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Perioperative neurocognitive disorders (PNDs) are one of the most common complications in perioperative patients, and neuroinflammatory reaction mediated by microglia plays a key role in their formation, but the underlying mechanism remains unknown. Given that the triggering receptor expressed on myeloid cells 1 (TREM1) is a key regulator of inflammation, this study aimed to observe the role of TREM1 on the sevoflurane-induced inflammatory activation in microglia. BV2 microglia were subjected to varying sevoflurane concentrations and durations to assess their viability using CCK8 and the expression of TREM1, iNOS, and ARG using enzyme-linked immunosorbent assays. Additionally, TREM1 knockdown lentivirus was employed to examine its impacts on microglia response to sevoflurane and altered expression of inflammatory markers, IL-1β, TNF-α, TGF-β, IL-10, iNOS, and ARG, as detected using qRT-PCR and immunofluorescence for INOS/Iba-1 and ARG/Iba-1. Our findings underscore the potent inflammatory activation induced by prolonged, high-concentration sevoflurane exposure on microglia. We highlight the potential role of TREM1 as a modulator of microglial polarization and a potential target for the treatment and prevention of sevoflurane-induced PNDs.

Dementia represents a significant health issue, afflicting both patients and their families. To assess the global trends in the incidence, prevalence, mortality, and disability-adjusted life years (DALYs) of Alzheimer's disease (AD) and other dementias in the elderly population, the Global Burden of Disease Study (1999−2019) was used. The average annual percentage change (AAPC) was estimated using linear regression. Stratified analysis of the global trends by age, sex, region, national level, and social development index (SDI) were also performed. The global incidence of AD and other dementias increased from 507.96 per 100,000 in 1990 to 569.39 per 100,000 in 2019, showing a significant increase in this period. In males, the incidence increased from 387.56 per 100,000 population in 1990 to 462.40 per 100,000 in 2019 (AAPC = 0.61), whereas females experienced a slower rise (AAPC = 0.31) and had a higher incidence in 2019 (662.93 per 100,000 population). The most significant increase was observed in individuals aged 60−64 and those in the middle-SDI quintile. Regionally, the high-income Asia Pacific had the highest incidence (890.01 per 100,000 population) and DALYs (3043.86 per 100,000) in AD and other dementias in 2019. As for national trends, Japan had the most pronounced increase in the incidence and DALYs of AD and other dementias during the 1990−2019 period. These findings highlight the growing burden of dementias on life expectancy at a population level, which is significant for healthcare professionals and decision-makers to conduct the ongoing debate on the policy of AD and other dementias.

Alzheimer's disease (AD) is a neurodegenerative disease, which is mainly characterized by the abnormal deposition of β-amyloid peptide (Aβ) and Tau. Since Tau aggregation is more closely associated with synaptic loss, neurodegeneration, and cognitive decline than Aβ, the correlation between Tau and cognitive function in AD has gradually gained attention. The posttranslational modifications (PTMs) of Tau are key factors contributing to its pathological changes, which include phosphorylation, acetylation, ubiquitination, glycosylation, glycation, small ubiquitin-like modifier mediated modification (SUMOylation), methylation, succinylation, etc. These modifications change the structure of Tau, regulating Tau microtubule interactions, localization, degradation, and aggregation, thereby affecting its propensity to aggregate and leading to neuronal injury and cognitive impairments. Among numerous PTMs, drug development based on phosphorylation, acetylation, ubiquitination, and SUMOylation primarily involves enzymatic reactions, affecting either the phosphorylation or degradation processes of Tau. Meanwhile, methylation, glycosylation, and succinylation are associated with maintaining the structural stability of Tau. Current research is more extensive on phosphorylation, acetylation, ubiquitination, and methylation, with related drugs already developed, particularly focusing on phosphorylation and ubiquitination. In contrast, there is less research on SUMOylation, glycosylation, and succinylation, requiring further basic research, with the potential to become novel drug targets. In conclusion, this review summarized the latest research on PTMs of Tau and related drugs, highlighting the potential of targeting specific PTMs for developing novel therapeutic strategies in AD.

Tic disorders represent a developmental neuropsychiatric condition whose causes can be attributed to a variety of environmental, neurobiological, and genetic factors. From a neurophysiological perspective, the disorder has classically been associated with neurochemical imbalances (particularly dopamine and serotonin) and structural and functional alterations affecting, in particular, brain areas and circuits involved in the processing and coordination of movements: the basal ganglia, thalamus, motor cortical area, and cingulate cortex; however, more recent research is demonstrating the involvement of many more brain regions and neurotransmission systems than previously observed, such as the prefrontal cortex and cerebellum. In this paper, therefore, we summarize the evidence to date on these abnormalities with the intent to illustrate and clarify the main neuroanatomical differences between patients with tic disorders and healthy individuals.

Neuromyelitis optica spectrum disorder (NMOSD) is a group of autoimmune disorders characterized by inflammatory involvement of the optic nerve, spinal cord, and central nervous system. NMOSD is often associated with other autoimmune disorders, including Sjogren's syndrome (SS). While NMOSD typically occurs at a peak in young or older individuals, the coexistence of NMOSD and SS in a youngster is rare. Here, we presented a case of a 14-year-old girl with NMOSD and SS who responded well to immunosuppressive therapy but experienced a severe relapse after discontinuation of therapy. We described the clinical course of a case over 8 years, underscoring the importance of long-term treatment for NMOSD and SS. This case, along with the review of relevant literature, will raise awareness of this type of disease and facilitate early diagnosis and treatment to avoid serious sequelae.

The rapid advancement of artificial intelligence (AI) has sparked renewed discussions on its trustworthiness and the concept of eXplainable AI (XAI). Recent research in neuroscience has emphasized the relevance of XAI in studying cognition. This scoping review aims to identify and analyze various XAI methods used to study the mechanisms and features of cognitive function and dysfunction. In this study, the collected evidence is qualitatively assessed to develop an effective framework for approaching XAI in cognitive neuroscience. Based on the Joanna Briggs Institute and preferred reporting items for systematic reviews and meta-analyses extension for scoping review guidelines, we searched for peer-reviewed articles on MEDLINE, Embase, Web of Science, Cochrane Central Register of Controlled Trials, and Google Scholar. Two reviewers performed data screening, extraction, and thematic analysis in parallel. Twelve eligible experimental studies published in the past decade were included. The results showed that the majority (75%) focused on normal cognitive functions such as perception, social cognition, language, executive function, and memory, while others (25%) examined impaired cognition. The predominant XAI methods employed were intrinsic XAI (58.3%), followed by attribution-based (41.7%) and example-based (8.3%) post hoc methods. Explainability was applied at a local (66.7%) or global (33.3%) scope. The findings, predominantly correlational, were anatomical (83.3%) or nonanatomical (16.7%). In conclusion, while these XAI techniques were lauded for their predictive power, robustness, testability, and plausibility, limitations included oversimplification, confounding factors, and inconsistencies. The reviewed studies showcased the potential of XAI models while acknowledging current challenges in causality and oversimplification, particularly emphasizing the need for reproducibility.

Hydrocephalus is the most common and devastating condition affecting the fetus. The aim of this study was to provide a comprehensive overview of the relevant literature through bibliometric analysis. The survey covers the articles related to congenital hydrocephalus published in the Web of Science Core Collection (WoSCC) database from January 1, 2003 to December 31, 2022. In addition to repeated literature, reviews and articles are included. We visualized the annual publication number, citation frequency, country/region, institution, author, periodical, and keywords with a range of software such as VOSviewer (1.6.18), Microsoft Excel 2019 (Redmond) and online analysis platform (https://bibliometric.com/ document). The results showed that the United States made the most important contribution to the research on fetal hydrocephalus. China's contribution has grown and developed strongly in recent years. The key words were mainly divided into four categories: basic research, epidemiology, treatment, and diagnostics. The number of publications related to fetal hydrocephalus has increased significantly, and it has a good development prospect in prenatal diagnosis and treatment.

Sterile-α and Toll/interleukin 1 receptor (TIR) motif-containing protein 1 (SARM1), a key intracellular molecule that plays numerous important biological functions in the nervous system, has attracted much attention. Recent studies have shown that SARM1 plays a key role in nerve injury, degeneration, and neurodegenerative diseases. Therefore, understanding the role of SARM1 in the central nervous system (CNS) will enhance our knowledge of the pathogenesis of CNS diseases and aid in the development of new therapeutic strategies. This review will explore the biological functions of SARM1 in the nervous system and its potential roles in nerve injury and disease, thus providing new directions for future research and treatment.

Cancer cells immediately expand and penetrate adjoining tissues, as opposed to metastasis, that is the spread of cancer cells through the circulatory or lymphatic systems to more distant places via the invasion process. We found that a lack of studies discussed tumor development with the nervous system, by the aspects of cancer-tissue invasion (biological) and chemical modulation of growth that cascades by releasing neural-related factors from the nerve endings via chemical substances known as neurotransmitters. In this review, we aimed to carefully demonstrate and describe the cancer invasion and interaction with the nervous system, as well as reveal the research progress and the emerging neuroscience of cancer. An initial set of 160 references underwent systematic review and summarization. Through a meticulous screening process, these data were refined, ultimately leading to the inclusion of 98 studies that adhered to predetermined criteria. The outcomes show that one formidable challenge in the realm of cancer lies in its intrinsic heterogeneity and remarkable capacity for rapid adaptation. Despite advancements in genomics and precision medicine, there is still a need to identify new molecular targets. Considering cancer within its molecular and cellular environment, including neural components, is crucial for addressing this challenge. In conclusion, this review provides good referential data for direct, indirect, biological, and chemical interaction for nerve tissue–tumor interaction, suggesting the establishment of new therapy techniques and mechanisms by controlling and modifying neuron networks that supply signals to tumors.

This study aimed to detect median effective dosage (ED₅₀) of midazolam oral solution (MOS) for preschool children in preoperative sedation. Thirty children (3–6 years old, with a body mass index (BMI) of 18–28 kg/m², American Society of Anesthesiologists status (ASA) I-II) scheduled for the hidden penis correction surgery under general anesthesia were selected. The effective dosage of MOS for preschool children in preoperative sedation was measured by sequential method. The initial dose was set at 0.5 mg/kg, with a concentration gradient of 0.1 mg/kg. Sedation was deemed successful if the patients’ Ramsay sedation scores were ≥4 and Frankl treatment compliance rating scale was ≥3, without any grade III or higher adverse events during anesthesia. If these criteria were met, the dosage for the next patient was reduced by one gradient based on the last patient's dosage, otherwise, the dosage for the next patient was increased by one gradient. This process was repeated until the 7th inflection point from unsuccessful to successful sedation was reached, at which point the trial was terminated. Probit regression analysis was used to calculate the ED₅₀, 95% effective doses (ED₉₅) and 95% confidence interval (CI) of MOS. Adverse reactions such as bradycardia, nausea, vomiting, and blurred vision were recorded during sedation. This study revealed that the ED₅₀ and ED₉₅ of MOS for preschool children preoperative sedation are 0.627 mg/kg (95% CI 0.582–0.669 mg/kg) and 0.795 mg/kg (95% CI 0.712–1.211 mg/kg), respectively, providing a reference for the administration of MOS in this population.