Hormonal contraceptives (HCs) contain synthetic gonadal hormones that act on receptors widely distributed throughout the brain, thereby altering the body's endogenous hormonal milieu in ways that may influence brain and behavior. Although HCs are among the most commonly prescribed medications for female adolescents, their effects on the developing brain and mental health remain poorly understood. This gap is concerning given that adolescence is marked by substantial hormonal change, neurodevelopment, and a sharp rise in depression risk among female youth. In this review, we synthesize current evidence on associations between adolescent HC use, depression risk, and brain structure and function. Epidemiological studies have consistently reported associations between HC use during adolescence and increased depression risk, but causal interpretation is limited by residual confounding. Neuroimaging research remains scarce, particularly in adolescents, and rarely accounts for heterogeneity in HC formulations and characteristics of use or for endogenous hormonal variation related to puberty or the menstrual cycle. We outline 3 considerations to guide future research: accounting for HC heterogeneity, incorporating developmental features of adolescent menstrual cycles, and situating HC use within its broader developmental and sociocultural context. We conclude by emphasizing the need for rigorous developmentally sensitive research to counter misinformation and better support adolescents' reproductive and mental health care needs. Hormonal contraceptives (HCs) are widely used by adolescent girls, but their potential effects on the developing brain and mental health are not well understood. This matters because puberty brings major hormonal and brain changes, and depression risk rises for girls during adolescence. Many population studies link adolescent HC use to higher depression risk, but these findings may reflect other differences between users and nonusers. In this review, we evaluate evidence linking adolescent HC use with depression risk and with brain structure and function. We highlight key research gaps and priorities to reduce misinformation about HCs and better support adolescents’ reproductive and mental health.
Over the past century, research on meditation and mindfulness has aimed to characterize the behavioral phenomenology and the neurophysiology of the contemplative mind. In recent years, investigators have extended this work beyond single participants to dyads and larger groups using hyperscanning (the simultaneous recording of neural activity from two or more individuals). This narrative review synthesizes interbrain connectivity research and explores dyadic synchrony findings within mindfulness and meditation practices. Among the selected studies (n = 7), interbrain synchronization was observed across protocols and spectral bands in five studies. Anterior theta phase synchrony was evident during cooperation tasks following mindfulness induction. Motor coordination tasks with shared breathing and physical mirroring elicited alpha, theta, and delta coherence in frontal brain regions. Gamma synchrony increased in socio-emotional paradigms and among expert meditators practicing together. Dyadic coupling in lower-frequency spectral bands was potentiated when breath focus was combined with a shared goal. The evidence reviewed suggests that interbrain synchrony varies as a function of expertise, task heterogeneity, and personality traits such as agreeableness.
To explore the current management status and challenges of brain-computer interface (BCI) rehabilitation medical devices. The existing classification system in China faces several problems, including a single classification dimension, insufficient risk adaptation, and having difficulties in coping with technological iteration. This study aims to propose scientific classification ideas and promote the healthy and orderly development of such devices in the medical field. By sorting out the regulatory experience of the United States, the European Union and Japan, combining the current situation of BCI technology research and classification management in China, this study analyzes the technical characteristics of BCI products and the current status of "ambiguous definition and classification, and pending update of regulations and standards". On this basis, a three-dimensional classification model based on "function, risk and invasiveness" is constructed. The core function of these products is defined as "collecting electroencephalographic signals to identify patients' intentions for rehabilitation training or adjuvant therapy". Subdivisions such as "invasive/non-invasive" and "rehabilitation training/augmentative and alternative communication/mental illness treatment" are achieved. For example, multi-functional devices for stroke patients are classified as "medium risk". International practices are integrated to overcome the limitations of traditional classification, providing a path for China to learn from international ideas. Space is reserved for technological iteration, such as new electrodes and artificial intelligence algorithms. By clarifying functional purposes and risks, the proposed classification idea provides a basis for supervision. It can be optimized with the expansion of technology and scenarios, and it helps make the classification of BCI products more scientific . 探讨脑机接口（brain-computer interface，BCI）类康复医疗器械的管理现状与挑战，解决我国现有分类体系“维度单一、风险适配不足、难以应对技术迭代”的问题，提出科学分类的思路，促进其在医疗领域健康有序发展。. 梳理美、欧、日的监管经验，结合我国BCI技术研究与分类管理现状，分析BCI类产品技术特点及“定义分类模糊、法规标准有待更新”的现状，构建“功能、风险、侵入性”三维分类模型。. 明确该类产品以“采集脑电信号识别患者意图、用于康复训练或辅助治疗”为核心功能，通过模型实现“侵入式/非侵入式”“康复训练/辅助交流/精神疾病治疗类”细分（如脑卒中患者多功能设备可定为“中风险”）；融合国际经验，解决传统分类局限，为我国借鉴国际思路提供路径，且为技术迭代（如新型电极、AI算法）预留空间。. 该分类思路通过明确功能、用途与风险，为监管提供依据，可随技术与场景的拓展优化，助力BCI类产品的分类工作更具科学性。.
Alzheimer's disease (AD) is one of the most diagnosed neurodegenerative disorders worldwide and presents a significant challenge for both affected individuals and their caregivers. Alzheimer's disease is characterized by the accumulation of amyloid plaques and dysfunctional tau protein in the brain, along with the final development of dementia. Recently, in addition to the strongly developing ischemic etiology of AD, it is suggested that the gut and oral microbiota may also participate in the development of this disease. This involvement may stem from an unbalanced diet and the consumption of foods containing harmful chemical additives. An unhealthy diet can compromise the integrity of the gut barrier, facilitating the translocation of bacterial pathogens and leading to a pro-inflammatory T-cell response mediated by innate immune cells. This inflammatory response can disrupt systemic homeostasis and may contribute to neuroinflammation. The brain and gut interact through a complex network known as the "gut-brain-microbiota axis," and emerging studies suggest that the intestinal microbiota and their metabolites may play a significant role in the pathogenesis of Alzheimer's disease. Moreover, these inflammatory mediators and microbial metabolites can reach the brain via the gut-brain axis, potentially exacerbating neurodegenerative processes. Preclinical and limited clinical evidence indicates that low-fiber diets are associated with alterations in intestinal microbiota composition, which may contribute to the onset and progression of Alzheimer's disease. This review aims to explore the potential connections between AD and the gut microbiome, emphasizing the significance of dietary factors in shaping these relationships. A comprehensive understanding of the interactions between the human microbiome and the brain, particularly in the context of diet and its ingredients, may enhance our understanding of AD etiology and inform the development of preventative strategies, through dietary modifications or therapeutic interventions. This area of research holds promise for identifying novel approaches to prevent or slow the progression of AD.
To explore the prevalence and outcomes of dysphagia in paediatric acquired brain injury, associated with aetiology, unilateral and bilateral injury, and brain regions involved, while considering age, sex, and length of stay. This was a retrospective observational cohort study of 85 children with acquired brain injury (50 males, 35 females; age range 6 months to 16 years, mean 8 years 2 months, SD 5 years 3 months). Aetiologies included traumatic brain injury (TBI) (n = 24), stroke/vascular injury (n = 23), hypoxic/ischaemic injury (n = 8), infection (n = 15), autoimmune conditions (n = 8), and other causes (n = 7). Dysphagia at admission and discharge was recorded; magnetic resonance imaging review identified lesion laterality and regions involved. One-year follow-up evaluated recovery in children with dysphagia at discharge. Dysphagia prevalence at admission varied (TBI 83%, stroke/vascular 52%, hypoxic 100%, infection 87%, autoimmune 63%, other 43%), decreasing at discharge (TBI 33%, stroke/vascular 8%, hypoxic 87%, infection 13%, autoimmune 25%, other 0%). At admission, 97.6% of children with bilateral injury presented with dysphagia, compared to 47.7% with unilateral injury. All children with unilateral injury had resolved dysphagia at discharge, compared to 47.5% with bilateral injury. Children with both cortical and subcortical injury showed low resolution of dysphagia at discharge (33%). Dysphagia is prevalent in paediatric acquired brain injury. Bilateral injuries, particularly involving cortical and subcortical regions, are associated with persistent dysphagia.
Background Brain abscess following sinonasal mucormycosis is a rare and life-threatening complication. Since our knowledge is mostly based on case reports, a well-documented way of treatment for such cases is yet to be found. Case Description A retrospective case series study was conducted at a tertiary hospital. Patients whose brain abscesses were treated without opening the dura during surgery were selected for the study. The patients received radical debridement of necrotic tissues as well as the infected bones adjacent to the brain abscess. Then, they were treated medically. Three patients were included in the study. All patients had a history of diabetes and COVID-19 before developing symptoms of sinonasal infection. The average size of the abscesses was less than 2 cm. Conclusion Removing infected tissues and bones surrounding the brain abscess without opening the dura can be a viable treatment option for mucormycosis-induced brain abscesses of less than 2 cm.
Kynurenine pathway (KP), the principal route of tryptophan (TRY) metabolism, is implicated in schizophrenia (SCZ), but findings remain inconsistent, particularly regarding peripheral-central associations and links to immune dysregulation. We measured KP metabolites, cytokines, and metabolic risk factors in serum from drug-naïve (DN) and risperidone-treated (RT) SCZ patients versus healthy controls (HC) as well as in post-mortem brain tissue from an independent cohort by assessing KP metabolites, enzyme expression (mRNA, protein) and cytokine profiles. We recruited a total of 227 participants from the clinical services of a large neuropsychiatric hospital, which included DN SCZ (n = 66), RT SCZ (n = 87), and HC (n = 74). Additionally, brain KP metabolite levels and the mRNA and protein expression of key enzymes and cytokines were evaluated in the dorsolateral prefrontal cortex (DLPFC) samples from the post-mortem cohort of 10 SCZ patients and 17 controls. KP metabolites were measured using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Both DN and RT groups exhibited significantly reduced TRY (p < 0.05), elevated kynurenine (KYN), kynurenic acid (KYNA), KYN/TRY ratio and serotonin (SER) in serum (p < 0.001), alongside higher TNF-α, and IFN-γ and lower IL-10 (p < 0.001 for both). These alterations were correlated with metabolic risk factors, symptom severity of SCZ, and immune markers, and these remained associated with disease status after adjusting for confounders. Post-mortem analyses confirmed increased brain KYN (p < 0.05) and KYNA (p < 0.001) in the DLPFC of SCZ, accompanied by upregulation of Tryptophan 2,3-dioxygenase (TDO2) (p < 0.001) and Kynurenine aminotransferase II (KAT II) (p < 0.05) expression and elevated pro-inflammatory cytokines. Our findings provide convergent evidence for KP dysregulation in SCZ, linking immune activation with enhanced change toward KYNA synthesis both systemically and centrally. The observed alterations across independent serum and post-mortem brain cohorts support the potential relevance of these molecular signatures to SCZ pathophysiology and their possible therapeutic implications.
Depressive disorders are highly heterogeneous syndromes characterized not only by depressed mood but also by cognitive impairment, sleep-circadian rhythm disturbances, altered appetite, somatic discomfort, and metabolic or gastrointestinal comorbidities. In recent years, the microbiota-gut-brain axis (MGBA) has been increasingly recognized as an integrative biological framework linking abnormalities in mood regulation, immune responses, endocrine function, metabolism, and neuroplasticity. This review provides a systematic synthesis of gut microbial ecology and host phenotypic features associated with depressive disorders, with particular emphasis on the depletion of short-chain fatty acid-producing commensals, the enrichment of potentially pro-inflammatory taxa, and the functional remodeling of key metabolic pathways, including the tryptophan-kynurenine pathway, short-chain fatty acids, bile acids, and trimethylamine N-oxide. We further discuss how bidirectional gut-to-brain and brain-to-gut communication may contribute to the onset and progression of depressive disorders through intestinal barrier disruption, low-grade systemic inflammation, hypothalamic-pituitary-adrenal axis activation, vagal signaling, and dysregulation of neurotransmitter and neurotrophic pathways. Current interventional evidence suggests that dietary and lifestyle modification, psychobiotics, and fecal microbiota transplantation may exert antidepressant potential in selected populations; however, the overall effect sizes remain limited and between-study heterogeneity is substantial. Patients with prominent gastrointestinal symptoms, metabolic abnormalities, or low-grade inflammatory states may represent priority candidates for MGBA-targeted interventions; nevertheless, a putative microbiota-responsive phenotype should not be simply equated with high stress exposure alone, and its definition requires prospective validation integrating stress burden, host responses, and microbial/metabolic readouts. Overall, MGBA research is gradually moving beyond descriptive profiling of microbial composition toward functional integration and clinical translation; however, causal inference, multi-omics standardization, and the identification of stratification biomarkers remain major challenges. Future studies should incorporate phenotype-based stratification, strengthened functional readouts, and precision intervention designs to determine which patients are most likely to benefit from microbiota-targeted therapies.
HER2-positive (HER2+) breast cancer (BC) is associated with a high incidence of brain metastases (BMs), which negatively affect prognosis and quality of life. Local therapies, such as whole-brain radiotherapy (WBRT), stereotactic radiotherapy, stereotactic radiosurgery, and neurosurgery, allow temporary control of metastatic spread. Systemic treatments are limited by the blood-brain barrier (BBB), which restricts the passage of many therapeutic molecules. Research initially focused on small molecule tyrosine kinase inhibitors due to their low molecular weight. Recent evidence suggests that tumor-induced disruption of the BBB may increase its permeability, potentially allowing larger molecules, including antibody-drug conjugates, to cross. Although trastuzumab deruxtecan (T-DXd) has demonstrated intracranial activity, evidence of durable complete responses in heavily pretreated patients with active BMs remains limited. We report a case of a HER2+ BC patient with multiple (>20) active BMs, previously treated with WBRT and trastuzumab emtansine (T-DM1), who developed intracranial progression. Third-line treatment with T-DXd resulted in a complete radiological intracranial response, which has been maintained for more than 20 months under ongoing therapy, with associated improvement in neurological symptoms and quality of life. This case provides preliminary evidence that T-DXd may achieve deep and durable intracranial responses even in heavily pretreated patients with active BMs, including those previously treated with WBRT and T-DM1. The exceptional duration of response observed in this case appears to exceed historical expectations and warrants further investigation in this high-risk population.
Bilingualism is increasingly common in families worldwide, yet bilingual individuals remain underrepresented in developmental neuroscience research. In simultaneous bilingualism, children typically acquire two languages simultaneously from birth, while their parents tend to learn the societal language later in life. These differences in language acquisition may influence how parents and children communicate, particularly when interacting in a second language. Neural synchrony, the temporal alignment of brain activity between individuals, has emerged as a key mechanism underlying social connection, communication, and learning in early development. However, little is known about how language choice affects neural synchrony in bilingual parent-child interactions. This study used functional near-infrared spectroscopy (fNIRS) hyperscanning to simultaneously record brain activity from 15 bilingual mother-child dyads during naturalistic play. Each dyad completed three conditions: collaborative play in the mother's native language, collaborative play in English (the mother's second language), and independent play. Neural activity was recorded from the prefrontal cortex (PFC) and temporoparietal junction (TPJ), regions associated with social cognition, joint attention, and mentalising. Families took part in a naturalistic free play paradigm, allowing them to interact in a comfortable and ecologically valid manner. Both native- and English-language play elicited significantly greater neural synchrony across the PFC and the TPJ than independent play, validating the use of naturalistic free play paradigms. No significant overall differences emerged between native and English play, indicating that bilingual dyads maintain inter-brain coupling across languages when both partners are proficient. Exploratory analyses suggested a trend toward higher child-directed synchrony in English play and age-related trends in mother-directed synchrony; however, these effects did not reach statistical significance. Our findings show that bilingualism does not compromise mother-child neural synchrony, supporting the inclusion of linguistically diverse families in developmental neuroscience. They underscore the value of naturalistic paradigms and highlight the need for future research on language proficiency, partner familiarity, and behavioral correlates of synchrony. This work highlights the importance of studying bilingual families in ecologically valid contexts to better understand how language use influences neural coupling in early development.
Vascular endothelial growth factor receptor tyrosine kinase inhibitors (VEGFR TKIs) are widely used in the treatment of metastatic renal cell carcinoma (RCC). Although hemorrhagic events are recognized adverse effects of these agents, intracranial hemorrhage is rare, and the safety of re-administration of VEGFR TKIs after central nervous system (CNS) hemorrhage remains unclear. We report a 52-year-old man with metastatic clear cell RCC who initially received first-line immunotherapy with ipilimumab and nivolumab, resulting in disease progression, followed by second-line sunitinib, which achieved a partial response. However, he subsequently developed sudden neurological deterioration, and brain imaging revealed multifocal cerebellar hemorrhages without evidence of brain metastasis; the absence of metastasis was confirmed by surgical and histopathological examination. After surgical management, complete radiologic resolution of the hemorrhage was confirmed 4 weeks postoperatively. Pazopanib was subsequently initiated based on the prior favorable response to VEGFR TKI therapy; however, recurrent cerebellar hemorrhage occurred within 4 weeks of rechallenge, leading to rapid clinical deterioration and death despite supportive care. This case highlights that VEGFR TKI-associated intracranial hemorrhage can occur even in the absence of brain metastases and may recur with fatal consequences upon rechallenge. These findings suggest that early VEGFR TKI rechallenge (<1-2 months) after CNS hemorrhage may be unsafe, and that careful risk-benefit assessment with an adequate waiting period is essential when considering re-administration.
Functional magnetic resonance imaging (fMRI) provides a crucial window for understanding brain functional connectivity (FC) in psychiatric disorders, yet its complex spatiotemporal dynamics pose substantial challenges for modeling. Existing methods often rely on static FC, making it difficult to capture the dynamic plasticity of brain, while generally ignoring structural differences across functional networks or discarding informative weak connections due to excessive sparsification. Here, we propose SPSGL, a biologically inspired deep learning framework designed to construct novel brain connectivity patterns from fMRI signals. SPSGL transforms voxel-wise time series into frequency-domain, feature-driven functional brain graphs and employs a biologically inspired gated edge-update mechanism to capture dynamic changes in connectivity strength. On this basis, core functional networks and whole-brain patterns are mapped as structural priors to explicitly guide multi-head attention in forming complementary subspace foci that emphasize neurobiologically meaningful connections. Further combined with Orthonormal Clustering Readout (OCRead), our model achieves adaptive learning of multi-scale brain graph representations and functional parcellations. Across five psychiatry-related computational tasks, SPSGL demonstrates superior performance compared with existing approaches. Moreover, it identifies task-relevant functional connections and hub regions associated with aberrant coupling among the default mode, sensorimotor, and subcortical networks, highlighting potential neuroimaging biomarkers and uncovering shared brain network factors shared across diverse psychiatric conditions. Overall, SPSGL provides a unified, interpretable, and high-performing framework for fMRI-based brain connectivity analysis, advancing mechanistic understanding and potential clinical translation in mental health research. Our code is publicly available on https://github.com/zhaoqi106/SPSGL. The online version contains supplementary material available at 10.1007/s13755-026-00467-6.
Although lactate levels and lactate clearance are associated with outcomes in shock states, their prognostic value in brain-dead potential organ donors remains unclear and is not mentioned in clinical guidelines as a perfusion marker to guide clinical intervention. We aimed to evaluate whether lactate levels and lactate clearance may predict losses of brain-dead potential organ donors to cardiac arrest. This was a secondary analysis embedded within the cluster-randomized DONORS trial. Participants were stratified according to baseline lactate level: <2 mmol/L and ≥2 mmol/L. Individuals with lactate measurements at enrollment and after 6 h were classified according to lactate clearance: <10% or ≥10%. The primary outcome was loss of potential donors to cardiac arrest prior to organ procurement. Among 1043 participants, those with baseline lactate ≥2 mmol/L were more likely to develop cardiac arrest (53/386 [13.7%] vs. 62/657 [9.4%]; p = 0.016) and less likely to become actual donors (151/386 [39.1%] vs. 308/657 [46.9%]; p = 0.022). In adjusted analyzes, baseline lactate ≥2.0 mmol/L was associated with increased risk of cardiac arrest (OR, 1.59; 95% CI, 1.09-2.33; p = 0.016). High lactate clearance was associated with more cardiac arrests (OR, 3.44; 95% CI, 1.61-7.14; p = 0.001). Elevated baseline lactate identifies brain-dead potential donors at increased risk of cardiac arrest, whereas a lactate clearance <10% was associated with a higher risk.
For implantable closed loop neuromodulation systems, real-time neural sensing, biomarker detection, and targeted stimulation are essential components for delivering personalized therapy. Current limitations in sampling rate and the number of available recording channels in implantable systems may pose significant challenges, especially in epilepsy research where high-frequency biomarkers and multi-site monitoring are essential. The Brain Interchange (BIC) system of CorTec is an externally powered, wireless implantable system that enables sensing and stimulation up to 32 channels at 1 kHz addressing the current limitations in the field. In this study, we present a modular closed loop neuromodulation environment developed for the BIC, enabling real-time data streaming, event detection, and flexible stimulation control. The framework integrates a Simulink-based processing pipeline, real-time communication, and a graphical user interface supporting both open and closed loop paradigms. System performance was evaluated through impedance measurement, latency assessment across three stimulation modes, and real-time closed loop stimulation using electrocardiogram (ECG) for in-lab demonstration. This modular environment provides a flexible platform for developing and validating neuromodulation algorithms and can be extended to incorporate advanced biomarker detection and multi-channel neural interfaces for future clinical research.
Objectives Early prediction of neurological outcomes in patients with out-of-hospital cardiac arrest (OHCA) is critical for guiding treatment decisions. Machine learning (ML) model and grey-white matter ratio (GWR), both derived from brain computed tomography (CT), can be used to predict the neurological outcome. However, their relative performance shortly post-return of spontaneous circulation (ROSC) and whether combining the ML model with prehospital information can improve predictive performance remains unclear. This study aimed (1) to compare the predictive performance for poor neurological outcome between the ML model and manually measured GWR in the early phase after ROSC in patients with OHCA, and (2) to assess the predictive ability of the combination of the ML model and prehospital information. Methods This single-center retrospective study included adult patients who underwent brain CT within two hours post-ROSC. The endpoint was consecutive coma post-ROSC. Three slice levels (basal ganglia, centrum semiovale, high convexity) of brain CT images were used to generate the ML model and the GWR. Residual Network 101 (ResNet-101) with transfer learning was constructed in the ML model. Results Among the 143 cases, 88 patients had a persistent coma, and 55 awoke from coma. Across 10 repeated five-fold cross-validations, the area under the receiver operating characteristic curves (AUCs) for predicting persistent coma between the three-slice ensembled ML model and the average GWR were not significantly different (ML model: 0.796 (interquartile range (IQR): 0.737-0.826), GWR: 0.821 (IQR: 0.763-0.854); p = 0.121). In the regression analysis, the AUC of the model based on prehospital information was 0.846 (95% CI: 0.772-0.92), which improved to 0.905 (95% CI: 0.856-0.953) after adding the ML score. Conclusion The ML model achieved moderate predictive performance, with no significant difference compared with the conventional GWR method. The combination of the ML model and prehospital information could improve predictive performance.
Longstanding distinctions between "verbal" and "mathematical" minds continue to shape educational assessment, curriculum design, and how learners are categorized by perceived cognitive strengths. Yet plenty of evidence from psychology and cognitive neuroscience points to a more unified model of intelligence that refutes the false dichotomy. In this article, I propose dual-domain cognitive fluency (DDCF) as a way to describe how the human mind can move fluidly between words and numbers and derive meaning from both. Building on research in symbolic cognition, executive function, and cognitive flexibility, this article identifies three dimensions: symbolic translation between modalities, cognitive flexibility across task demands, and layered reasoning, which integrates propositional logic with linguistic abstraction. DDCF captures the symbolic agility now required in knowledge-based environments where the integration of representational systems matters more than isolated domain expertise. Examples range from data storytelling in journalism to algebraic modeling in the social sciences-contexts in which verbal and quantitative reasoning operate in tandem. These insights matter for pedagogy, curriculum design, and the evolving demands of data-intensive workplaces. Far from a niche ability, dual-domain fluency reflects a generalizable cognitive capacity that existing models of intelligence have struggled to measure, reward, or systematically support.
The vigilance decrement in speed and accuracy of response is prevalent in studies of sustained attention. The amplitudes of Event-Related Potentials (ERPs) elicited by task stimuli also show temporal decline. However, it is difficult to link the behavioral performance decrement to loss of efficiency in the specific brain circuits that control human attention. A recent study published by the authors used an extended duration-version of the Attention Network Test to explore temporal changes in behavioral and electroencephalographic indices in executive control, alerting, and orienting attention networks. This study found evidence for temporal decline in ERPs associated with the alerting network, as well as slowing of uncued reaction time. This study, like most psychophysiological studies of sustained attention, analyzed group data. The present article provides new analyses of data from the authors' previous study to investigate individual differences in loss of attention on the extended ANT, and their relationships with positive and negative affect. Data analyses addressed the temporal stability of attention network metrics, inter-relationships between different metrics, and associations between metrics and affective states. Results illustrated some challenges in assessment of brain networks at the individual level on tasks requiring sustained attention. Issues included differential temporal stability of metrics, divergence of behavioral and ERP measures, and distinguishing changes in network function from changes in baseline response. The ANT is well-supported by group data as a tool for investigating attentional functioning. However, the present results suggest that caution is necessary in utilizing network indices at the individual level in clinical and other applied contexts.
Traditional neuroscience describes the cerebral cortex as a mosaic of discrete, functionally specialized regions. However, a complementary view has emerged, demonstrating that the brain is also organized along continuous gradients that capture large-scale transitions in connectivity, microstructure, and function. These gradients, derived using dimensionality reduction techniques on neuroimaging data, provide a low-dimensional manifold framework that unifies our understanding of how cortical architecture supports cognitive flexibility, learning, and clinical disorders. In this review, we integrate evidence from genetics, phylogeny, development, and multimodal neuroimaging to outline how macroscale gradients emerge from underlying biological constraints, become progressively decoupled from local microstructure in transmodal cortex, and dynamically reorganize during cognitive and clinical states. We further discuss how this framework provides new insights into individual differences, disease mechanisms, and recovery following brain injury. By bridging anatomy, function, and behavior, gradient-based approaches offer a powerful lens for mapping the architecture of human cognition and its disruption in disease.
The publisher identified, after publication of this article [1], that the publication year was incorrectly printed as 2024 instead of 2025. This error has now been corrected. The original article can be found online at: https://www.eurekaselect.com/article/149361 We regret the error and apologize to readers. Details of the correction: Original Received Dates: October 24, 2024 Accepted: March 21, 2024 Corrected ; Received Dates: October 24, 2025 Accepted: March 21, 2025.
In recent years, allicin has received extensive attention in the field of neuroprotection. This mini-review summarizes the extraction, detection, synthesis, toxicity, novel drug delivery systems of allicin and its research progress in neurological diseases. We found that allicin can exert neuroprotective effects in Alzheimer's disease, Parkinson's disease, traumatic brain injury, cerebral ischemia-reperfusion injury, cerebral hemorrhage, and subarachnoid hemorrhage by inhibiting oxidative stress, neuroinflammation, and apoptosis, regulating mitochondrial function, and improving blood-brain barrier integrity. However, current studies are mostly limited to animal experiments and lack high-quality clinical research evidence. Additionally, the unstable chemical properties and low bioavailability of allicin have limited its clinical translation. In the future, more randomized controlled clinical trials should be conducted and new delivery systems should be developed to improve its stability and targeting. This mini-review aims to provide a theoretical basis for further research and application of allicin in neurological diseases.