Human Brain Research Articles

Genetic Insights Into Hypothalamic Hamartoma: Unraveling Somatic Variants.

Hypothalamic hamartomas (HHs) are rare developmental brain lesions associated with drug-resistant epilepsy and often subjected to epilepsy surgery. Brain somatic variants in genes affecting the Sonic hedgehog (Shh) and primary cilia signaling pathways have been implicated in approximately 50% of nonsyndromic HH cases. This study aims to characterize a new cohort of 9 HH cases and elucidate their genetic etiology. We recruited 9 HH cases including 8 nonsyndromic cases of which 4 were type IV HH. Genomic DNA was extracted from peripheral blood and surgical brain tissues, and somatic variants were investigated using high-depth whole-exome sequencing. Pathogenic somatic variants in known HH genes (GLI3, OFD1, and PRKACA) were identified in 7 of the 9 cases. In addition, a 2-hit mutational event comprising a germline variant (predicted to impair kinase activity) and a somatic loss-of-heterozygosity was identified in TNK2, a gene encoding a brain-expressed tyrosine kinase. Our findings reinforce the role of somatic variants in Shh and cilia genes in HH cases while also shedding light on TNK2 as a potential novel disease-causing gene. This study emphasizes the increasing importance of brain mosaicism in epilepsy disorders and underscores the critical role of genetic diagnosis derived from resected brain tissue.

Glutathione Therapy in Diseases: Challenges and Potential Solutions for Therapeutic Advancement.

An endogenous antioxidant, reduced glutathione (GSH), is found at high concentrations in nearly all typical cells. GSH synthesis is a controlled process, and any disruption in the process of GSH synthesis could result in GSH depletion. Cellular oxidative damage results from GSH depletion. Various pathological conditions such as aging, cardiovascular disease (CVD), psychiatric disorders, neurological disorders, liver disorders, and diabetes mellitus are more affected by this stress. There are various reasons for GSH reduction, but replenishing it can help to improve this condition. However, there are challenges in this field. Low bioavailability and poor stability of GSH limit its delivery to tissues, mainly brain tissue. Today, new approaches are used for the optimal amount and efficiency of drugs and alternative substances such as GSH. The use of nano-materials and liposomes are effective methods for improving the treatment effects of GSH. The difficulties of GSH decrease and its connection to the most important associated disorders are reviewed for the first time in this essay. The other major concerns are the molecular mechanisms involved in them; the impact of treatment with replacement GSH; the signaling pathways impacted; and the issues with alternative therapies. The utilization of nano-materials and liposomes as potential new approaches to solving these issues is being considered.

LOX-Mediated ECM Mechanical Stress Induces Piezo1 Activation in Hypoxic-Ischemic Brain Damage and Identification of Novel Inhibitor of LOX

Hypoxic-ischemic encephalopathy (HIE) poses a significant challenge in neonatal medicine, often resulting in profound and lasting neurological deficits. Current therapeutic strategies for hypoxia-ischemia brain damage (HIBD) remain limited. Ferroptosis has been reported to play a crucial role in HIE and serves as a potential therapeutic target. However, the mechanisms underlying ferroptosis in HIBD remain largely unclear. In this study, we found that elevated lysyl oxidase (LOX) expression correlates closely with the severity of HIE, suggesting LOX as a potential biomarker for HIE. LOX expression levels and enzymatic activity were significantly increased in HI-induced neuronal models both in vitro and in vivo. Notably, we discovered that HI-induced brain tissue injury results in increased stiffness and observed a selective upregulation of the mechanosensitive ion channel Piezo1 in both brain tissue of HIBD and primary cortex neurons. Mechanistically, LOX increases its catalytic substrates, the Collagen I/III components, promoting extracellular matrix (ECM) remodeling and possibly mediating ECM cross-linking, which leads to increased stiffness at the site of injury and subsequent activation of the Piezo1 channel. Piezo1 senses these stiffness stimuli and then induces neuronal ferroptosis in a GPX4-dependent manner. Pharmacological inhibition of LOX or Piezo1 ameliorated brain neuronal ferroptosis and improved learning and memory impairments. Furthermore, we identified traumatic acid (TA) as a novel LOX inhibitor that effectively suppresses LOX enzymatic activity, mitigating neuronal ferroptosis and promoting synaptic plasticity. In conclusion, our findings elucidate a critical role for LOX-mediated ECM mechanical stress-induced Piezo1 activation in regulating ferroptotic cell death in HIBD. This mechanistic insight provides a basis for developing targeted therapies aimed at ameliorating neurological outcomes in neonates affected by HIBD.

CvFormer: Cross-view transFormers with pre-training for fMRI analysis of human brain

In recent years, functional magnetic resonance imaging (fMRI) has been widely utilized to diagnose neurological disease, by exploiting the region of interest (RoI) nodes as well as their connectivities in human brain. However, most of existing works only rely on either RoIs or connectivities, neglecting the potential for complementary information between them. To address this issue, we study how to discover the rich cross-view information in fMRI data of human brain. This paper presents a novel method for cross-view analysis of fMRI data of the human brain, called Cross-view transFormers (CvFormer). CvFormer employs RoI and connectivity encoder modules to generate two separate views of the human brain, represented as RoI and sub-connectivity tokens. Then, basic transformer modules can be used to process the RoI and sub-connectivity tokens, and cross-view modules integrate the complement information across two views. Furthermore, CvFormer uses a global token for each branch as a query to exchange information with other branches in cross-view modules, which only requires linear time for both computational and memory complexity instead of quadratic time. To enhance the robustness of the proposed CvFormer, we propose a two-stage strategy to train its parameters. To be specific, RoI and connectivity views can be firstly utilized as self-supervised information to pre-train the CvFormer by combining it with contrastive learning and then fused to finetune the CvFormer using label information. Experiment results on two public ABIDE and ADNI datasets can show clear improvements by the proposed CvFormer, which can validate its effectiveness and superiority.

Towards a Systemic Concept of the Brain Ishemia Stroke: Monte Carlo Driven in silico Model.

The work proposes a new mathematical model of dynamic processes of a typical spatially heterogeneous biological system, and sets and solves a mathematical problem of modeling the dynamics of the system of neurovascular units of the brain in conditions of ischemic stroke. There is a description of only a small number of mathematical models of stroke in the literature. This model is being studied and a numerical and software implementation of the corresponding mathematical problem is proposed. This work is the first attempt ever aiming to employ a Monte Carlo computational approach for In Silico simulation of the most critical parameters in molecular and cellular pathogenesis of the brain ischemic stroke. In this work, a new mathematical model of the development of ischemic stroke is proposed in the form of a discrete model based on neurovascular units (NVU) as elements. As a result of testing the program with the assignment of empirically selected coefficients, data were obtained on the evolution of the states of the lattice of the cellular automaton of the model for the spread of stroke in a region of the brain tissue. A resulting new theoretical model of the particular pathologically altered biosystem might be taken as a promising tool for further studies in neurology; general pathology and cell biology. For the first time, a mathematical model has been constructed that allows us to represent the spatial dynamics of the development of the affected area in ischemic stroke of the brain, taking into account neurovascular units as single morphofunctional structures.

Tanshinone IIA Against Cerebral Ischemic Stroke and Ischemia-Reperfusion Injury: A Review of the Current Documents.

Stroke is a well-known neurological disorder that carries significant morbidity and mortality rates worldwide. Cerebral Ischemic Stroke (CIS), the most common subtype of stroke, occurs when thrombosis or emboli form elsewhere in the body and travel to the brain, leading to reduced blood perfusion. Cerebral Ischemia/Reperfusion Injury (CIRI) is a common complication of CIS and arises when blood flow is rapidly restored to the brain tissue after a period of ischemia. The therapeutic approaches currently recognized for CIS, such as thrombolysis and thrombectomy, have notable side effects that limit their clinical application. Recently, there has been growing interest among researchers in exploring the potential of herbal agents for treating various disorders and malignancies. One such herbal agent with medicinal applications is tanshinone IIA, an active diterpene quinone extracted from Salvia miltiorrhiza Bunge. Tanshinone IIA has shown several pharmacological benefits, including anti-inflammatory, antioxidant, anti-apoptotic, and neuroprotective properties. Multiple studies have indicated the protective role of tanshinone IIA in CIS and CIRI. This literature review aims to summarize the current findings regarding the molecular mechanisms through which this herbal compound improves CIS and CIRI.

Genome-Wide and Transcriptome-Wide Association Studies on Northern New England and Ohio Amyotrophic Lateral Sclerosis Cohorts.

Amyotrophic lateral sclerosis (ALS) is an age-associated, fatal neurodegenerative disorder causing progressive paralysis and respiratory failure. The genetic architecture of ALS is still largely unknown. We performed a genome-wide association study (GWAS) and transcriptome-wide association study (TWAS) to understand genetic risk factors for ALS using a population-based case-control study of 435 ALS cases and 279 controls from Northern New England and Ohio. Single nucleotide polymorphism (SNP) genotyping was conducted using the Illumina NeuroChip array. Odds ratios were estimated using covariate-adjusted logistic regression. We also performed a genome-wide SNP-smoking interaction screening. TWAS analyses used PrediXcan to estimate associations between predicted gene expression levels across 15 tissues (13 brain tissues, skeletal muscle, and whole blood) and ALS risk. GWAS analyses identified the p.A382T missense variant (rs367543041, p = 3.95E-6) in the TARDBP gene, which has previously been reported in association with increased ALS risk and was found to share a close affinity with the Sardinian haplotype. Both GWAS and TWAS analyses suggested that ZNF235 is associated with decreased ALS risk. Our results support the need for future evaluation to clarify the role of these potential genetic risk factors for ALS and to understand genetic susceptibility to environmental risk factors.

Prediction Models Of The Aphasia Severity After Stroke By Lesion Load Of Cortical Language Areas and White Matter Tracts: An Atlas-based Study.

ObjectiveTo construct relatively objective, atlas-based multivariate models for predicting early aphasia severity after stroke, using structural magnetic resonance imaging. MethodsWe analyzed the clinical and imaging data of 46 patients with post-stroke aphasia. The aphasia severity was identified with a Western Aphasia Battery Aphasia Quotient. The assessments of stroke lesions were indicated by the lesion load of both the cortical language areas (Areas-LL) and four white matter tracts (i.e., the superior longitudinal fasciculus, SLF-LL; the inferior frontal occipital fasciculi, IFOF-LL; the inferior longitudinal, ILF-LL; and the uncinate fasciculi, UF-LL) extracted from human brain atlas. Correlation analyses and multiple linear regression analyses were conducted to evaluate the correlations between demographic, stroke- and lesion-related variables and aphasia severity. The predictive models were then established according to the identified significant variables. Finally, the receiver operating characteristic (ROC) curve was utilized to assess the accuracy of the predictive models. ResultsThe variables including Areas-LL, the SLF-LL, and the IFOF-LL were significantly negatively associated with aphasia severity (p < 0.05). In multiple linear regression analyses, these variables accounted for 59.4% of the variance (p < 0.05). The ROC curve analyses yielded the validated area under the curve (AUC) 0.84 both for Areas-LL and SLF-LL and 0.76 for IFOF-LL, indicating good predictive performance (p < 0.01). Adding the combination of SLF-LL and IFOF-LL to this model increased the explained variance to 62.6% and the AUC to 0.92. ConclusionsThe application of atlas-based multimodal lesion assessment may help predict the aphasia severity after stroke, which needs to be further validated and generalized for the prediction of more outcome measures in populations with various brain injuries.

Evaluating the Efficacy of CortexID Quantitative Analysis in Localization of the Epileptogenic Zone in Patients with Temporal Lobe Epilepsy.

There remains a critical need for precise localization of the epileptogenic foci in individuals with drug-resistant epilepsy (DRE). 18F-Fluorodeoxyglucose positron emission tomography (FDG-PET) imaging can reveal hypometabolic regions during the interval between seizures in patients with epilepsy. However, visual-based qualitative analysis is time-consuming and strongly influenced by physician experience. CortexID Suite is a quantitative analysis software that helps to evaluate PET imaging of the human brain. Therefore, we aimed to evaluate the efficacy of CortexID quantitative analysis in the localization of the epileptogenic zone in patients with temporal lobe epilepsy (TLE). A total of 102 patients with epilepsy who underwent 18F-FDG-PET examinations were included in this retrospective study. The PET visual analysis was interpreted by two nuclear medicine physicians, and the quantitative analysis was performed automatically using CortexID analysis software. The assumed epileptogenic zone was evaluated comprehensively by two skilled neurologists in the preoperative assessment of epilepsy. The accuracy of epileptogenic zone localization in PET visual analysis was compared with that in CortexID quantitative analysis. The diagnostic threshold for the difference in the metabolic Z-score between the right and left sides of medial temporal lobe epilepsy (MTLE) was calculated as 0.87, and that for lateral temporal lobe epilepsy (LTLE) was 2.175. In patients with MTLE, the area under the curve (AUC) was 0.922 for PET visual analysis, 0.853 for CortexID quantitative analysis, and 0.971 for the combined diagnosis. In patients with LTLE, the AUC was 0.842 for PET visual analysis, 0.831 for CortexID quantitative analysis, and 0.897 for the combined diagnosis. These results indicate that the diagnostic efficacy of CortexID quantitative analysis is not inferior to PET visual analysis (p > 0.05), while combined analysis significantly increases diagnostic efficacy (p < 0.05). Among the 23 patients who underwent surgery, the sensitivity and specificity of PET visual analysis for localization were 95.4% and 66.7%, and the sensitivity and specificity of CortexID quantitative analysis were 100% and 50%. The diagnostic efficacy of CortexID quantitative analysis is comparable to PET visual analysis in the localization of the epileptogenic zone in patients with TLE. CortexID quantitative analysis combined with visual analysis can further improve the accuracy of epileptogenic zone localization.

PPARs (Peroxisome Proliferator-activated Receptors) and Their Agonists in Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disease leading to dementia because of complex phathomechanisms like amyloid β (Aβ) aggregation, tau aggregates, and neurofibrillary tangles. Peroxisome proliferator-activated receptor (PPAR) agonists have been reported recently with neuroprotective and anti-inflammatory properties. PPARs belong to the superfamily of nuclear hormone receptors and function as ligand-activated transcription factors. These have emerged as crucial players in the pathogenesis of AD. This review presented the potential of PPARs and their agonists in treating neurodegenerative diseases like AD. <P> </P> PPARs regulate the expression of specific genes vital for synaptic function and neurotransmitter release. PPAR agonists play a critical role in increasing the clearance of Aβ peptides by lowdensity lipoprotein receptor-related protein 1 (LRP1) in the microvascular endothelial cells of the human brain. Studies have shown that PPAR agonists reduce the level of APoE-mRNA, contributing to the accumulation of Aβ plaques and up-regulation of PPAR. A knockout of miR-128 has been found to inhibit AD-like cognitive decline, amyloid precursor protein (APP) amyloidogenic processing, and inflammatory responses in AD. <P> </P> PPARs are involved in the pathomechanism of AD, and therefore, PPAR agonists could be viable options for controlling the neurodegenerative symptoms and may be useful in treating AD.

Extracellular vesicle-mediated trafficking of molecular cues during human brain development

Extracellular vesicle-mediated trafficking of molecular cues during human brain development

Evaluation of knowledge of risk factors and warning signs of stroke among paramedical students

Stroke is a medical emergency caused by a blockage or rupture in the blood vessels that supply blood to the brain. This prevents brain tissue from receiving oxygen, leading to the death of brain cells within minutes and causing neurological damage, disability, or death. Aim: The aim of the present study was to assess baseline knowledge regarding stroke risk factors, symptoms, treatment, and information resources. The “golden hour” is a time span of 60 minutes or less after stroke symptoms begin. There are two types of stroke, namely ischemic and hemorrhagic stroke. Ischemic stroke is further divided into thrombotic and embolic stroke. Hemorrhagic stroke is further divided into intracerebral hemorrhage and subarachnoid hemorrhage. Methods: The research method used in the study is a quantitative research approach. Purposive sampling techniques were used and 1050 participants were assessed The questionnaire consists of demographic details such as department, level of education, family history, and knowledge questions based on risk factors and management. Results: This study comprises 1040 patients who fulfill the inclusion criteria. The survey assessed the knowledge of risk factors and warning signs of stroke among future healthcare professionals (pharmacy, nursing, and AHS). The current findings reported that 51.8% of the paramedical students had knowledge about stroke, while the majority of them reported poor knowledge overall. The findings identified that 57.4% of the student population were knowledgeable about risk factors, 69.9% were knowledgeable about warning signs, and 51.8% were knowledgeable about management. These results were similar to many previous studies conducted around the world. Conclusion: Better knowledge about stroke, recognizing the risk factors, and being able to provide immediate management are essential for paramedical students. This is crucial for reducing stroke incidence and improving survival rates of patients by providing better medical help through early detection, rapid intervention, and better long-term health outcomes not only in a medical setup but also in their respective environments.

Modeling electrical impedance in brain tissue with diffusion tensor imaging for functional neurosurgery applications

Abstract Objective. Decades ago, neurosurgeons used electrical impedance measurements in the brain for coarse intraoperative tissue differentiation. Over time, these techniques were largely replaced by more refined imaging and electrophysiological localization. Today, advanced methods of diffusion tensor imaging (DTI) and finite element method (FEM) modeling may permit non-invasive, high-resolution intracerebral impedance prediction. However, expectations for tissue-impedance relationships and experimentally verified parameters for impedance modeling in human brains are lacking. This study seeks to address this need. Approach. We used FEM to simulate high-resolution single- and dual-electrode impedance measurements along linear electrode trajectories through (1) canonical gray and white matter tissue models, and (2) selected anatomic structures within whole-brain patient DTI-based models. We then compared intraoperative impedance measurements taken at known locations along deep brain stimulation (DBS) surgical trajectories with model predictions to evaluate model accuracy and refine model parameters. Main results. In DTI-FEM models, single- and dual-electrode configurations performed similarly. While only dual-electrode configurations were sensitive to white matter fiber orientation, other influences on impedance, such as white matter density, enabled single-electrode impedance measurements to display significant spatial variation even within purely white matter structures. We compared 308 intraoperative single-electrode impedance measurements in five DBS patients to DTI-FEM predictions at one-to-one corresponding locations. After calibration of model coefficients to these data, predicted impedances reliably estimated intraoperative measurements in all patients (R=0.784±0.116, n=5). Through this study, we derived an updated value for the slope coefficient of the DTI conductance model published by Tuch et al., k=0.0649 S·s/mm3 (original k=0.844), for use specifically in humans at physiological frequencies. Significance. This is the first study to compare impedance estimates from imaging-based models of human brain tissue to experimental measurements at the same locations in vivo. Accurate, non-invasive, imaging-based impedance prediction has numerous applications in functional neurosurgery, including tissue mapping, intraoperative electrode localization, and DBS.

Infection route influence the consequences of Nocardia farcinica infection in BALB/c mice

BackgroundNocardia, a rare but potentially fatal pathogen, can induce systemic infections with diverse manifestations. This study aimed to investigate the tissue and organ damage caused by Nocardia farcinica (N. farcinica) in mice via different infection routes, evaluate the resulting host immune responses, and assess its invasiveness in brain tissue.MethodsBALB/c mice were infected with N. farcinica through intranasal, intraperitoneal, and intravenous routes (doses: 1 × 10^8, 1 × 10^7, 1 × 10^7 CFU in 50 µl PBS). Over a 7-day period, body temperature, weight, and mortality were monitored, and samples were collected for histopathological analysis and bacterial load assessment. Serum was isolated for cytokine detection via ELISA. For RNA-seq analysis, mice were infected with 1 × 107 CFU through three infection routes, after which brain tissue was harvested.ResultsIntraperitoneal and intravenous N. farcinica infections caused significant clinical symptoms, mortality, and neural disruption in mice, resulting in severe systemic infection. Conversely, intranasal infection primarily affected the lungs without causing significant damage to other organs. Intraperitoneal and intravenous infections significantly increased serum cytokines, particularly TNF-α and IFN-γ. RNA-seq analysis of brains from intravenously infected mice revealed significant differential gene expression, whereas the intranasal and intraperitoneal routes showed limited differences (only three genes). The enriched Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways in the intravenous group were primarily related to immune processes.ConclusionThe study demonstrated that intravenous N. farcinica infection induces significant clinical symptoms, triggers an inflammatory response, damages multiple organs, and leads to systemic infections.

The molecular landscape of vascular cells in the human brain

The molecular landscape of vascular cells in the human brain

Deciphering the spatial distribution of Gli1-lineage cells in dental, oral, and craniofacial regions

Abstract The craniofacial bone, crucial for protecting brain tissue and supporting facial structure, undergoes continuous remodeling through mesenchymal (MSCs) or skeletal stem cells (SSCs) in their niches. Gli1 is an ideal marker for labeling MSCs and osteoprogenitors in this region, and Gli1-lineage cells are identified as pivotal for bone growth, development, repair, and regeneration. Despite its significance, the distribution of Gli1-lineage cells across the dental, oral, and craniofacial (DOC) regions remains to be systematically explored. Utilizing tissue-clearing and light sheet fluorescence microscopy (LSFM) with a Gli1CreER; tdTomatoAi14 mouse model, we mapped the spatial distribution of Gli1-lineage cells throughout the skull, focusing on calvarial bones, sutures, bone marrow, teeth, periodontium, jaw bones, and the temporomandibular joint (TMJ). We found Gli1-lineage cells widespread in these areas, underscoring their significance in DOC regions. Additionally, we observed their role in repairing calvarial bone defects, providing novel insights into craniofacial biology and stem cell niches and enhancing our understanding of stem cells and their progeny’s behavior in vivo.

Tetrabenazine, a vesicular monoamine transporter 2 inhibitor, inhibits vesicular storage capacity and release of monoamine transmitters in mouse brain tissue

AbstractBackground and PurposeTetrabenazine (TBZ), used for treating hyperkinetic disorders, inhibits vesicular monoamine transporter‐2 (VMAT‐2), which sequesters monoamines into vesicles for exocytosis. However, our knowledge of the effect of TBZ on monoaminergic transmission is limited. Herein, we provide neurochemical evidence regarding the effect of VMAT‐2 inhibition on vesicular neurotransmitter release from the prefrontal cortex (PFC) and striatum (STR) (brain regions involved in characteristic TBZ treatment side effects). The interaction between TBZ and MDMA was also assessed regarding motor behaviour in mice.Experimental ApproachVesicular storage capacity and release of [3H]‐noradrenaline ([3H]‐NA), [3H]‐dopamine ([3H]‐DA), [3H]‐serotonin ([3H]‐5‐HT), and [3H]‐acetylcholine ([3H]‐ACh) was studied in mouse PFC and STR ex vivo slice preparations using electrical field stimulation. Additionally, locomotor activity was assessed in vehicle‐treated mice and compared with that of MDMA, TBZ, and co‐administered animals (n = 6) using the LABORAS system.Key ResultsTBZ lowered the storage capacity and inhibited the vesicular release of [3H]‐NA and [3H]‐DA from the PFC, and [3H]‐DA and [3H]‐5‐HT from the STR in a concentration‐dependent manner. Unlike vesamicol (vesicular ACh uptake inhibitor), TBZ failed to inhibit the vesicular release of [3H]‐ACh from the PFC. When the vesicular storage of the investigated monoamines was inhibited by TBZ in the PFC and STR, MDMA induced the release of transmitters through transporter reversal; MDMA dose dependently increased locomotor activity in vivo.Conclusion and ImplicationsOur observations provide neurochemical evidence explaining the mechanism of VMAT‐2 inhibitors in the brain and support the involvement of dopaminergic and noradrenergic transmission in hyperkinetic movement disorders.

Rapid reconfiguration of cortical networks after repeated exposure to visual-vestibular conflicts

Visual-vestibular conflicts can induce motion sickness and further postural instability. Visual-vestibular habituation is recommended to reduce the symptoms of motion sickness and improve postural stability with an altered multisensory reweighting progress. However, it is unclear how the human brain reweights multisensory information after repeated exposure to visual-vestibular conflicts. Therefore, we synchronized a rotating platform and a virtual scene to present visual-vestibular congruent (natural visual stimulation) and incongruent (conflicted visual stimulation) conditions and collected EEG and center of pressure (COP) data. We constructed the effective brain connectivity of region of interest (ROI) derived from source-space EEG in theta-band activity, and quantified the postural stability and the inflow and outflow of each ROI. We found repeated exposure to congruent and incongruent conditions both decreased COP path length and increased COP complexity. Besides, we found that repeated exposure to the incongruent environment decreased the inflow into visual cortex, suggesting the brain down-weighted the less reliable visual information for postural stability. In contrast, repeated exposure to the congruent environment increased the inflow into posterior parietal cortex and the outflow from visual cortex and S1, suggesting an increase in efficiency of multisensory integration. We concluded that repeated exposure to congruent and incongruent conditions both improved postural stability with different multisensory reweighting patterns as revealed by different dynamic changes of brain networks.

Artificial intelligence role in advancement of human brain connectome studies

Artificial intelligence role in advancement of human brain connectome studies

Nanoplastics exposure-induced mitochondrial dysfunction contributes to disrupted stem cell differentiation in human cerebral organoids

Nanoplastics are ubiquitous in our daily lives, raising concerns about their potential impact on the human brain. Many studies reported that nanoplastics permeate the blood-brain barrier and influence cellular processes in mouse models. However, the neurotoxic effects of ingesting nanoplastics on human brain remain poorly understood. Here, we treated cerebral organoids with polystyrene nanoplastics to model the effects of nanoplastic exposure on human brain. Importantly, we found that mitochondria might be the significant organelles affected by polystyrene nanoplastics using immunostaing and RNA-seq analysis. Subsequently, we observed the increased cell death and decreased cell differentiation in our cerebral organoids. In conclusion, our findings shed insights on the mechanisms underlying the toxicity of nanoplastics on human brain organoids, providing an evaluation system in detection potential environmental toxicity on human brain.