Ibrain最新文献

Borderline personality disorder (BPD) is a dysfunctional, stable, and pervasive alteration in personality functioning with the inability to adapt to the environment, mental rigidity, and ego-syntonic. High suicidality in BPD patients underlines the significance of research into its pathology. While extensive research on the psychological and behavioral manifestations of BPD can be found in literature, the neuropsychological aspects of the disorder are still partially unknown, although the roles of certain brain structures in the manifestation of the pathology, such as the amygdala, hippocampus, insula, medial prefrontal and cingulate cortices, nucleus accumbens, and temporo-occipital areas, have already been clarified. This review aims to synthesize current knowledge of the neuroanatomical and functional correlates of BPD, providing insights that may inform future research and therapeutic strategies.

Alzheimer's disease (AD) is a common cause of dementia characterized by the presence of two proteinaceous deposits in the brain. These pathologies may be a consequence of complex interactions between neurons and glia before the onset of cognitive impairments. Curcumin, a bioactive compound found in turmeric, is a promising candidate for AD because it alleviates neuropathologies in mouse models of the disease. Although its clinical efficacy has been hindered by low oral bioavailability, the development of new formulations may overcome this limitation. The purpose of this study was to determine the effects of a bioavailable curcumin formulation in a mouse model of AD. The formulation was administered to mice in drinking water after encapsulation into micelles using a previously validated method. A neuropathological assessment was performed to determine if it slows or alters the course of the disease. Cognitive performance was not included because it had already been assessed by a previous study. The bioavailable curcumin formulation was unable to alter the size or number of amyloid plaques in a transgenic mouse model. In addition, mechanisms that regulate amyloid beta production were unchanged, suggesting that the disease had not been altered. The number of reactive astrocytes in the hippocampus and dentate gyrus was not altered by curcumin. However, protein levels of glial fibrillary acidic protein were increased overall in the brain, suggesting that it may have aggravated neuroinflammation. Therefore, a higher dosage, despite its enhanced oral bioavailability, may have a potential risk for neuroinflammation.

Fei-Sun Y, Huang M, Qin H-Y, et al. Protective effect of isoflurane preconditioning on neurological function in rats with HIE. ibrain. 2022;8:500-515.

We have identified an error in Figure 9 of our online publication, specifically in the experimental data. The issue stems from the repetition of the third enlarged image in the lower right corner of the figure was duplicate (the Row, “42d Protreatment” and the Column, “CA2”) and unintentionally included during the figure preparation process. However, we would like to clarify that there is no mistake in the corresponding text of the publication. To correct this figure, the restructured version of the figure is present below:

Updated Figure 9

We apologize for this error.

General anesthesia typically involves three key components: amnesia, analgesia, and immobilization. Monitoring the depth of anesthesia (DOA) during surgery is crucial for personalizing anesthesia regimens and ensuring precise drug delivery. Since general anesthetics act primarily on the brain, this organ becomes the target for monitoring DOA. Electroencephalogram (EEG) can record the electrical activity generated by various brain tissues, enabling anesthesiologists to monitor the DOA from real-time changes in a patient's brain activity during surgery. This monitoring helps to optimize anesthesia medication, prevent intraoperative awareness, and reduce the incidence of cardiovascular and other adverse events, contributing to anesthesia safety. Different anesthetic drugs exert different effects on the EEG characteristics, which have been extensively studied in commonly used anesthetic drugs. However, due to the limited understanding of the biological basis of consciousness and the mechanisms of anesthetic drugs acting on the brain, combined with the effects of various factors on existing EEG monitors, DOA cannot be accurately expressed via EEG. The lack of patient reactivity during general anesthesia does not necessarily indicate unconsciousness, highlighting the importance of distinguishing the mechanisms of consciousness and conscious connectivity when monitoring perioperative anesthesia depth. Although EEG is an important means of monitoring DOA, continuous optimization is necessary to extract characteristic information from EEG to monitor DOA, and EEG monitoring technology based on artificial intelligence analysis is an emerging research direction.

The immune response in the central nervous system (CNS) is a highly specialized and tightly regulated process essential for maintaining neural health and protecting against pathogens and injuries. The primary immune cells within the CNS include microglia, astrocytes, T cells, and B cells. They work together, continuously monitor the CNS environment for signs of infection, injury, or disease, and respond by phagocytosing debris, releasing cytokines, and recruiting other immune cells. In addition to providing neuroprotection, these immune responses must be carefully balanced to prevent excessive inflammation that can lead to neuronal damage and contribute to neurodegenerative diseases. Dysregulated immune responses in the CNS are implicated in various neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Wnt signaling is a crucial pathway in the CNS that regulates various cellular processes critical for brain development, function, and maintenance. Despite enhancing immune responses in the health CNS, dysregulated Wnt signaling exacerbates neuroinflammation in the neurodegenerative brains. This review summarized the role of Wnt signaling in regulating immune response under different conditions. We then examined the role of immune response in healthy brains and during the development of neurodegenerative diseases. We also discussed therapeutic intervention in various neurodegenerative diseases through the modulation of the Wnt signaling pathway and neuroinflammation and highlighted challenges and limitations in current clinical trials.

In central nervous system (CNS) surgery, the accurate identification of tumor boundaries, achieving complete resection of the tumor, and safeguarding healthy brain tissue remain paramount challenges. Despite the expertise of neurosurgeons, the infiltrative nature of the tumors into the surrounding brain tissue often hampers intraoperative differentiation between tumorous and non-tumorous tissue, thus hindering total tumor removal. Optical coherence tomography (OCT), with its unique advantages of high-resolution imaging, efficient image acquisition, real-time intraoperative detection, and radiation-free and noninvasive properties, offers accurate diagnostic capabilities and invaluable intraoperative guidance for minimally invasive CNS tumor diagnosis and treatment. Various OCT systems have been employed in neurological tumor research, including polarization-sensitive OCT systems, orthogonal polarization OCT systems, Doppler OCT systems, and OCT angiography systems. In addition, OCT-based diagnostic and therapeutic techniques have been explored for the surgical resection of CNS tumors. This review aims to compile and evaluate the research progress surrounding the principles of OCT systems and their applications in CNS tumors, providing insights into potential future research avenues and clinical applications.

Neurodegenerative disorders encompass a group of age-related conditions characterized by the gradual decline in both the structure and functionality of the central nervous system (CNS). RNA modifications, arising from the epitranscriptome or RNA-modifying protein mutations, have recently been observed to contribute significantly to neurodegenerative disorders. Specific modifications like N6-methyladenine (m6A), N1-methyladenine (m1A), 5-methylcytosine (m5C), pseudouridine and adenosine-to-inosine (A-to-I) play key roles, with their regulators serving as crucial therapeutic targets. These epitranscriptomic changes intricately control gene expression, influencing cellular functions and contributing to disease pathology. Dysregulation of RNA metabolism, affecting mRNA processing and noncoding RNA biogenesis, is a central factor in these diseases. This review underscores the complex relationship between RNA modifications and neurodegenerative disorders, emphasizing the influence of RNA modification and the epitranscriptome, exploring the function of RNA modification enzymes in neurodegenerative processes, investigating the functional consequences of RNA modifications within neurodegenerative pathways, and evaluating the potential therapeutic advancements derived from assessing the epitranscriptome.

Parkinson's disease (PD) is a common degenerative disease of the central nervous system that is characterized by movement disorders and non-motor symptoms (NMSs). The associated NMSs primarily include neuropsychiatric symptoms, autonomic dysfunction, sleep-wake disorders, pain, fatigue, and hyposmia. These NMSs can occur at any stage of PD, especially before the onset of motor symptoms, and may affect a patient's quality of life more than motor symptoms. Although PD is most commonly diagnosed in people over 65 years, some patients exhibit symptom onset before the age of 50, which is clinically known as early-onset Parkinson's disease (EOPD). The high heterogeneity and incidence of EOPD-associated NMSs can lead to the misdiagnosis of EOPD as other neurodegenerative diseases. In this review, we discuss the research progress related to NMSs in patients with EOPD, focusing on neuropsychiatric disorders, autonomic dysfunction, sleep disorders, and sensory impairment, and outline the association of NMSs with different genotypic alterations, with the aim of providing assistance in the clinical management of patients.

The management of deep brain stimulation (DBS)-related surgical site infection (SSI) is challenging. This article aimed to report the efficacy of negative pressure wound therapy (NPWT) in treating DBS-related SSI while preserving all DBS devices. As a retrospective case series in a single center, localized DBS-related SSI was treated with complete debridement and NPWT, with preserving all DBS devices. Successful infection control was defined as no clinical or microbiological evidence of recurrent infection 3 months after NPWT. Five patients (three females, two males, median age: 64 years) received NPWT for their DBS-related SSI. The infection was located in the chest, parietal, and retroauricular areas. Only one patient had the extension wires removed due to the heavy contamination, while no DBS devices were removed in the other patients. All patients showed successful infection control without any remarkable side effects 3 months after debridement and NPWT. These findings suggest that NPWT may effectively promote wound healing with a high probability of preserving all DBS devices in DBS-related SSI.

This study aims to explore the expression profile of PANoptosis-related genes (PRGs) and immune infiltration in Alzheimer's disease (AD). Based on the Gene Expression Omnibus database, this study investigated the differentially expressed PRGs and immune cell infiltration in AD and explored related molecular clusters. Gene set variation analysis (GSVA) was used to analyze the expression of Gene Ontology and Kyoto Encyclopedia of Genes and Genomes in different clusters. Weighted gene co-expression network analysis was utilized to find co-expressed gene modules and core genes in the network. By analyzing the intersection genes in random forest, support vector machine, generalized linear model, and extreme gradient boosting (XGB), the XGB model was determined. Eventually, the first five genes (Signal Transducer and Activator of Transcription 3, Tumor Necrosis Factor (TNF) Receptor Superfamily Member 1B, Interleukin 4 Receptor, Chloride Intracellular Channel 1, TNF Receptor Superfamily Member 10B) in XGB model were selected as predictive genes. This research explored the relationship between PANoptosis and AD and established an XGB learning model to evaluate and screen key genes. At the same time, immune infiltration analysis showed that there were different immune infiltration expression profiles in AD.