Journal of integrative neuroscience最新文献

Background: Autism spectrum disorder (ASD) has been reported to confer an increased risk of natural premature death. Telomere erosion caused by oxidative stress is a common consequence in age-related diseases. However, whether telomere length (TL) and oxidative indicators are significantly changed in ASD patients compared with controls remains controversial. The aim of this study was to determine the associations of ASD with TL and oxidative indicators by performing a meta-analysis of all published evidence.

Methods: The PubMed and Embase databases were searched for articles published up to April, 2024. The effect size was expressed as standardized mean difference (SMD) and 95% confidence interval (CI) via Stata 15.0 software.

Results: Thirty-nine studies were included. Pooled results showed that compared with controls, children and adolescents with ASD were associated with significantly shorter TL (SMD = -0.48; 95% CI = -0.66- -0.29; p < 0.001; particularly in males), lower total antioxidant capacity (TAC: SMD = -1.15; 95% CI = -2.01- -0.30; p = 0.008), and higher oxidative DNA (8-hydroxy-2^'-deoxyguanosine, 8-OHdG: SMD = 0.63; 95% CI = 0.03-1.23; p = 0.039), lipid (hexanolyl-lysine, HEL: SMD = 0.37; 95% CI = 0.13-0.62; p = 0.003), and protein (3-nitrotyrosine, 3-NT: SMD = 0.86; 95% CI = 0.21-1.51; p = 0.01; dityrosine, DT: SMD = 0.66; 95% CI = 0.521-0.80; p < 0.01) damage. There were no significant differences between ASD and controls in 8-isoprostane and oxidative stress index after publication bias correction, and in N-formylkynurenine during overall meta-analysis.

Conclusions: TL, 8-OHdG, TAC, HEL, 3-NT, and DT represent potential biomarkers for prediction of ASD in children and adolescents.

Background: White matter (WM) is a principal component of the human brain, forming the structural basis for neural transmission between cortico-cortical and subcortical structures. The impairment of WM integrity is closely associated with the aging process, manifesting as the reorganization of brain networks based on graph theoretical analysis of complex networks and increased volume of white matter hyperintensities (WMHs) in imaging studies.

Methods: This study investigated changes in the robustness of WM brain networks during aging and assessed their correlation with WMHs. We constructed WM brain networks for 159 volunteers from a community sample dataset using diffusion tensor imaging (DTI). We then calculated the robustness of these networks by simulating neurodegeneration based on network attack analysis, and studied the correlations between WM network robustness, age, and the proportion of WMHs.

Results: The analysis revealed a moderate, negative correlation between WM network robustness and age, and a weak and negative correlation between WM network robustness and the proportion of WMHs.

Conclusions: These findings suggest that WM pathologies are associated with aging and offer new insights into the imaging characteristics of the aging brain.

The complicated neurological syndrome known as multiple sclerosis (MS) is typified by demyelination, inflammation, and neurodegeneration in the central nervous system (CNS). Managing this crippling illness requires an understanding of the complex interactions between neurophysiological systems, diagnostic techniques, and therapeutic methods. A complex series of processes, including immunological dysregulation, inflammation, and neurodegeneration, are involved in the pathogenesis of MS. Gene predisposition, autoreactive T cells, B cells, and cytokines are essential participants in the development of the disease. Demyelination interferes with the ability of the CNS to transmit signals, which can cause a variety of neurological symptoms, including impaired motor function, sensory deficiencies, and cognitive decline. Developing tailored therapeutics requires understanding the underlying processes guiding the course of the disease. Neuroimaging, laboratory testing, and clinical examination are all necessary for an accurate MS diagnosis. Evoked potentials and cerebrospinal fluid studies assist in verifying the diagnosis, but magnetic resonance imaging (MRI) is essential for identifying distinctive lesions in the CNS. Novel biomarkers have the potential to increase diagnostic precision and forecast prognosis. The goals of MS treatment options are to control symptoms, lower disease activity, and enhance quality of life. To stop relapses and reduce the course of the disease, disease-modifying treatments (DMTs) target several components of the immune response. DMTs that are now on the market include interferons, glatiramer acetate, monoclonal antibodies, and oral immunomodulators; each has a unique mode of action and safety profile. Symptomatic treatments improve patients' general well-being by addressing specific symptoms, including pain, sphincter disorders, fatigue, and spasticity. Novel treatment targets, neuroprotective tactics, and personalized medicine techniques will be the main focus of MS research in the future. Improving long-term outcomes for MS patients and optimizing disease treatment may be possible by utilizing immunology, genetics, and neuroimaging developments. This study concludes by highlighting the complexity of multiple MS, including its changing therapeutic landscape, diagnostic problems, and neurophysiological foundations. A thorough grasp of these elements is essential to improving our capacity to identify, manage, and eventually overcome this intricate neurological condition.

Background: Volume alterations in the parietal subregion have received less attention in Alzheimer's disease (AD), and their role in predicting conversion of mild cognitive impairment (MCI) to AD and cognitively normal (CN) to MCI remains unclear. In this study, we aimed to assess the volumetric variation of the parietal subregion at different cognitive stages in AD and to determine the role of parietal subregions in CN and MCI conversion.

Methods: We included 662 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database, including 228 CN, 221 early MCI (EMCI), 112 late MCI (LMCI), and 101 AD participants. We measured the volume of the parietal subregion based on the Human Brainnetome Atlas (BNA-246) using voxel-based morphometry among individuals at various stages of AD and the progressive and stable individuals in CN and MCI. We then calculated the area under the curve (AUC) of the receiver operating characteristic (ROC) curve to test the ability of parietal subregions to discriminate between different cognitive groups. The Cox proportional hazard model was constructed to determine which specific parietal subregions, alone or in combination, could be used to predict progression from MCI to AD and CN to MCI. Finally, we examined the relationship between the cognitive scores and parietal subregion volume in the diagnostic groups.

Results: The left inferior parietal lobule (IPL)_6_5 (rostroventral area 39) showed the best ability to discriminate between patients with AD and those with CN (AUC = 0.688). The model consisting of the left IPL_6_4 (caudal area 40) and bilateral IPL_6_5 showed the best combination for predicting the CN progression to MCI. The left IPL_6_1 (caudal area 39) showed the best predictive power in predicting the progression of MCI to AD. Certain subregions of the volume correlated with cognitive scales.

Conclusion: Subregions of the angular gyrus are essential in the early onset and subsequent development of AD, and early detection of the volume of these regions may be useful in identifying the tendency to develop the disease and its treatment.

Background: Deficits in emotion recognition have been shown to be closely related to social-cognitive functioning in schizophrenic. This study aimed to investigate the event-related potential (ERP) characteristics of social perception in schizophrenia patients and to explore the neural mechanisms underlying these abnormal cognitive processes related to social perception.

Methods: Participants included 33 schizophrenia patients and 35 healthy controls (HCs). All participants underwent electroencephalogram recording while completing the Emotion Intensity Recognition Task (EIRT). Behavioral data and ERP components were analyzed using repeated measures analysis of variance.

Results: Schizophrenia patients had longer reaction times (RTs) to sad faces compared with disgusted faces, and had lower accuracy than the HCs. Additionally, schizophrenia patients had lower accuracy than the HCs for disgusted faces, surprised faces, angry faces, and fearful faces. Late Positive Potential (LPP) mean amplitudes of the HCs were larger than the schizophrenia patients for sad faces in the frontal lobe and central lobe. For happy faces, the HCs elicited larger LPP mean amplitudes than schizophrenia patients in the frontal lobe and central lobe. For surprised faces, the LPP mean amplitudes were higher in the HCs in the central lobe and parietal lobe than in schizophrenia patients. The HCs exhibited larger LPP mean amplitudes for angry faces in the frontal lobe, central lobe, and parietal lobe than in schizophrenia patients. For fearful faces, the HCs elicited a larger LPP mean amplitude than schizophrenia patients in the frontal lobe, central lobe, and parietal lobe.

Conclusions: Schizophrenia patients present impaired social perception, and the observed ERP patterns provide valuable insights into the neural mechanisms underlying the EIRT results, highlighting the differences between HCs and schizophrenia patients. These findings underscore the potential of the EIRT as a biomarker for cognitive and emotional dysregulation in schizophrenia.

Clinical trial registration: No: ChiCTR2300078149. Registered 29 November, 2023; https://www.chictr.org.cn/showproj.html?proj=211510.

Mitochondria are organelles of eukaryotic cells delimited by two membranes and cristae that consume oxygen to produce adenosine triphosphate (ATP), and are involved in the synthesis of vital metabolites, calcium homeostasis, and cell death mechanisms. Strikingly, normal mitochondria function as an integration center between multiple conditions that determine neural cell homeostasis, whereas lesions that lead to mitochondrial dysfunction can desynchronize cellular functions, thus contributing to the pathophysiology of traumatic brain injury (TBI). In addition, TBI leads to impaired coupling of the mitochondrial electron transport system with oxidative phosphorylation that provides most of the energy needed to maintain vital functions, ionic homeostasis, and membrane potentials. Furthermore, mitochondrial metabolism produces signaling molecules such as reactive oxygen species (ROS), regulating calcium levels and controlling the expression profile of intrinsic pro-apoptotic effectors influenced by TBI. Hence, the set of these functions is widely referred to as 'mitochondrial function', although the complexity of the relationship between such components limits such a definition. In this review, we present mitochondria as a therapeutic target, focus on TBI, and discuss aspects of mitochondrial structure and function.

Background: In neuroscience, Ca²⁺ imaging is a prevalent technique used to infer neuronal electrical activity, often relying on optical signals recorded at low sampling rates (3 to 30 Hz) across multiple neurons simultaneously. This study investigated whether increasing the sampling rate preserves critical information that may be missed at slower acquisition speeds.

Methods: Primary neuronal cultures were prepared from the cortex of newborn pups. Neurons were loaded with Oregon Green BAPTA-1 AM (OGB1-AM) fluorescent indicator. Spontaneous neuronal activity was recorded at low (14 Hz) and high (500 Hz) sampling rates, and the same neurons (n = 269) were analyzed under both conditions. We compared optical signal amplitude, duration, and frequency.

Results: Although recurring Ca²⁺ transients appeared visually similar at 14 Hz and 500 Hz, quantitative analysis revealed significantly faster rise times and shorter durations (half-widths) at the higher sampling rate. Small-amplitude Ca²⁺ transients, undetectable at 14 Hz, became evident at 500 Hz, particularly in the neuropil (putative dendrites and axons), but not in nearby cell bodies. Large Ca²⁺ transients exhibited greater amplitudes and faster temporal dynamics in dendrites compared with somas, potentially due to the higher surface-to-volume ratio of dendrites. In neurons bulk-loaded with OGB1-AM, cell nucleus-mediated signal distortions were observed in every neuron examined (n = 57). Specifically, two regions of interest (ROIs) on different segments of the same cell body displayed significantly different signal amplitudes and durations due to dye accumulation in the nucleus.

Conclusions: Our findings reveal that Ca²⁺ signal undersampling leads to three types of information loss: (1) distortion of rise times and durations for large-amplitude transients, (2) failure to detect small-amplitude transients in cell bodies, and (3) omission of small-amplitude transients in the neuropil.

Objective: To study the use of a dementia screening tool in our clinic cohort of adults with Down syndrome.

Study design: A retrospective chart review of patients with Down syndrome was conducted to follow the use of the Adaptive Behaviour Dementia Questionnaire (ABDQ) in a dementia screening protocol. The ABDQ results for patients aged 40 years and older at a Down syndrome specialty clinic program were assessed. Based on caregiver feedback, an ABDQ with modified instructions was piloted and the impact assessed.

Results: As part of our clinic's initiative to implement a new clinical protocol to screen for dementia, the ABDQ was completed by 47 caregivers of adults with Down syndrome, aged 39 years and above, from December, 2021 to April, 2023. Based on clinical impressions at the same timepoint, the ABDQ had a sensitivity of 0%, specificity of 97.4%, positive predictive value of 0%, and negative predictive value of 80.4%. Nine patients were deemed to have mild cognitive impairment and/or dementia by clinical impressions, but they did not identify as positive on the ABDQ. The Down syndrome clinic team modified the ABDQ in an effort to provide clearer language and increased sensitivity. The modified ABDQ showed a sensitivity of 0%, specificity of 93.8%, positive predictive value of 0% and negative predictive value of 75%.

Conclusion: Neither the original ABDQ nor a modified version adequately identified patients with cognitive impairment and/or dementia within the Down syndrome clinical program. The inability to replicate findings from the initial ABDQ validation may be due to differences in setting and format.

Background: Sports fatigue in soccer athletes has been shown to decrease neural activity, impairing cognitive function and negatively affecting motor performance. Transcranial direct current stimulation (tDCS) can alter cortical excitability, augment synaptic plasticity, and enhance cognitive function. However, its potential to ameliorate cognitive impairment during sports fatigue remains largely unexplored. This study investigated the effect of dual-site tDCS targeting the dorsolateral prefrontal cortex (DLPFC) or primary motor cortex (M1) on attention, decision-making, and working memory in elite soccer athletes during sports fatigue.

Methods: Sports fatigue was induced in 23 (non-goalkeeper) elite soccer athletes, who then participated in three counterbalanced intervention sessions: dual-site tDCS over the M1, dual-site tDCS over the DLPFC, and sham tDCS. Following tDCS, participants completed the Stroop, Iowa Gambling, and 2-back tasks.

Results: We found a significant improvement in Stroop task accuracy following dual-site anodal tDCS over the M1 compared with the sham intervention in the incongruent condition (p = 0.036). Net scores in the Iowa Gambling task during blocks 4 (p = 0.019) and 5 (p = 0.014) significantly decreased under dual-site tDCS targeting the DLPFC compared with the sham intervention. No differences in 2-back task performance were observed between sessions (all p > 0.05).

Conclusions: We conclude that dual-site anodal tDCS applied to the M1 enhanced attention performance while tDCS targeting the DLPFC increased risk propensity in a decision-making task during sports fatigue in elite soccer athletes. However, dual-site anodal tDCS targeting either the M1 or DLPFC did not significantly influence working memory performance during sports fatigue in this population. These preliminary findings suggest that dual-site tDCS targeting the M1 has beneficial effects on attention performance, potentially informing future research on sports fatigue in athletes.

Clinical trial registration: No: NCT06594978. Registered 09 September, 2024; https://clinicaltrials.gov/search?cond=NCT06594978.

Introduction: The effects of remimazolam (Re) in combination with andrographolide (AP) on learning, memory, and motor abilities in rats following cardiopulmonary bypass (CPB) surgery were studied.

Methods: We hypothesized that the combination of Re and AP could improve postoperative cognitive dysfunction (POCD) in rats after CPB by modulating nervous system inflammation. Cognitive function was assessed using the Morris Water Maze test, and the concentrations of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6) in serum were measured by enzyme-linked immunosorbent assay (ELISA). Apoptosis was evaluated using western blotting and the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) staining assay.

Results: The results indicated that both Re and AP independently improved cognitive function in rats after CPB and inhibited the secretion of inflammatory factors and apoptosis in hippocampal tissues. Combined administration of Re and AP enhanced the alleviation of POCD compared with monotherapy. The adenosine monophosphate-activated protein kinase/silent information regulator of transcription 1 (AMPK/SIRT1) signaling pathway was activated by the combination of Re and AP.

Conclusions: Collectively, the combination of Re and AP treatment significantly improves POCD in rats after CPB through activation of the AMPK/SIRT1 signaling pathway.