Search Results (1,389)

Electroencephalography (EEG) is the only brain imaging method light enough and with the temporal precision to assess electrocortical dynamics during human locomotion. However, head motion during whole-body movements produces artifacts that contaminate the EEG and reduces ICA decomposition quality. We compared commonly used motion artifact removal approaches for reducing the motion artifact from the EEG during running and identifying stimulus-locked ERP components during an adapted flanker task. EEG was recorded from young adults during dynamic jogging and static standing versions of the Flanker task. Motion artifact removal approaches were evaluated based on their ICA’s component dipolarity, power changes at the gait frequency and harmonics, and ability to capture the expected P300 ERP congruency effect. Preprocessing the EEG using either iCanClean with pseudo-reference noise signals or artifact subspace reconstruction (ASR) led to the recovery of more dipolar brain independent components. In our analyses, iCanClean was somewhat more effective than ASR. Power was significantly reduced at the gait frequency after preprocessing with ASR and iCanClean. Finally, preprocessing using ASR and iCanClean also produced ERP components similar in latency to those identified in the standing flanker task. The expected greater P300 amplitude to incongruent flankers was identified when preprocessing using iCanClean. ASR and iCanClean may provide effective preprocessing methods for reducing motion artifacts in human locomotion studies during running. Full article

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition with early-life origins. Maternal obesity has been associated with increased ASD risk, yet the mechanisms and timing of susceptibility remain unclear. Using a mouse model combining in vitro fertilization (IVF) and embryo transfer, we separated the effects of pre-conception and gestational obesity. We found that maternal high fat diet (HFD) exposure prior to conception alone was sufficient to induce ASD-like behaviors in male offspring—including altered vocalizations, reduced sociability, and increased repetitive grooming—without anxiety-related changes. These phenotypes were absent in female offspring and those exposed only during gestation. Cortical transcriptome analysis revealed dysregulation and isoform shifts in genes implicated in ASD, including Homer1 and Zswim6. Whole-genome bisulfite sequencing of hippocampal tissue showed hypomethylation of an alternative Homer1 promoter, correlating with increased expression of the short isoform Homer1a, which is known to disrupt synaptic scaffolding. This pattern was specific to mice with ASD-like behaviors. Our findings show that pre-conceptional maternal obesity can lead to lasting, isoform-specific transcriptomic and epigenetic changes in the offspring’s brain. These results underscore the importance of maternal health before pregnancy as a critical and modifiable factor in ASD risk. Full article

The purpose of this work was to study the effects of lactoferrin (Lf) on acute (days 3 and 15) and early-delayed (day 30) changes in the dentate gyrus of mouse hippocampus caused by whole-body gamma-irradiation. Male C57BL/6 mice received Lf (4 mg per mouse, i.p. injection) immediately after whole-body gamma-irradiation at a dose of 7.5 Gy from a ⁶⁰Co source. The effect of Lf on mouse behavior was evaluated using “Open field” and “Elevated plus-maze” tests. The proportion of cells with DNA replication was determined by 5-ethynyl-2′-deoxyuridine incorporation (thymidine analog) and detected by a click reaction with azide Alexa Fluor 568. Lf treatment increased animal survival during the experiment (30 days), compensated for radiation-induced body weight loss, and prevented suppression of motor and exploratory activities. A pronounced anti-radiation effect of Lf on mouse brain cells has been demonstrated. A single injection of the protein allowed preserving 2-fold more proliferating cells and immature neurons in the dentate gyrus of the hippocampus of irradiated animals during the acute period of post-radiation injury development. Full article

Adolescence represents a critical period of neurodevelopment during which brain-derived neurotrophic factor (BDNF) plays a fundamental role in neuronal survival and synaptic plasticity. While exercise-BDNF relationships are well-documented in adults, evidence in adolescents remains limited and inconsistent. This systematic review examined the effects of exercise modalities on circulating BDNF concentrations in adolescent populations. A systematic search was conducted following PRISMA guidelines across multiple databases (FECYT, PubMed, SPORTDiscus, ProQuest Central, SCOPUS, Cochrane Library) through June 2025. Inclusion criteria comprised adolescents, exercise interventions, BDNF outcomes, and randomized controlled trial design. Methodological quality was assessed using the PEDro scale. From 130 initially identified articles, 8 randomized controlled trials were included, with 4 rated as excellent and the other 4 as good quality. Exercise modalities included aerobic, resistance, concurrent, high-intensity interval training, Taekwondo, and whole-body vibration, with durations ranging 6–24 weeks. Four studies demonstrated statistically significant BDNF increases following exercise interventions, four showed no significant changes, and one reported transient reduction. Positive outcomes occurred primarily with vigorous-intensity protocols implemented for a minimum of six weeks. Meta-analysis was not feasible due to high heterogeneity in populations, interventions, and control conditions. Moreover, variation in post-exercise sampling timing further limited comparability of BDNF results. Future research should standardize protocols and examine longer interventions to clarify exercise-BDNF relationships in adolescents. Full article

Hydrogen-rich water (HRW) has shown neuroprotective effects in acute brain injury, but its role in chronic radiation-induced brain injury (RIBI) remains unclear. This study investigated the long-term efficacy of HRW in mitigating cognitive impairment and neuronal damage caused by chronic RIBI. Fifty male Sprague Dawley rats were randomly divided into five groups: control, irradiation (IR), IR with memantine, IR with HRW, and IR with combined treatment. All but the control group received 20 Gy whole-brain X-ray irradiation, followed by daily interventions for 60 days. Behavioral assessments, histopathological analyses, oxidative stress measurements, ¹⁸F-FDG PET/CT imaging, transcriptomic sequencing, RT-qPCR, Western blot, and serum ELISA were performed. HRW significantly improved anxiety-like behavior, memory, and learning performance compared to the IR group. Histological results revealed that HRW reduced neuronal swelling, degeneration, and loss and enhanced dendritic spine density and neurogenesis. PET/CT imaging showed increased hippocampal glucose uptake in the IR group, which was alleviated by HRW treatment. Transcriptomic and molecular analyses indicated that HRW modulated key genes and proteins, including CD44, CD74, SPP1, and Wnt1, potentially through the MIF, Wnt, and SPP1 signaling pathways. Serum CD44 levels were also lower in treated rats, suggesting its potential as a biomarker for chronic RIBI. These findings demonstrate that HRW can alleviate chronic RIBI by preserving neuronal structure, reducing inflammation, and enhancing neuroplasticity, supporting its potential as a therapeutic strategy for radiation-induced cognitive impairment. Full article

Diffuse axonal brain injury (DAI) is a common, debilitating consequence of traumatic brain injury, yet its detection and severity grading remain challenging in clinical and experimental settings. This study evaluated the sensitivity of diffusion tensor imaging (DTI), histology, and neurological severity scoring (NSS) in assessing injury severity in a rat model of isolated DAI. A rotational injury model induced mild, moderate, or severe DAI in male and female rats. Neurological deficits were assessed 48 h after injury via NSS. Magnetic resonance imaging, including DTI metrics, such as fractional anisotropy (FA), relative anisotropy (RA), axial diffusivity (AD), mean diffusivity (MD), and radial diffusivity (RD), was performed prior to tissue collection. Histological analysis used beta amyloid precursor protein immunohistochemistry. Sensitivity and variability of each method were compared across brain regions and the whole brain. Histology was the most sensitive method, requiring very small groups to detect differences. Anisotropy-based MRI metrics, especially whole-brain FA and RA, showed strong correlations with histology and NSS and demonstrated high sensitivity with low variability. NSS identified injury but required larger group sizes. Diffusivity-based MRI metrics, particularly RD, were less sensitive and more variable. Whole-brain FA and RA were the most sensitive MRI measures of DAI severity and were comparable to histology in moderate and severe groups. These findings support combining NSS and anisotropy-based DTI for non-terminal DAI assessment in preclinical studies. Full article

Psychological stress and dietary behavior are interdependent forces that greatly influence mental and physical health. Thus, both what and how we eat impact our well-being. Maladaptive eating patterns, such as eating in response to emotional cues rather than physiological hunger, have become increasingly common amid modern stressors and an ultra-processed food environment. This narrative review synthesizes interdisciplinary findings from nutritional psychiatry, microbiome science, and behavioral nutrition to explore how stress physiology, gut–brain interactions, and dietary quality shape emotional regulation and eating behavior. It highlights mechanisms (e.g., HPA-axis dysregulation, blunted interoception, and inflammatory and epigenetic pathways) and examines the evidence for mindful and intuitive eating; phytochemical-rich, whole-food dietary patterns; and the emerging role of precision nutrition. Trauma-informed approaches, cultural foodways, structural barriers to healthy eating, and clinical implementation strategies (e.g., interprofessional collaboration) are considered in the context of public health equity to support sustainable mental wellness through dietary interventions. Ultimately, restoring a healthy relationship with food positions nutrition not only as sustenance but as a modifiable regulator of affect, cognition, and stress resilience, central to mental and physical well-being. Full article

Military personnel deployed to Iraq and Afghanistan were exposed to emissions from open-air burn pits, where plastics, metals, and medical waste were incinerated. These exposures have been linked to deployment-related respiratory diseases (DRRD) and may also impact neurological health via the lung–brain axis. To investigate molecular mechanisms, adult male rats were exposed to filtered air, naphthalene (a representative volatile organic compound), or a combination of naphthalene and carbon black (surrogate for particulate matter; CBN) via whole-body inhalation (six hours/day, three consecutive days). Lung, brain, and plasma samples were collected 24 h after the final exposure. Pro-inflammatory biomarkers were assessed using multiplex electrochemiluminescence and western blot. Differentially expressed genes (DEGs) were identified by RNA sequencing, and elastic net modeling was used to define exposure-predictive gene signatures. CBN exposure altered inflammatory biomarkers across tissues, with activation of nuclear factor kappa B (NF-κB) signaling. In the lung, gene set enrichment revealed activated pathways related to proliferation and inflammation, while epithelial–mesenchymal transition (EMT) and oxidative phosphorylation were suppressed. In the brain, EMT, inflammation, and senescence pathways were activated, while ribosomal function and oxidative metabolism were downregulated. Elastic net modeling identified a lung gene signature predictive of CBN exposure, including Kcnq3, Tgfbr1, and Tm4sf19. These findings demonstrate that inhalation of a surrogate burn pit mixture induces inflammatory and metabolic gene expression changes in both lung and brain tissues, supporting the utility of this animal model for understanding systemic effects of airborne military toxicants and for identifying potential biomarkers relevant to DRRD and Veteran health. Full article

Alzheimer’s disease (AD) and ischemic stroke (IS) are prevalent neurological disorders that frequently co-occur in the same individuals. Recent studies have demonstrated that AD and IS share several common risk factors and pathogenic elements, including an overlapping genomic architecture. However, the relationship between IS risk gene polymorphisms and AD has been less extensively studied. We aimed at determining whether IS risk gene polymorphisms were associated with the risk of AD and the severity of AD in AD patients. We utilized data of AD patients and normal controls (NCs) sourced from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. IS risk single nucleotide polymorphisms (SNPs) were identified through the most recent and largest IS genome-wide association study (GWAS) meta-analysis. Subsequently, we conducted SNP-based association analysis of IS-risk SNPs with the risk of AD, along with amyloid, tau, and neuroimaging for AD. The generalized multifactor dimensionality reduction (GMDR) model was used to assess the interactions among IS-risk SNPs and apolipoprotein E (ApoE) ε4. Protein–protein interactions (PPIs) of the IS-risk genes product and APOE were explored using the STRING database. Seven IS-risk SNPs were involved in the study. Five SNPs were found to be associated with at least one measurement of cerebrospinal fluid (CSF) levels of amyloid-beta 1–42 (Aβ₄₂), total tau (t-tau), and phosphorylated tau 181 (p-tau₁₈₁), as well as the volumes of the hippocampus, whole brain, entorhinal cortex, and mid-temporal regions. After multiple testing corrections, we found that T allele of rs1487504 contributed to an increased risk of AD in non-ApoE ε4 carriers. The combination of rs1487504 and ApoE ε4 emerged as the optimal two-factor model, and its interaction was significantly related to the risk of AD. Additionally, C allele of rs880315 was significantly associated with elevated levels of CSF Aβ₄₂ in AD patients, and A allele of rs10774625 was significantly related to a reduction in the volume of the entorhinal cortex in AD patients. This study found that IS risk SNPs were associated with both the risk of AD and AD major indicators in the ADNI cohort. These findings elucidated the role of IS in AD from a genetic perspective and provided an innovative approach to predict AD through IS-risk SNPs. Full article

Background: Autism spectrum disorder (ASD) is characterised by atypical behavioural and cognitive diversity, yet the neural underpinnings linking brain activity and individual presentations remain poorly understood. In this study, we investigated the relationship between resting-state functional magnetic resonance imaging (fMRI) signal complexity and intelligence (full-scale intelligence quotient (FIQ); verbal intelligence quotient (VIQ); and performance intelligence quotient (PIQ)) in male adults with ASD (n = 14) and matched neurotypical controls (n = 15). Methods: We used three complexity-based metrics: Hurst exponent (H), fuzzy approximate entropy (fApEn), and fuzzy sample entropy (fSampEn) to characterise resting-state fMRI signal dynamics, and correlated these measures with standardised intelligence scores. Results: Using a whole-brain measure, ASD participants showed significant negative correlations between PIQ and both fApEn and fSampEn, suggesting that increased neural irregularity may relate to reduced cognitive–perceptual performance in autistic individuals. No significant associations between entropy (fApEn and fSampEn) and PIQ were found in the control group. Group differences in brain–behaviour associations were confirmed through formal interaction testing using Fisher’s r-to-z transformation, which showed significantly stronger correlations in the ASD group. Complementary regression analyses with interaction terms further demonstrated that the entropy (fApEn and fSampEn) and PIQ relationship was significantly moderated by group, reinforcing evidence for autism-specific neural mechanisms underlying cognitive function. Conclusions: These findings provide insight into how cognitive functions in autism may not only reflect deficits but also an alternative neural strategy, suggesting that distinct temporal patterns may be associated with intelligence in ASD. These preliminary findings could inform clinical practice and influence health and social care policies, particularly in autism diagnosis and personalised support planning. Full article

(1) Background: Evidence from non-human animal and spaceflight analog studies have suggested that traveling to outer space could have a significant impact on the structural properties of the hippocampus, a brain region within the medial temporal lobe that is critical for learning and memory. Here, we tested this hypothesis in a group of astronauts who participated in a six-month mission in the International Space Station (ISS). (2) Methods: We collected magnetic resonance imaging (MRI) scans from a sample of 17 (9 males, 8 females) astronauts before and after the ISS mission, and calculated percent gray matter volume changes in the whole hippocampus and its (anterior, body, and posterior) subregions in both hemispheres. (3) Following the six-month mission in the ISS, we found a significantly decreased volume in the whole left hippocampus; in addition, when looking at subregions separately, we detected a significantly decreased volume in the anterior subregion of the left hippocampus and the body subregion of the right hippocampus. We also found a significantly decreased volume in the whole right hippocampus of male astronauts as compared to female astronauts. (4) Conclusions: This study, providing the very first evidence of hippocampal volumetric changes in astronauts following a six-month mission to the ISS, could have significant implications for cognitive performance during future long-duration spaceflights. Full article

Pathogenic variants in the MAP1B gene have been associated with neurological impairment, including intellectual disability, attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder, brain malformations, cognitive hearing loss, short stature, and dysmorphic features. However, few cases with detailed clinical characterization have been reported. We describe a 12-year-old boy carrying a loss-of-function MAP1B variant, presenting with severe elimination disorders despite normal intelligence. He was referred to the genetics service due to persistent elimination issues, including daytime urinary incontinence, nocturnal enuresis, and fecal incontinence. He had normal motor and cognitive development, with an IQ of 99; however, he also presented with ADHD, short stature, microcephaly, and myopia. Brain MRI revealed bilaterial subependymal periventricular nodular heterotopia (PVNH). Audiometry showed normal bilateral hearing. Testing fragile X syndrome (FXS) and karyotype analyses yielded normal results. Whole exome sequencing (WES) revealed a nonsense pathogenic variant in MAP1B (c.895 C>T; p.Arg299*). No other family members showed a similar phenotype; however, a great-uncle and a great-aunt had a history of nocturnal enuresis until age 10. The patient’s deceased mother had short stature and psychiatric disorders, and a history of consanguinity was reported on the maternal side. This case broadens the phenotypic spectrum associated with MAP1B syndrome, suggesting that elimination disorder, frequently reported in FXS, should also be evaluated in MAP1B pathogenic variant carriers. In addition, the presence of short stature also appears to be part of the syndrome. Full article

Alzheimer’s disease (AD) involves the accumulation of amyloid-β (Aβ) plaques, whose quantification plays a central role in understanding disease progression. Automated segmentation of Aβ deposits in histopathological micrographs enables large-scale analyses but is hindered by the high cost of detailed pixel-level annotations. Weakly supervised learning offers a promising alternative by leveraging coarse or indirect labels to reduce the annotation burden. We evaluated a weakly supervised approach to segment and analyze thioflavin-S-positive parenchymal amyloid pathology in AD and age-matched brains. Our pipeline integrates three key components, each designed to operate under weak supervision. First, robust preprocessing (including retrospective multi-image illumination correction and gradient-based background estimation) was applied to enhance image fidelity and support training, as models rely more on image features. Second, class activation maps (CAMs), generated by a compact deep classifier SqueezeNet, were used to identify, and coarsely localize amyloid-rich parenchymal regions from patch-wise image labels, serving as spatial priors for subsequent refinement without requiring dense pixel-level annotations. Third, a patch-based convolutional neural network, U-Net, was trained on synthetic data generated from micrographs based on CAM-derived pseudo-labels via an extensive object-level augmentation strategy, enabling refined whole-image semantic segmentation and generalization across diverse spatial configurations. To ensure robustness and unbiased evaluation, we assessed the segmentation performance of the entire framework using patient-wise group k-fold cross-validation, explicitly modeling generalization across unseen individuals, critical in clinical scenarios. Despite relying on weak labels, the integrated pipeline achieved strong segmentation performance with an average Dice similarity coefficient (≈0.763) and Jaccard index (≈0.639), widely accepted metrics for assessing segmentation quality in medical image analysis. The resulting segmentations were also visually coherent, demonstrating that weakly supervised segmentation is a viable alternative in histopathology, where acquiring dense annotations is prohibitively labor-intensive and time-consuming. Subsequent morphometric analyses on automatically segmented Aβ deposits revealed size-, structural complexity-, and global geometry-related differences across brain regions and cognitive status. These findings confirm that deposit architecture exhibits region-specific patterns and reflects underlying neurodegenerative processes, thereby highlighting the biological relevance and practical applicability of the proposed image-processing pipeline for morphometric analysis. Full article

The insulin-like growth factor binding protein, acid-labile subunit (IGFALS), plays a crucial role in glucose metabolism and immune regulation, key processes in recovery from surgery. Here, we studied the perioperative serum IGFALS dynamics and explored potential clinical implications. A total of 79 patients undergoing elective cardiac surgery with implementation of cardiopulmonary bypass had their serum isolated at baseline, 24 h, seven days, and three months postoperatively to assess serum concentrations of IGFALS and insulin growth factor 1 (IGF-1). Markers of perioperative injury included troponin I (TnI), high-mobility group box 1 (HMGB-1), and heat shock protein 60 (Hsp-60). Inflammatory status was assessed via interleukin-6 (IL-6) and interleukin-8 (IL-8). Additionally, we measured in vitro cytokine production to viral stimulation of whole blood and monocytes. Surrogates of neuronal distress included neurofilament light chain (NF-L), total tau (τ), phosphorylated tau at threonine 181 (τp181), and amyloid β40 and β42. Renal impairment was defined by RIFLE criteria. Cardiac dysfunction was denoted by serum N-terminal pro-brain natriuretic peptide (NT-proBNP) levels. Serum IGFALS levels declined significantly after surgery and remained depressed even at 3 months. Administration of acetaminophen and acetylsalicylic acid differentiated IGFALS levels at the 24 h postoperatively. Serum IGFALS 24 h post-operatively correlated with production of cytokines by leukocytes after in vitro viral stimulation. Serum amyloid-β1-42 was significantly associated with IGFALS at baseline and 24 h post-surgery Patients discharged home had higher IGFALS levels at 28 days and 3 months than those discharged to healthcare facilities or who died. These findings suggest that IGFALS may serve as a prognostic biomarker for recovery trajectory and postoperative outcomes in cardiac surgery patients. Full article

Hemorheology is a branch of science that studies and explains the causes of blood flow disorders. In many vascular disorders whole blood viscosity, plasma viscosity, aggregability, and deformability of erythrocytes can be a diagnostic factor. In this paper we analyze whether statin therapy affects hemorheological values in a group of patients with clinically diagnosed silent ischemic foci of the brain (CSVCL). The study includes an analysis of the hemorheological parameter values such as whole blood viscosity, plasma viscosity, and selected biochemical parameters. Aggregability and deformability of erythrocytes were determined using the mathematical Quemada model. Our results indicate a modifying effect of statins on hemorheological parameters. Full article