Neuroscience最新文献

This neuroimaging study sought to characterize differences in cortical gray-white matter contrast (GWC) between individuals with anorexia nervosa (AN) and age-matched healthy controls (HC) and compare these findings with conventional cortical thickness (CT) measures. The study included 58 female participants (29 AN, 29 HC). T1-weighted images were acquired using a 3 T scanner and processed with FreeSurfer. GWC maps were calculated at each cortical vertex. Vertex-wise general linear models assessed group differences in GWC controlling for age only, and controlling for age and vertex-wise CT. A separate model tested CT differences. Models were corrected for multiple comparisons using cluster-wise correction. Spearman correlations related mean GWC in significant clusters to BMI at scan, age at onset, and illness duration. The age-only model revealed two clusters in the left hemisphere with higher GWC in patients with AN, namely the inferior temporal cortex and medial orbitofrontal cortex. No clusters survived in the model controlling for age and CT. The CT analysis revealed no significant group differences. Mean GWC in clusters did not correlate with clinical severity indices in AN. Patients with AN exhibit focal increases in GWC despite the absence of detectable cortical thinning, suggesting that the GWC can provide complimentary information in understanding the neurobiology of AN. The elimination of GWC differences when adjusting for CT likely reflects shared variance rather than true absence of effect. Lack of correlations with clinical indices may be due to limited sample size. Future longitudinal and multimodal studies are warranted to determine the underpinnings of GWC alterations.

The trade-off between proactive and reactive cognitive control refers to the dynamic regulation process by which individuals flexibly allocate cognitive resources according to task demands-representing a core feature of cognitive control flexibility. Previous research has shown that emotion can significantly affect this trade-off, but most studies have focused on emotional valence and arousal, lacking a systematic investigation into how emotional motivation influences the trade-off in cognitive control. Using the AX-Continuous Performance Task paradigm, the present study systematically examined the mechanisms by which different emotional motivations impact the trade-off between proactive and reactive control. Results showed that proactive control increased under both approach and avoidance motivation, as indicated by higher Proactive Control Index scores and larger CNV amplitudes than baseline. In contrast, reactive control improved only under avoidance motivation: behaviorally, avoidance enhanced BX performance, and electrophysiologically it produced a larger P3a amplitude than both approach and baseline. Approach motivation did not produce a reliable change in reactive control. These findings suggest that approach and avoidance motivation differentially modulate proactive and reactive control, thereby influencing the dynamic trade-off between cognitive control modes and revealing a regulatory process through which emotion may shape cognitive control strategy selection.

This study aims to explore the role of the central nervous system network outside the auditory system in the development process of noise - induced central injury. A noise-exposed rat model was established with unilateral narrow-band noise. Auditory brainstem response (ABR) measured hearing thresholds at Click and 8, 16, 24, 32 kHz pre- and post-noise exposure. Experimental rats were split into transcutaneous auricular vagus nerve stimulation (ta-VNS) and sham subgroups for 2-week intervention. Resting-state fMRI (rs-fMRI) was performed on all groups (ta-VNS, sham, control) post-noise exposure and 2 weeks post-intervention. After noise exposure, 22 rats had elevated hearing thresholds at 8, 24, 32 kHz. fMRI revealed increased ALFF/ReHo in the entorhinal cortex, amygdalar cortex, and hippocampus, decreased values in the prelimbic cortex, basal forebrain, striatum, and cingulate cortex, and enhanced cingulate cortex-basal forebrain functional connectivity. The rats were divided into ta-VNS (n = 10) and sham (n = 12) subgroups for 2-week intervention. Compared with the control group (n = 9), both subgroups showed similar brain activation/inhibition in regions like the entorhinal cortex pre- vs. post-intervention. However, the ta-VNS group reversed noise-induced reduced neural activity in the prelimbic cortex and basal forebrain, and significantly enhanced their functional connectivity. Noise exposure increased entorhinal cortex, hippocampus, and amygdala activity in rats, potentially linked to aversive emotions and abnormal auditory memory. The prelimbic cortex-centered network may gate noise-induced aversive perception, with cingulate cortex activity/connectivity disrupted. ta-VNS may alleviate such perception by reversing reduced neural activity in gating-related regions and enhancing their connectivity, plus strengthening brainstem-limbic and brainstem-cerebellum functional links.

Parkinson's Disease (PD) is a neurodegenerative disorder primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra, leading to classical motor symptoms such as tremors, rigidity, and bradykinesia. In later stages, patients frequently develop non-classical symptoms, including respiratory dysfunctions, which may result from neurodegeneration in brainstem regions involved in respiratory control, such as the pre-Bötzinger Complex (preBötC) and the retrotrapezoid nucleus (RTN). These changes are likely driven by oxidative stress and neuroinflammation. Given the antioxidant and anti-inflammatory properties of omega-3 polyunsaturated fatty acids, this study investigated whether omega-3 supplementation could prevent respiratory-related neuroanatomical and respiratory dysfunctional alterations in a mouse model of PD induced by bilateral injection of 6-hydroxydopamine into the striatum. Omega-3 supplementation prevented respiratory dysfunction by preventing neuronal loss in the preBötC and RTN, reducing glial reactivity and oxidative stress, and maintaining respiratory frequency. These findings support the therapeutic potential of omega-3 in mitigating respiratory dysfunction in PD.

Humans primarily rely on bodily sensations to experience emotions. Alexithymia, however, alters individuals' emotional experiences. Despite this, limited research has examined whether individuals with different levels of alexithymia experience the same emotions when exposed to identical bodily sensations. The present studies aimed to explore the altered representation of interoceptive sensations in individuals with alexithymia. In Study 1, we measured how participants associated interoceptive sensations with emotion categories using a computer mouse. In Study 2, event-related potentials (ERPs) were recorded simultaneously while participants performed the same task. Mouse trajectories and the N400 component were analyzed, and ANOVA was conducted to examine the differences in both mouse trajectories and N400 amplitudes. In Study 1, we found that individuals with high alexithymia (HA) exhibited less direct and more curved mouse trajectories compared to those with low alexithymia (LA). Study 2 confirmed these behavioral findings and further revealed that HA individuals exhibited greater N400 amplitudes than LA individuals. Our findings suggest that HA individuals experience deficits in the representation of interoceptive sensations, with the N400 serving as a potential index of these deficits in individuals with alexithymia.

Abnormal activity within supplementary motor area (SMA) has been associated with impaired speech and limb movement in neurological conditions. Normalizing aberrant neural activity through non-invasive neuromodulation techniques over SMA has demonstrated promising effects in ameliorating motor and non-motor functions. However, there is limited research on the application of transcranial electrical stimulation (tES) over the left SMA as a potential non-invasive protocol to improve speech production. In this study, we examined the effects of several tES protocols, including high-definition transcranial alternating current stimulation (HD-tACS), transcranial random noise stimulation (tRNS), and direct current stimulation (HD-tDCS), targeting the left SMA in neurotypical adults, on speech and limb reaction times. In a sham-controlled dual-experiment design, two groups of neurologically intact adult participants underwent multiple stimulation sessions: Experiment 1) sham HD-tACS, HD-tACS tuned to each individual's frequency of maximal SMA beta activity (15-30 Hz) during speech (tuned-to-speech) or limb (tuned-to-limb), or HD-tRNS; Experiment 2) sham, anodal or cathodal HD-tDCS. Following the stimulation, the participants were instructed to perform a speech-limb interleaved task. Personalized beta HD-tACS and HD-tRNS - but not HD-tDCS - over the left SMA significantly improved reaction times for both speech and limb movement compared to sham. There was no difference in reaction times between HD-tACS and HD-tRNS for either speech or limb movement. These findings demonstrate comparable neuromodulatory effects of HD-tACS and HD-tRNS in improving speech and limb reaction times in younger adults. This study is exploratory and warrants replication with a larger sample within a single-group design.

Early life stress (ELS) is a significant factor in the development of eating disorders (ED), not as a single cause, but as a powerful influence that creates a vulnerability across an individual's biology and psychology. This review explains how various forms of ELS, such as trauma, neglect, and chronic adversity, can permanently alter brain systems. For example, chronic stress hormone exposure can dysregulate the hypothalamic-pituitary-adrenal (HPA) axis, leading to abnormal cortisol levels and impaired stress self-regulation later in life. This dysregulation can lead to difficulties in managing emotions and coping with stress later in life. Furthermore, ELS impacts the brain's neurochemical systems, including serotonin, dopamine, and norepinephrine, which are responsible for mood, reward, and impulse control. Lasting changes to these systems can explain why some people use food to cope with distress, leading to behaviors like binge eating or extreme restriction. ELS also leaves a biological memory via epigenetic modifications, notably DNA methylation, altering gene expression without changing the DNA sequence to link early experiences to long-term risk. From a psychological perspective, ELS often leads to low self-esteem, self-criticism, and an impaired ability to regulate emotions. These psychological traits, along with a person's neurobiological profile, can make them more susceptible to developing an eating disorder as a way to gain a sense of control over their lives. By integrating genetic, epigenetic, neurobiological, and psychosocial factors, this review clarifies how ELS acts as a multifaceted embedder of vulnerability, contributing to the onset and persistence of EDs.

Background: Alzheimer's disease (AD) is increasingly recognized as a multifactorial network disorder in which amyloid and tau pathology interact with mitochondrial dysfunction, neuroinflammation, metabolic impairment, vascular dysregulation, and synaptic failure. This review provides an integrative, systems-level synthesis of these mechanisms with emphasis on diagnostic and therapeutic implications.

Methods: A structured narrative review was conducted using PubMed, Scopus, Web of Science, and Embase (2010-2025). Eligible studies included clinical trials, biomarker validation studies, cohort analyses, and mechanistic investigations. Evidence was synthesized by mechanistic domain with focus on cross-system interactions and translational relevance.

Findings: Convergent data indicate that soluble Aβ species, tau propagation, glial dysregulation, insulin resistance, mitochondrial bioenergetic failure, lipid imbalance, and BBB dysfunction form a self-reinforcing neurodegenerative network. Diagnostic advances-including plasma p-tau181/217, Aβ42/40 ratio, GFAP, sTREM2, neuronal exosomes, and multimodal machine-learning models-enable earlier staging and refinement of therapeutic selection. Therapeutic development is shifting from linear amyloid removal to multi-target strategies incorporating anti-tau agents, glial-modulating compounds, metabolic and microbiome interventions, medical nutrition, and multidomain lifestyle programs. Across trials, combined strategies targeting interacting mechanisms demonstrate stronger biomarker and cognitive effects than single-axis approaches.

Conclusions: AD management requires a systems-oriented therapeutic architecture in which interventions are selected based on mechanistic dominance, biomarker stage, and potential synergy. We outline a multi-target strategy integrating amyloid/tau modulation, neuroimmune regulation, metabolic-vascular stabilization, and synaptic support. Future work should prioritize biomarker-guided stratification, treatment sequencing, and prevention-oriented combination designs.

Acute pain processing emerges from complex interactions among multiple brain regions, with local ion channels critically shaping neuronal communication. To better understand the role of HCN4 channels during acute pain in mice, a genetic brain-specific HCN4-KO was compared with pharmacological inhibition by the selective HCN4 channel blocker EC18. Stimulus-driven BOLD-fMRI measurements using graded peripheral thermal stimulation allowed brain-wide investigation of both discriminative and suppressive processes within ascending and descending pain pathways. Classical BOLD parameters and graph-theoretical analyses revealed that compared to controls, HCN4-KO showed a significant increase in brain activity in regions responsible for discriminative tasks, emotional pain processing and pain suppression including sensory cortex, amygdala and hypothalamus across both high and low thermal stimulation intensities. In striking contrast, acute inhibition of HCN4 with EC18 decreased activity in these same regions compared with both KO and control mice. Furthermore, comparing pre- and post-stimulation resting-state measurements revealed that HCN4-KO and controls exhibited a stimulation-induced increase in functional connectivity, whereas EC18-treated mice demonstrated a connectivity decrease. Taken together, genetic loss of HCN4 produced a hypersensitive phenotype in thermal pain processing, whereas acute pharmacological inhibition of the channel elicited an opposing hyposensitive phenotype.