Neuroscience最新文献

Psychogenic erectile dysfunction (pED) is often accompanied by abnormal brain activities. This study aimed to develop an automaticclassifier to distinguish pED from healthy controls (HCs) by identified brain-basedcharacteristics. Resting-state functional magnetic resonance imaging data were acquired from 45 pED patients and 43 HCs. Regional homogeneity (ReHo) and functional connectivity (FC) values were calculated and compared between groups. Moreover, based on altered ReHo and FC values, support vector machine (SVM) classifier, incorporating recursive feature elimination (RFE), an SVM-RFE diagnostic model was established using leave-one-out cross-validation. Patients demonstrated reduced ReHo values in the left middle temporal gyrus (had decreased FC values with the left medial superior frontal gyrus and cuneus), orbital part of inferior frontal gyrus (had decreased FC values within the same region), triangular part of inferior frontal gyrus, anterior cingulate gyrus (had decreased FC values with the left inferior temporal gyrus, anterior cingulate gyrus, cuneus and right supplementary motor area) and middle frontal gyrus. The right calcarine fissure displayed increased ReHo values. The diagnostic model demonstrated excellent performance, achieving an accuracy rate of 90.80%. This study identified altered regional activity and FC in specific brain regions of pED patients, which might be related to the development of pED. The application of machine learning confirmed the distinctive characteristics of these functional changes in the brain. The high accuracy of our diagnostic model suggested a promising direction for developing objective diagnostic tools for psychological disorders.

Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by motor symptoms such as tremors, rigidity, and bradykinesia. Magnetic resonance imaging (MRI) offers a non-invasive means to study PD and its progression. This study utilized the unilateral 6-hydroxydopamine (6-OHDA) rat model of parkinsonism to assess whether white matter microstructural integrity measured using advanced free-water diffusion tensor imaging metrics (fw-DTI) and gray matter density using voxel-based morphometry (VBM) can serve as imaging biomarkers of pathological changes following nigrostriatal denervation. By comparing the 6-OHDA-lesioned vs. sham-lesioned rats, we aimed to identify complementary gray matter and white matter changes indicative of disease pathophysiology. Results showed widespread gray matter atrophy and subtle changes in white matter integrity in the 6-OHDA lesioned rats. Gray matter atrophy predominantly affected ipsilateral cortical regions, with some bilateral regions also showing atrophy. Conversely, higher volumes were observed in some regions of the contralateral gray matter in the 6-OHDA model. Furthermore, increased fw-FA and fw-AX were observed in regions including the brainstem, thalamus, superior and inferior colliculus, and fornix. Smaller clusters of decreased fw-FA and fw-AX were found in the corpus callosum. Regions of both increased and decreased diffusivity were noted in fw-RD, primarily in the brainstem, while the f index was elevated in several regions in the 6-OHDA lesioned group, except for a cluster in the contralateral thalamus. In conclusion, this study underscores the significant potential role for gray and white matter imaging biomarkers in delineating disease pathology in parkinsonism.

Transcranial alternating current stimulation (tACS) modulates brain oscillations and corticomotor plasticity. We examined the effects of four tACS frequencies (20 Hz, 40 Hz, 60 Hz, and 80 Hz) on motor cortex (M1) excitability and motor performance. In a randomised crossover design, 12 adults received 20-minute tACS sessions, with Sham as control. Corticomotor and intracortical excitability was measured up to 60-minutes post-tACS. Motor performance was evaluated using the Grooved Pegboard Test (GPT) and sensorimotor assessments. Our findings demonstrated frequency-dependent modulation of corticomotor excitability based on MEP amplitude. 20 Hz and 40 Hz tACS reduced MEPs, while 60 Hz and 80 Hz increased MEPs. Inhibition (cortical silent period, SP) was reduced across all tACS frequencies compared to Sham, with 20 Hz and 40 Hz showing consistent reductions, 60 Hz showing effects at post-0 and post-30, and 80 Hz at post-60. Furthermore, 60 Hz tACS decreased intracortical inhibition at post-0, while intracortical facilitation increased with 20 Hz and 60 Hz at post-0, and 40 Hz at post-60. Motor performance remained unaffected across frequencies. Regression analyses revealed that shorter SP at 60 min post 60 Hz tACS predicted faster reaction times, while greater MEP amplitudes at 60 min following 80 Hz tACS predicted improved hand dexterity. Overall, beta and gamma tACS frequencies modulate M1 excitability, with consistent effects on SP, suggesting potential use in conditions involving SP elongation, such as stroke and Huntington's disease. These findings highlight 60 Hz tACS as a potential tool for motor rehabilitation therapies.

Although inflammation and oxidative stress have been increasingly recognised as components of Alzheimer's disease (AD) and Parkinson's disease (PD) pathologies. Few studies have investigated peripheral inflammation, and none have examined oxidative stress in Dementia with Lewy bodies (DLB). The purpose of our study was to characterize and compare those biomarkers in DLB with those in AD and amnestic mild cognitive impairment (aMCI). Plasma samples were obtained from Chinese patients with DLB (n = 50), AD (n = 59), and aMCI (n = 30), and healthy controls (HCs) (n = 54). Peripheral inflammatory biomarkers, including interferon-gamma (IFN-γ), interleukins (IL-1β, IL-2, IL-4, IL-6, IL-10, IL-12p70, IL-17A), tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP). Oxidative stress markers, such as superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px), were also assessed. The findings revealed that DLB patients had higher IL-6 levels than AD and HCs and elevated IL-10 and IL-17A levels compared to HCs. In terms of oxidative stress, the levels of SOD were significantly lower and MDA were significantly higher in the DLB and AD compared with HCs. Significant positive correlations were found between Unified Parkinson's Disease Rating Scale (UPDRS) scores and CRP levels. Our study identifies a unique peripheral immune and oxidative stress profile in DLB, characterized by elevated IL-6, MDA, and reduced SOD levels, distinguishing it from AD. These findings, linked to α-synuclein (α-Syn) pathology, provide novel insights into DLB mechanisms and highlight potential biomarkers for disease monitoring, targeted therapies, and future clinical trials.

Background: The rupture of intracranial aneurysms (IAs) leads to aneurysmal subarachnoid hemorrhage (aSAH), which is associated with significant disability and mortality rates. This study aims to identify metabolic markers causally linked to the occurrence of IAs and aSAH through Mendelian randomization (MR), thereby offering novel predictive and therapeutic targets.

Methods: We conducted a genome-wide association study (GWAS) on IAs and aSAH, analyzing 1,400 metabolomic indices from the Canadian Longitudinal Study on Aging (CLSA) cohort (n = 8,299). Subsequently, we employed two-sample Mendelian randomization to ascertain potential causal relationships between each metabolite and the conditions IAs and aSAH by various MR methodologies, including MR Egger, Weighted median, Inverse variance weighted (IVW), MR-PRESSO, Simple mode, and Weighted mode. The heterogeneity of instrumental variables was assessed using Cochran's Q statistics, and metabolic pathway analyses were performed via the Metaconflict 5.0 platform.

Results: Our analysis found that 87 metabolites/metabolic ratios were associated with IAs, and 85 metabolites/metabolic ratios were associated with aSAH. After false discovery rate (FDR) correction and sensitivity analyses, nine metabolites/metabolic ratios were significantly causally associated with aSAH. Conversely, while 87 metabolites and their ratios initially showed potential causal links with IA, none demonstrated significant causal associations post-FDR correction. The study also pinpointed eight significant metabolic pathways implicated in both IAs and aSAH.

Conclusion: This study found that nine circulating metabolites and their ratios with significant causal associations to aSAH, while no metabolites and their ratios were causally linked to IAs. These results suggest possible mechanisms and predictive molecular targets for IAs and aSAH.

This study investigates the neural and physiological mechanisms underlying External Referent Decision Awareness (ERDA) within organizational contexts, focusing on hierarchical roles (Head, Peer, Staff). Twenty-two professionals participated, and electroencephalographic (EEG frequency band: Delta, Theta, Alpha, Beta, Gamma) and autonomic indices (skin conductance and cardiovascular indices) were recorded, while personality traits and decision-making styles were assessed. Results revealed higher Delta and Theta activation in the left temporo-parietal junction (TPJ) during Peer-related decisions, reflecting increased social cognition and ambiguity regulation in those contexts. Gamma activity, associated with high-order cognitive processes, was prominent in the left frontal cortex across all roles, indicating complex decision evaluation. These findings underscore the complexity of low-frequency bands (Delta and Theta), involved in emotional regulation and social cognition, while high-frequency bands (Gamma) reflect cognitive integration and decision complexity. Furthermore, autonomic data showed higher Skin Conductance Levels (SCL) for Head decisions, suggesting greater emotional involvement.The findings revealed a significant negative correlation between avoidant decision-making styles and the neural and behavioral evaluations of leader decisions, suggesting reduced engagement of neurocognitive systems involved in reward processing and evaluative judgment in individuals with a tendency to avoid decision-making. Additionally, higher extraversion correlated with more favorable evaluations of decisions made by Staff, potentially indicating greater activation in neural circuits associated with social reward and group dynamics. In conclusion, these findings suggest that neural activity and personality traits interact to shape hierarchical decision-making awareness, highlighting the need for tailored leadership and decision-making strategies in organizations.

Exercise-induced fatigue (EF) is characterized by a decline in maximal voluntary muscle force following prolonged physical activity, influenced by both peripheral and central factors. Central fatigue involves complex interactions within the central nervous system (CNS), where astrocytes play a crucial role. This study explores the impact of astrocytic calcium signals on EF. We used adeno-associated viruses (AAV) to express GCaMP7b in astrocytes of the dorsal striatum in mice, allowing us to monitor calcium dynamics. Our findings reveal that EF significantly increases the frequency of spontaneous astrocytic calcium signals. Utilizing genetic tools to either enhance or reduce astrocytic calcium signaling, we observed corresponding decreases and increases in exercise-induced fatigue time, respectively. Furthermore, modulation of astrocytic calcium signals influenced corticostriatal synaptic plasticity, with increased signals impairing and decreased signals ameliorating long-term depression (LTD). These results highlight the pivotal role of astrocytic calcium signaling in the regulation of exercise-induced fatigue and synaptic plasticity in the striatum.

Peripuberty is a significant period of neurodevelopment with long-lasting effects on the brain and behavior. Blocking type 1 corticotropin-releasing factor receptors (CRFR1) in neonatal and peripubertal rats attenuates detrimental effects of early-life stress on neural plasticity, behavior, and stress hormone action, long after exposure to the drug has ended. CRFR1 antagonism can also impact neural and behavioral development in the absence of stressful stimuli, suggesting sustained alterations under baseline conditions. To investigate this further, we administered the CRFR1 antagonist (CRFR1a) R121919 to young adolescent male and female rats across 4 days. Following each treatment, rats were tested for locomotion, social behavior, mechanical allodynia, or prepulse inhibition (PPI). Acute CRFR1 blockade immediately reduced PPI in peripubertal males, but not females. In adulthood, each assay was repeated without CRFR1a exposure to test for persistent effects of the adolescent treatment. Males continued to experience deficits in PPI while females displayed altered locomotion, PPI, and social behavior. The amygdala was collected to measure long-term effects on gene expression. In the adult amygdala, peripubertal CRFR1a induced alterations in pathways related to neural plasticity and stress in males. In females, pathways related to central nervous system myelination, cell junction organization, and glutamatergic regulation of synaptic transmission were affected. Understanding how acute exposure to neuropharmacological agents can have sustained impacts on brain and behavior, in the absence of further exposures, has important clinical implications for developing adolescents.

Major depressive disorder (MDD) is a complex neuropsychiatric disorder potentially influenced by factors such as stress and inflammation. Chronic stress can lead to maladaptive brain changes that may trigger immune hyperactivation, contributing to MDD's pathogenesis. While the involvement of inflammation in MDD is well established, the effects of inflammatory preconditioning in animals subsequently exposed to chronic stress remain unclear. This study aimed to investigate the impact of inflammatory preconditioning on behavioral, biochemical, and molecular changes in adult male Swiss mice subjected to chronic restraint stress (CRS). The mice received a single injection of lipopolysaccharide (LPS) 24 h before thefirst CRS and performed 6 h daily for 28 days. Behavioral tests were conducted 24 h after the last CRS, across 4 days, and euthanasia followed 24 h after the final tests. Results indicated that only the LPS + CRS group exhibited depressive- and anxiety-like behaviors, accompanied by demotivation and apathy. Biochemical and molecular analyses revealed anoxidative imbalance in the hippocampus, marked by elevated H₂O₂ levels and MPO activity. In the prefrontal cortex, theLPS + CRS group demonstrated a central inflammatory imbalance, with reduced IL-10 levels, increased Iba1 gene expression, and decreased Gfap and Bdnf gene expression. A trend toward elevated IL-17 levels was also observed at the peripheral level. These findings indicate that inflammatory preconditioning contributes significantly to behaviors phenotypically associated with MDD. Furthermore, the study suggests that these behavioral changes are linked to a dysfunctional immune response and impaired neuroplasticity.