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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.

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.

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.

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.

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.

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.