Disorders; tau Proteins
PubMed: 34089505
DOI: 10.1007/s12264-021-00716-6 -
Neurology Feb 2022Evidence on timing of memory change after first and recurrent strokes is limited and inconsistent. We investigated memory trajectories before and after first and...
BACKGROUND AND OBJECTIVES
Evidence on timing of memory change after first and recurrent strokes is limited and inconsistent. We investigated memory trajectories before and after first and recurrent strokes in 18 European countries and tested whether the country-level acute stroke care was associated with memory change after stroke.
METHODS
Data were from the Survey of Health, Ageing and Retirement in Europe (2004-2019). Incident first and recurrent strokes were identified among baseline stroke-free individuals. Within each country, each participant with incident stroke (case group) was matched with a stroke-free individual (control group) using propensity score matching. We applied multilevel segmented linear regression to quantify acute and accelerated memory changes (measured by the sum score of immediate and delayed word recall tests; 0-20 words) before and after first and recurrent strokes in both groups. Associations between stroke and memory were compared between countries with different levels of acute stroke care indicators.
RESULTS
The final analytical sample included 35,164 participants who were stroke-free at baseline (≥50 years). A total of 2,362 incident first and 341 recurrent strokes between 2004 and 2019 were identified. In case groups, mean acute decreases in memory scores were 0.48 (95% confidence interval [CI] 0.31, 0.65) and 1.14 (95% CI 0.80, 1.48) words after first and recurrent stroke, respectively, independent of a range of confounders. No such acute decreases were observed in the control group after a hypothetical nonstroke onset date. In both groups, memory declined over time but decline rates were similar (-0.07 [95% CI -0.10, -0.05] vs -0.06 [95% CI -0.08, -0.05] words per year). The mean acute decreases in memory scores after first and recurrent strokes were smaller in countries with better access to endovascular treatment.
DISCUSSION
We found acute decreases but not accelerated declines in memory after first and recurrent strokes. Improved endovascular therapy might be associated with smaller memory loss after stroke but more evidence based on individual-level data is needed. More effort should be made in early assessment and intensive prevention of stroke among the ageing population and promoting access to and delivery of acute stroke care among patients with stroke.
Topics: Aging; Europe; Humans; Memory Disorders; Stroke; Time Factors
PubMed: 34893555
DOI: 10.1212/WNL.0000000000013171 -
Proceedings of the Japan Academy.... 2020Memory retrieval is not a passive process. When a memory is retrieved, the retrieved memory is destabilized, similar to short-term memory just after learning, and... (Review)
Review
Memory retrieval is not a passive process. When a memory is retrieved, the retrieved memory is destabilized, similar to short-term memory just after learning, and requires memory reconsolidation to re-stabilize the memory. Recent studies characterizing destabilization and reconsolidation showed that a retrieved memory is not always destabilized and that there are boundary conditions that determine the induction of destabilization and reconsolidation according to certain parameters, such as the duration of retrieval and the memory strength and age. Moreover, the reconsolidation of contextual fear memory is not independent of memory extinction; rather, these memory processes interact with each other. There is an increasing number of findings suggesting that destabilization following retrieval facilitates the modification, weakening, or strengthening of the original memory, and the resultant updated memory is stabilized through reconsolidation. Reconsolidation could be targeted therapeutically to improve emotional disorders such as post-traumatic stress disorder and phobia. Thus, this review summarizes recent findings to understand the mechanisms and function of reconsolidation.
Topics: Animals; Brain; Extinction, Psychological; Fear; Humans; Memory Consolidation; Memory Disorders; Mental Disorders; Phobic Disorders; Signal Transduction; Stress Disorders, Traumatic
PubMed: 32161213
DOI: 10.2183/pjab.96.008 -
Physiological Research Apr 2024ADHD is a common chronic neurodevelopmental disorder and is characterized by persistent inattention, hyperactivity, impulsivity and are often accompanied by learning and... (Review)
Review
ADHD is a common chronic neurodevelopmental disorder and is characterized by persistent inattention, hyperactivity, impulsivity and are often accompanied by learning and memory impairment. Great evidence has shown that learning and memory impairment of ADHD plays an important role in its executive function deficits, which seriously affects the development of academic, cognitive and daily social skills and will cause a serious burden on families and society. With the increasing attention paid to learning and memory impairment in ADHD, relevant research is gradually increasing. In this article, we will present the current research results of learning and memory impairment in ADHD from the following aspects. Firstly, the animal models of ADHD, which display the core symptoms of ADHD as well as with learning and memory impairment. Secondly, the molecular mechanism of has explored, including some neurotransmitters, receptors, RNAs, etc. Thirdly, the susceptibility gene of ADHD related to the learning and impairment in order to have a more comprehensive understanding of the pathogenesis. Key words: Learning and memory, ADHD, Review.
Topics: Attention Deficit Disorder with Hyperactivity; Humans; Animals; Memory Disorders; Learning; Disease Models, Animal; Learning Disabilities; Memory
PubMed: 38710050
DOI: 10.33549/physiolres.935202 -
The New England Journal of Medicine Feb 2024
Topics: Humans; COVID-19; Memory, Episodic; Memory Disorders; Health Status; Prospective Studies
PubMed: 38416436
DOI: 10.1056/NEJMc2311200 -
Genes Jun 2021Formaldehyde (FA) is a highly reactive substance that is ubiquitous in the environment and is usually considered as a pollutant. In the human body, FA is a product of... (Review)
Review
Formaldehyde (FA) is a highly reactive substance that is ubiquitous in the environment and is usually considered as a pollutant. In the human body, FA is a product of various metabolic pathways and participates in one-carbon cycle, which provides carbon for the synthesis and modification of bio-compounds, such as DNA, RNA, and amino acids. Endogenous FA plays a role in epigenetic regulation, especially in the methylation and demethylation of DNA, histones, and RNA. Recently, epigenetic alterations associated with FA dysmetabolism have been considered as one of the important features in age-related cognitive impairment (ARCI), suggesting the potential of using FA as a diagnostic biomarker of ARCI. Notably, FA plays multifaceted roles, and, at certain concentrations, it promotes cell proliferation, enhances memory formation, and elongates life span, effects that could also be involved in the aetiology of ARCI. Further investigation of and the regulation of the epigenetics landscape may provide new insights about the aetiology of ARCI and provide novel therapeutic targets.
Topics: Animals; Cognitive Dysfunction; DNA Methylation; Formaldehyde; Histone Code; Humans; Memory Disorders; Mutagens
PubMed: 34199279
DOI: 10.3390/genes12060913 -
Progress in Neuro-psychopharmacology &... Dec 2023Neurocognitive impairment is a transdiagnostic feature across several psychiatric and cardiometabolic conditions. The relationship between inflammatory and lipid...
INTRODUCTION
Neurocognitive impairment is a transdiagnostic feature across several psychiatric and cardiometabolic conditions. The relationship between inflammatory and lipid metabolism biomarkers and memory performance is not fully understood. This study aimed to identify peripheral biomarkers suitable to signal memory decline from a transdiagnostic and longitudinal perspective.
METHODS
Peripheral blood biomarkers of inflammation, oxidative stress and lipid metabolism were assessed twice over a 1-year period in 165 individuals, including 30 with schizophrenia (SZ), 42 with bipolar disorder (BD), 35 with major depressive disorder (MDD), 30 with type 2 diabetes mellitus (T2DM), and 28 healthy controls (HCs). Participants were stratified by memory performance quartiles, taking as a reference their global memory score (GMS) at baseline, into categories of high memory (H; n = 40), medium to high memory (MH; n = 43), medium to low memory (ML; n = 38) and low memory (L; n = 44). Exploratory and confirmatory factorial analysis, mixed one-way analysis of covariance and discriminatory analyses were performed.
RESULTS
L group was significantly associated with higher levels of tumor necrosis factor-alpha (TNF-α) and lower levels of apolipoprotein A1 (Apo-A1) compared to those from the MH and H groups (p < 0.05; ηp = 0.06-0.09), with small to moderate effect sizes. Moreover, the combination of interleukin-6 (IL-6), TNF-α, c-reactive protein (CRP), Apo-A1 and Apo-B compounded the transdiagnostic model that best discriminated between groups with different degrees of memory impairment (χ = 11.9-49.3, p < 0.05-0.0001).
CONCLUSIONS
Inflammation and lipid metabolism seem to be associated with memory across T2DM and severe mental illnesses (SMI). A panel of biomarkers may be a useful approach to identify individuals at greater risk of neurocognitive impairment. These findings may have a potential translational utility for early intervention and advance precision medicine in these disorders.
Topics: Humans; Diabetes Mellitus, Type 2; Depressive Disorder, Major; Tumor Necrosis Factor-alpha; Lipid Metabolism; Biomarkers; Inflammation; Memory Disorders
PubMed: 37327846
DOI: 10.1016/j.pnpbp.2023.110817 -
JCI Insight Jun 2023Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), and emerging evidence has shown that microRNAs (miRs) are...
Synaptic plasticity impairment plays a critical role in the pathogenesis of Alzheimer's disease (AD), and emerging evidence has shown that microRNAs (miRs) are alternative biomarkers and therapeutic targets for synaptic dysfunctions in AD. In this study, we found that the level of miR-431 was downregulated in the plasma of patients with amnestic mild cognitive impairment and AD. In addition, it was decreased in the hippocampus and plasma of APPswe/PS1dE9 (APP/PS1) mice. Lentivirus-mediated miR-431 overexpression in the hippocampus CA1 ameliorated synaptic plasticity and memory deficits of APP/PS1 mice, while it did not affect amyloid-β levels. Smad4 was identified as a target of miR-431, and Smad4 knockdown modulated the expression of synaptic proteins, including SAP102, and protected against synaptic plasticity and memory dysfunctions in APP/PS1 mice. Furthermore, Smad4 overexpression reversed the protective effects of miR-431, indicating that miR-431 attenuated synaptic impairment at least partially by Smad4 inhibition. Thus, these results indicated that miR-431/Smad4 might be a potential therapeutic target for AD treatment.
Topics: Mice; Animals; Mice, Transgenic; Alzheimer Disease; MicroRNAs; Neuronal Plasticity; Memory Disorders
PubMed: 37192007
DOI: 10.1172/jci.insight.166270