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        <title>Frontiers in Neuroscience | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/neuroscience</link>
        <description>RSS Feed for Frontiers in Neuroscience | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-13T07:19:10.120+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1808921</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1808921</link>
        <title><![CDATA[Roles of NRXN1 in neuropsychiatric disorders: from genetic lesion to molecular mechanism]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jiaxiang Liu</author><author>Yanxuan Zhang</author><author>Ruijia Jin</author><author>Yuxin Zhu</author><author>Jianrui Chen</author>
        <description><![CDATA[Numerous neuropsychiatric disorders frequently exhibit overlapping genetic risk factors, implying the molecular basis for their comorbidity. Nevertheless, the pathogenesis of these disorders remains elusive, particularly regarding how genetic variations impair the physiological function of risk genes and contribute to disease phenotypes. Neurexin 1 protein, encoded by NRXN1 gene, belongs to the neurexin family of presynaptic adhesion molecules. And neurexin 1 is involved in synaptogenesis and the maintenance of synaptic action. Genetic variations of NRXN1 have been demonstrated to be associated with a spectrum of neuropsychiatric disorders. Herein, this review focuses on the most recent and relevant literature concerning the genetic and molecular mechanisms through which NRXN1 variants contribute to the pathogenesis of neuropsychiatric disorders, particularly schizophrenia and autism spectrum disorder. Among them, we propose the isoform-dependent excitation-inhibition imbalance hypothesis of NRXN1 in autism spectrum disorder. And this hypothesis may account for both the elevated and decreased excitation-inhibition ratios observed in diverse individuals with autism spectrum disorder. Moreover, both schizophrenia and autism spectrum disorder involve deletions and alternative splicing of NRXN1, offering molecular evidence for their comorbidity. Then, we analyzed and summarized the current research status of NRXN1 in other neuropsychiatric disorders, including attention-deficit hyperactivity disorder, insomnia, epilepsy, suicide, and depression. Additionally, available limited researches on NRXN1-targeted therapeutic strategies and associated pharmacological studies are also incorporated. Finally, we discussed existing challenges in NRXN1 research within the context of neuropsychiatric disorders and proposed potential avenues to overcome these obstacles.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1827009</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1827009</link>
        <title><![CDATA[Federated training of spiking neural networks on edge hardware for audio processing]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Swaroop S. Kaimal</author><author>Ashwin JB</author><author>S. Sofana Reka</author><author>Prakash Venugopal</author>
        <description><![CDATA[Spiking Neural Networks have caught significant attention recently for their potential for energy-efficient computation on neuromorphic hardware and their event-driven processing. Spiking Neural networks employ spike-based learning paradigms, which require specialized training procedures such as Surrogate Gradient Descent. At the same time, Federated Learning allows collaborative model training on decentralized devices with preservation of data privacy protection. However, to date, few research has examined the suitability of Federated learning with ARM-based hardware. This work primarily investigates whether Federated Spiking Neural Networks training on ARM-based hardware is feasible with the Raspberry Pi 5 as a widely available and low-cost edge computing device for audio signal processing tasks. We perform a comparative analysis of federated Spiking Neural Network and federated convolutional neural networks on ARM processors and evaluate their performance on different data partitioning strategies using Dirichlet-based splits and various federated averaging algorithms. Using Federated learning, this work investigates the impact of data heterogeneity and aggregation strategies on model convergence, communication overhead, and latency in distributed training paradigms. The results provided showcases the important insights into the trade-offs of FL-SNN implementations on Von Neumann architectures and their applications in decentralized neuromorphic computing for audio processing.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1813618</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1813618</link>
        <title><![CDATA[Direct modulation of human GABA-A α1β2γ2 receptors by the endocannabinoid 2-arachidonoylglycerol: implications for cannabinoid-related ligands and limitations for anxiolytic drug development]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Edgar Mixcoha</author><author>Anabel Flores-Zamora</author><author>Ricardo Hernández-Miramontes</author><author>Jorge Alberto Hernández-Calderón</author><author>Susana Martiñón</author>
        <description><![CDATA[Anxiety disorders are associated with impaired inhibitory neurotransmission mediated by γ-aminobutyric acid type A (GABA-A) receptors. Although benzodiazepines remain effective anxiolytics, their clinical utility is limited by sedation, cognitive impairment, tolerance, and dependence, prompting the search for mechanistically distinct GABAergic modulators. Among cannabinoid-related molecules, the strongest evidence for direct GABA-A receptor modulation concerns the endocannabinoid 2-arachidonoylglycerol (2-AG), which potentiates recombinant human α1β2γ2 receptors through residues located in the M4 helix of the β2 subunit. Here, we review the structural architecture, biophysical properties, and pharmacological profile of the human GABA-A α1β2γ2 isoform as the relevant molecular framework for evaluating this mechanism, while discussing the broader relevance of cannabinoid-related ligands and selected phytocannabinoids without assuming mechanistic equivalence. We further assess the hypothesis that 2-AG reaches the β2-M4 site through a membrane-access route and identify five conceptual barriers that currently limit translation of this mechanism into anxiolytic drug development: supraphysiological effective concentrations, unresolved synaptic-versus-extrasynaptic actions, uncertain subtype selectivity, incomplete validation of lipid-environment effects, and lack of clinical evidence linking this mechanism to anxiolysis in humans. We conclude that direct modulation through β2-M4 defines a mechanistically intriguing allosteric pathway distinct from benzodiazepine action; however, its location on a shared β2 subunit and the micromolar concentrations required for modulation represent substantial obstacles to the rational design of anxioselective agents based on this mechanism.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1848705</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1848705</link>
        <title><![CDATA[Editorial: Research on the correlative mechanisms and clinical exploration of headache and cerebrovascular diseases]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Wei Wang</author><author>Feng Liu</author><author>Wei Shan</author><author>Lanfranco Pellesi</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1816238</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1816238</link>
        <title><![CDATA[Substance P–expressing neurons in the hypothalamic paraventricular nucleus mediate chronic cough hypersensitivity via the hypothalamus–airway neural pathway]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiaoyan Zhang</author><author>Jingyang Chen</author><author>Chun Lin</author><author>Tao Xiao</author><author>Bin Wu</author><author>Fei He</author>
        <description><![CDATA[Background and purposeIncreased cough sensitivity is the key pathophysiological mechanism of chronic cough. Although previous studies have focused on peripheral airway receptor sensitization, the role of the central nervous system—particularly the hypothalamic paraventricular nucleus (PVN)—remains unclear. Whether substance P (SP)–expressing PVN neurons contribute to cough hypersensitivity remains unknown.MethodsThree-week-old Hartley guinea pigs were divided into three groups: citric acid (CA), saline control (SA), and blank control (CON). A cough hypersensitivity model was induced by inhalation of 0.4 mol/L citric acid. Cough sensitivity was assessed using a capsaicin challenge, with the C5 threshold defined as the lowest capsaicin concentration inducing ≥5 coughs. Locomotor activity was evaluated using the open-field test. Airway inflammation and goblet cell hyperplasia were examined by HE and PAS staining. SP and c-Fos expression in the PVN were detected by immunofluorescence and Western blot. HSV retrograde tracing was used to analyze the PVN-airway neural pathway associated with cough hypersensitivity.ResultsCompared with the control groups, guinea pigs in the CA group exhibited a time-dependent increase in cough frequency and enhanced cough sensitivity, as indicated by a reduction in the C5 threshold. Histological analysis revealed increased inflammatory cell infiltration and goblet cell hyperplasia in the airways of the CA group. SP and c-Fos expression, along with the proportion of SP/Fos double-labeled neurons in the PVN, were significantly increased in the CA group (all P < 0.05). Viral tracing confirmed the presence of HSV-positive neurons in the PVN, supporting a neural connection between the PVN and the airways.ConclusionActivation of SP-expressing neurons in the PVN is associated with cough hypersensitivity and suggests the presence of a potential PVN–airway neural pathway. These findings provide a theoretical basis for the development of central-targeted therapies for chronic cough.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1838675</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1838675</link>
        <title><![CDATA[Multimodal CT radiomics-clinical ensemble machine learning model effectively predicts futile recanalization after endovascular treatment of acute ischemic stroke]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhenxiong Wang</author><author>Yidong Gao</author><author>Pan Xu</author><author>Di Wu</author><author>Wuying Li</author><author>Huameng Huang</author><author>Weihua Deng</author><author>Honggang Xu</author><author>Xinhua Wei</author><author>Xing Li</author>
        <description><![CDATA[BackgroundsFutile recanalization (FR) poses a significant challenge in endovascular treatment and there is a lack of reliable predictive models for assessing treatment outcomes in stroke. The aim of this study is to develop a robust CT radiomics-clinical ensemble model that predicts FR in patients with acute ischemic stroke (AIS) following endovascular treatment (EVT) utilizing machine learning techniques.MethodsThis study enrolled 101 patients diagnosed with AIS who underwent successful EVT. A total of 946 radiomics features were, respectively, extracted from non-contrast CT (NCCT), contrast-enhanced CT (CECT), and various CT perfusion maps (CBF, CBV, MTT, and TTP) using PyRadiomics prior to the endovascular intervention. Demographic characteristics, along with baseline clinical, laboratory, and angiographic variables, were incorporated as clinical features in the model analysis. Feature engineering was performed using SelectKBest. Five traditional machine learning algorithms were employed for modeling. The dataset was randomly split into a training cohort (n = 71, 70%) and an internal validation cohort (n = 30, 30%). Receiver operating characteristic (ROC) curves were utilized to evaluate the performance of each model.ResultsAmong the 101 patients, FR occurred in 66 individuals (65%), as determined by the modified Rankin Scale (mRS) at 90 days. The ensemble model integrating clinical data, NCCT, and CBV achieved the highest performance, with an area under the curve (AUC) of 0.918 using the CatBoost algorithm.ConclusionThe multimodal CT radiomics-clinical ensemble machine learning model demonstrated excellent predictive capability for identifying FR in AIS patients with large vessel occlusion prior to EVT.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1816533</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1816533</link>
        <title><![CDATA[LFP-LOC: an LFP power–based method for validating the anatomical placement of high-density neural probes in rodents]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Alberto Perna</author><author>Raffaele Adamo</author><author>Matteo Vincenzi</author><author>Gian Nicola Angotzi</author><author>João Filipe Ribeiro</author><author>Luca Berdondini</author>
        <description><![CDATA[High-density CMOS-based neural probes provide unprecedented spatiotemporal resolution for in-vivo electrophysiology, yet accurate validation of implant position remains challenging. Here we present LFP-LOC, a simple and interpretable method for intraoperative validation and refinement of probe anatomical location based on the spatial distribution of local field potential (LFP) power. Using spontaneous activity recordings performed in rodents, we compute power spectral densities in canonical LFP bands and apply dimensionality reduction and clustering to identify electrodes with shared spectral signatures. Across multiple implant sites, probe technologies, electrode layouts, and experimental conditions, the resulting clusters consistently align with anatomical boundaries. Applied to high-density probes with up to 1,024 electrodes/channels and sub-30 μm pitch, power features converge within approximately 20 s of recordings, allowing online intraoperative assessment. By leveraging the robust relationship between LFP power and brain structure, LFP-LOC enables rapid validation and adjustment of probe placement during surgery, complements histological validation, and may facilitate mesoscale electrophysiological studies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1794548</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1794548</link>
        <title><![CDATA[Long-term neurodevelopment in preterm neonates with necrotizing enterocolitis: systematic review and meta-analysis]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Katrien Vandenberghe</author><author>Liselotte Van Loo</author><author>Thomas Vandendriessche</author><author>Eline Vancoppenolle</author><author>Katrien Jansen</author><author>Maissa Rayyan</author><author>Anneleen Dereymaeker</author>
        <description><![CDATA[IntroductionNecrotizing enterocolitis (NEC) is a common complication in preterm infants and is associated with significant mortality and long-term morbidity, including gastrointestinal sequelae, brain injury, and developmental delays. This systematic review and meta-analysis examines long-term neurodevelopmental outcomes in infants born at less than 34 weeks’ gestation who survive NEC and identifies specific developmental domains most vulnerable to neurodevelopmental impairment.MethodsThe systematic review was performed according to the PRISMA guidelines. We systematically searched Pubmed (including MEDLINE), Embase and Web of Science for relevant articles. Studies were graded for quality using the GRADE system and bias was assessed using the ROBINS-E Risk of Bias tool. We performed gestational-age stratified subgroup analyses (22–28 weeks versus 29–34 weeks) and evaluated the risk of impairment in different neurodevelopmental domains.ResultsSurvivors of NEC are at increased risk of neurodevelopmental impairment (RR 1.42, 95% CI 1.32–1.53). Several neurodevelopmental domains are negatively impacted, such as motor skills (RR 2.08, 95% CI 1.86–2.32), cognition (RR 1.75, 95% CI 1.57–1.96), vision (RR 4.36, 95% CI 2.91–6.55), hearing (RR 4.09, 95% CI 2.91–5.77) and cerebral palsy (RR 2.48, 95% CI 2.15–2.86). The risk of epilepsy and behavioral problems does not differ between NEC survivors and age-matched controls. This increased risk of impairment after NEC persists after stratification for gestational age and extends into school-age.ConclusionNEC Survivors face an elevated risk of neurodevelopmental impairment, irrespective of gestational age, with deficits spanning multiple developmental domains. These findings highlight the need for targeted, long-term follow-up to enable timely detection and individualized interventions for developmental delays throughout childhood.Systematic review registrationhttp://www.crd.york.ac.uk/PROSPERO, identifier CRD42022322564.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1801865</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1801865</link>
        <title><![CDATA[Exercise as a multiscale recalibration of stress-related homeostatic balance]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yan Chen</author><author>Xin Qiu</author><author>Guoxin Ni</author><author>Jie Shao</author><author>Fan Yang</author>
        <description><![CDATA[Chronic stress disrupts homeostasis in the brain and body, leading to anxiety, depression, and cardiovascular and metabolic dysfunction. Although exercise can counter these effects, the mechanisms are scattered across fields and not yet integrated. This review proposes a multi-scale framework. Exercise is not only stress-relieving; it is also a controllable challenge that can recalibrate the system when repeated bouts are matched by sufficient recovery and bioenergetic support. We propose that repeated exercise engages a stress response–adaptation–recovery cycle, in which peripheral signals from skeletal muscles, liver, adipose tissue and gut convey body metabolic state to the brain and are consolidated into durable plasticity only when mitochondrial capacity, substrate availability, and redox balance permit recovery. These signals pass through the blood-brain barrier and engage plasticity switches, including neurotrophic signals, epigenetic modification and metabolic coupling, thus stabilizing the neural circuits of threat appraisal, reward processing and contextual memory. By integrating these dimensions, we clarify how exercise can transform short-term physical stress into lasting resilience and provide direction for future research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1837573</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1837573</link>
        <title><![CDATA[Steroid receptor coactivator-1: integrating steroid hormone signals to regulate brain function and disease]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yinghui Li</author><author>Bing Yang</author><author>Shiwei Xu</author><author>Tingting Xian</author><author>Ming Zhang</author>
        <description><![CDATA[Steroid receptor coactivator-1 (SRC-1), also known as nuclear receptor coactivator-1 (NCOA1), represents the first identified member of the p160 nuclear receptor coactivator family and plays a pivotal role in integrating steroid hormone signals, regulating gene transcription, and maintaining neural homeostasis in the central nervous system (CNS). SRC-1 exhibits region-specific, cell-type-specific, and sexually dimorphic expression patterns in the brain, with prominent distribution in key regions including the hippocampus, cerebral cortex, hypothalamus, and amygdala. Functional studies demonstrate that SRC-1 participates in diverse neural functions such as learning and memory, energy metabolism, emotional regulation, and reproductive behavior through modulation of synaptic plasticity-related genes, neurotrophic factors, and metabolic pathways. Aberrant SRC-1 expression is closely associated with neurodegenerative diseases, autism spectrum disorders, and glioblastoma. This review systematically summarizes the molecular structure, expression characteristics, physiological functions of SRC-1, and its roles in neurological disorders, while discussing its potential applications as a diagnostic biomarker and therapeutic target.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1824272</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1824272</link>
        <title><![CDATA[Effects of dexmedetomidine on perioperative neurocognitive disorders in elderly patients undergoing non-cardiac surgery: a scoping review]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Jinxiang Xie</author><author>Bokang Yang</author><author>Jiayi Xie</author><author>Abdulrahman Khaled Alwesabi</author><author>Chengying Ji</author><author>Zhaohui Gao</author><author>Boxiong Gao</author><author>Qijing Liu</author><author>Yatao Liu</author>
        <description><![CDATA[BackgroundPerioperative neurocognitive disorders (PNDs) are common and clinically significant complications in older surgical patients. Dexmedetomidine (DEX) has been investigated for neuroprotection; however, reported outcomes across PNDs subtypes remain inconsistent.MethodsFollowing PRISMA-ScR guidelines, we systematically searched PubMed, Embase, and Cochrane Library up to December 9, 2025. Eligible studies included patients aged ≥ 60 years undergoing non-cardiac surgery who received perioperative DEX. Data on study design, intervention characteristics, and cognitive outcomes were extracted and thematically synthesized.ResultsTwenty-seven studies (n = 9,890 patients) were included. DEX effects varied by PNDs subtype and assessment timing. For delayed neurocognitive recovery (dNCR), 13 of 19 studies demonstrated improved cognitive performance or reduced incidence. For postoperative delirium (POD), results were heterogeneous: 6 trials reported significant incidence reduction, whereas 4 found no effect. None of the four studies assessing long-term postoperative neurocognitive disorder (pNCD) showed benefit. Proposed mechanisms include anti-inflammatory, antisympathetic, analgesic, and neuroprotective pathways. Substantial heterogeneity was observed in DEX protocols, cognitive tools, diagnostic criteria, and application of the updated nomenclature.ConclusionDEX most consistently benefits dNCR, supporting its use in acute postoperative recovery. Its effect on POD is context-dependent, and no protective effect against long-term pNCD is evident. Considerable methodological diversity underscores the need for standardized diagnostic approaches and rigorously designed large-scale trials to clarify DEX’s role in perioperative cognitive protection.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1792685</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1792685</link>
        <title><![CDATA[Application of neuromodulation techniques in irritable bowel syndrome]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Yingchun Zhang</author><author>Liyuan Gao</author><author>Xiaoguang Zhang</author><author>Wenkai Sun</author><author>Meng Wang</author><author>Tingting Zhang</author><author>Xiaoyu Wang</author>
        <description><![CDATA[Irritable bowel syndrome (IBS) is a gut-brain interaction disorder characterized by abdominal pain/abdominal discomfort accompanied by changes in bowel motility. Its pathogenesis involves the interaction of multiple factors, including abnormalities of the brain-gut axis, intestinal microbiota dysbiosis, and visceral hypersensitivity. Traditional treatment strategies mainly focus on symptomatic relief, which have limitations such as insufficient targeting and significant side effects. Neuromodulation techniques, as an emerging treatment modality, modulate the central or peripheral nervous system through electrical and electromagnetic means, targeting key pathways of the brain-gut axis. These techniques can regulate gut motility and suppress inflammatory responses, thereby alleviating IBS symptoms. Currently, several techniques are widely applied, including electroacupuncture (EA), Sacral Nerve Stimulation (SNS), transcutaneous auricular vagus nerve stimulation (taVNS), and transcutaneous electrical nerve stimulation (TENS). Multiple clinical trials have confirmed their effectiveness in relieving abdominal pain, improving bowel dysfunction, and enhancing quality of life. However, there are still issues such as significant individual differences and insufficient long-term efficacy data. Future research should focus on the development of personalized treatment plans, exploration of combination therapy strategies, and technological innovation to further enhance their clinical value.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1801725</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1801725</link>
        <title><![CDATA[Case Report: Recurrent pathogenic mutation c.110G>A in DHDDS gene]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Ci Liu</author><author>Qiaoyu Ye</author><author>Jie Li</author><author>Siming Bu</author><author>Chenlu Ge</author><author>Xiangnan Wang</author><author>Moyuan Quan</author><author>Liang Wang</author>
        <description><![CDATA[Recent studies have demonstrated the close association of mutations in the dehydrodolichyl diphosphate synthase (DHDDS) gene with neurodevelopmental disorders and the onset of epilepsy. This report describes a female patient harboring a de novo heterozygous variant c.110G>A (p.Arg37His) in the DHDDS gene, characterized by childhood-onset myoclonus-like movement disorder (at age 6) and late-onset epilepsy (at age 17). The movement disorder was remarkably improved through the levetiracetam+ clonazepam+ haloperidol triple therapy, and epileptic seizures were also effectively controlled. A retrospective analysis of 59 epilepsy patients with DHDDS gene variants revealed significant clinical heterogeneity in disease phenotypes caused by DHDDS mutations. Epilepsy was identified as the predominant symptom, commonly accompanied by movement disorders and varying degrees of intellectual disability. Furthermore, while pathogenic mutations in DHDDS tend to be relatively clustered, no definitive genotype-phenotype correlation has been established. This study highlights the clinical manifestations, imaging features, treatment experiences, and genetic testing results through case reports and literature review, thereby providing crucial references for the clinical diagnosis, treatment, and further research of such diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1754510</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1754510</link>
        <title><![CDATA[Exploring the neuroprotective potential of ligustrazine: a preclinical meta-analysis and machine learning perspective on cerebral ischemia-reperfusion injury]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Lang Tu</author><author>Yimiao Luo</author><author>Xinyi Xu</author><author>Huiling Xiong</author><author>Zilong Zhang</author><author>Xiaoyuan Zhou</author>
        <description><![CDATA[ObjectiveThis study aimed to assess the efficacy of ligustrazine in treating cerebral ischemia-reperfusion (I/R) injury and construct a preclinical evidence framework by meta-analysis and machine learning.MethodsA systematic search was conducted for preclinical studies published in PubMed, Embase, Web of Science, and the Cochrane Library up to June 25, 2024. The inclusion criteria encompassed preclinical animal studies pertinent to the topic. Data extraction was performed independently by two individuals, Stata 17.0 software was used for quantitative analysis, R (version 4.3.3) and Python (version 3.11.4) were used for machine learning with neurological function score as the dependent variable.ResultsA total of 23 articles were included, involving 381 animals in the meta-analysis and 321 animals in the machine learning component. Ligustrazine significantly improved neurofunctional scores (NFS) [Longa criteria, SMD = −1.59, 95%CI (−2.16, −1.01), P < 0.001; mNSS criteria, SMD = −1.67, 95%CI (−2.36, −0.97), P < 0.001], cerebral infarct volume (%) [SMD = −2.56, 95%CI (−3.03, −2.09), P < 0.001], and BBB [SMD = −3.06, 95%CI (−4.53, −1.59), P < 0.001]. Furthermore, machine learning analyses, with NFS as the dependent variable, identified the time of first dose, duration, and dose as key determinants of neurofunctional improvement with ligustrazine. Notably, model interpretation suggested that greater improvements were more likely to occur when the initial administration of ligustrazine occurred within 24 h prior to (or 2.21 h post) the ischemic event, at a dosage of 23.53–34.69 mg/kg/day (or 45.71 to 75.65 mg/kg/day), and with an administration duration exceeding 71.43 h.ConclusionThe combination of meta-analysis and machine learning in this study not only confirms that ligustrazine is effective in reducing cerebral I/R injury, but also provides a framework for elucidating the preclinical intervention variables, thus offering novel insights for optimizing preclinical strategies of ligustrazine in cerebral I/R injury.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1788696</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1788696</link>
        <title><![CDATA[Haemodynamic correlates of bilateral 6 Hz transcranial alternating current stimulation during working memory enhancement revealed by fNIRS]]></title>
        <pubdate>2026-05-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Zhenghao Dong</author><author>Yingli Bi</author><author>Han Yang</author><author>Feilong Zhu</author><author>Jincheng Li</author><author>Mingxue Fan</author><author>Shiyan Wang</author><author>Zunke Gong</author>
        <description><![CDATA[IntroductionTheta-band transcranial alternating current stimulation (tACS) has been proposed to enhance working memory (WM) by entraining endogenous oscillations, yet the haemodynamic signatures accompanying theta-tACS–related WM gains remain unclear. We investigated whether 6 Hz tACS modulates prefrontal task-evoked haemodynamic responses during WM and whether such changes relate to behavioral improvement.MethodsIn a randomized, single-blind, sham-controlled design, healthy adults (18–30 years) were allocated to 6 Hz tACS or sham (initially n = 25 per group). Stimulation (1mA peak-to-peak, 20min, 30-sramp-up/down) was delivered bilaterally over the dorsolateral prefrontal cortex (DLPFC; F3/F4). Participants completed the Digit Span Test and N-back tasks (1-, 2-, 3-back) before and after stimulation. During N-back performance, fNIRS recorded bilateral DLPFC signals. Task-evoked oxygenated hemoglobin (HbO) β coefficients were estimated using a general linear model. Group differences in pre–post changes were tested using within-/between-group analyses and ANCOVA, with brain–behavior coupling assessed via Spearman correlation.ResultsAfter fNIRS quality control, 44 participants were included in the final analysis; six participants were excluded because more than 30% of channels were identified as low quality. Relative to sham, 6 Hz tACS produced greater improvements in backward Digit Span and total Digit Span. In the N-back task, accuracy improved selectively under the high-load 3-back condition (between-group change: [F(1.40) = 12.29, p_adj = 0.0034, η2p = 0.24)], whereas reaction time showed no significant between-group differences. fNIRS revealed post-stimulation increases in left DLPFC HbO-β during 3-back, with a significant between-group β-change at one channel [(F(1.40) = 10.69, p_adj = 0.035)]. Within the 6 Hz group, 3-back accuracy gains correlated positively with β-change in the left DLPFC (ρ = 0.44, p_adj = 0.039).ConclusionBilateral 6 Hz tACS selectively enhances high-load WM accuracy and is accompanied by increased task-evoked haemodynamic activation in the left DLPFC. The observed brain–behavior coupling suggests that theta-frequency neuromodulation may facilitate executive control under high cognitive demand via strengthened prefrontal neurovascular responses.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1815478</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1815478</link>
        <title><![CDATA[The glioma neuron symbiosis hypothesis—cellular and molecular mechanistic considerations]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Avital Schurr</author>
        <description><![CDATA[A recent hypothesis suggests that glioma cells and neurons engage in a symbiotic relationships, where neurons tend to use lactate, produced in abundance by the cancer cells, instead of glucose. Consequently, the glucose conserved by neurons becomes accessible to glioma cells, which have a high demand for it. The present monograph further develops this hypothesis, weighing specific cellular and molecular processes in both cell types that allow for these symbiotic relationships. The potential roles in the postulated symbiosis of the glycolytic pathway, the mitochondrial tricarboxylic acid cycle, and its coupled oxidative phosphorylation, glucose and lactate transporters, the excitatory neurotransmitter glutamate, lactate signaling via its receptor, and lactylation, are all considered here. The aim is to provide a wider foundation with greater detail for a better understanding of the proposed symbiosis that could offer several possible experimental avenues to verify its validity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1767180</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1767180</link>
        <title><![CDATA[Two-year longitudinal neuropsychological monitoring after unilateral and staged bilateral subthalamic nucleus deep brain stimulation]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Szczepan Iwański</author><author>Katarzyna Polanowska</author><author>Marcin Leśniak</author><author>Michał Sobstyl</author>
        <description><![CDATA[IntroductionDeep brain stimulation (DBS) is an increasingly popular therapeutic method for treating motor symptoms in Parkinson’s disease, but its impact on non-motor symptoms in long-term follow-up remains debated.MethodThe primary objective of this study was to monitor the cognitive functioning, mood, and quality of life in 2 years of unilateral and staged bilateral subthalamic nucleus DBS. A cohort of 30 patients was evaluated at three intervals: before DBS surgery, at 6 months, and 24 months post-surgery. The time points of neuropsychological assessments were set to control the impact of unilateral and bilateral DBS throughout the treatment. Two selected groups, unilateral and bilateral DBS, were also analyzed. The study employed a combination of computerized and paper-based tests to assess cognitive functions, alongside questionnaires to gauge emotional state and quality of life. The cognitive evaluation focused on three domains critical for daily activities: attention and processing speed, learning and episodic memory, and executive functions, including working memory and cognitive flexibility.ResultsAnalysis of the entire cohort from baseline through the two follow-up assessments revealed no decline in cognitive function, mood, or quality of life, alongside significant motor improvement. Additional analyses of the two subgroups—unilateral DBS and staged bilateral DBS—also showed no overall decline in any assessed domain over the 2-year follow-up period. However, comparison of cognitive outcomes with normative data indicated a higher proportion of patients meeting criteria for cognitive decline at the 24-month follow-up in the staged bilateral DBS group compared with the unilateral DBS group.ConclusionThe findings support the long-term overall stability of cognitive function, mood, and quality of life following unilateral and staged bilateral subthalamic DBS. Subgroup analyses did not reveal any significant decline in cognitive measures over time. Nevertheless, individual comparisons with normative data showed a higher proportion of patients with memory deficits in the staged bilateral DBS group after the two-year follow-up.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1817743</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1817743</link>
        <title><![CDATA[Estimation of head motion in structural MRI and its impact on cortical morphometry]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Charles Bricout</author><author>Samira Ebrahimi Kahou</author><author>Sylvain Bouix</author>
        <description><![CDATA[Motion-related artifacts are inevitable in Magnetic Resonance Imaging (MRI) and can bias automated neuroanatomical metrics such as cortical thickness. These biases can interfere with statistical analysis which is a major concern as motion has been shown to be more prominent in certain populations such as children or individuals with ADHD. Manual review cannot objectively quantify motion in anatomical scans, and existing quantitative automated approaches often require specialized hardware or custom acquisition protocols. Here, we train a 3D convolutional neural network to estimate a summary motion metric in retrospective routine research scans by leveraging a large training dataset of synthetically motion-corrupted volumes. We validate our method with one held-out site from our training cohort and with 14 fully independent datasets, including one with manual ratings, achieving a Spearman Rank correlation of 0.71 vs. manual labels. We also tested the correlation of our predicted motion score with morphometric measurements known to be impacted by motion, achieving significant correlation on most datasets. Furthermore, our predicted motion correlates with subject age in line with prior studies. Our approach shows good generalization across scanner brands and protocols, enabling objective, scalable motion assessment in structural MRI studies without prospective motion correction. Finally, we provide empirical evidence that our motion estimator significantly improve model fitness when studying cortical thickness and volume. Our final model is made openly and freely available through “Agitation," a tool usable as a CLI, python package and integrated in Nipoppy and Boutiques. By providing reliable motion estimates, our method offers researchers a tool to assess and account for potential biases in cortical morphometric analyses.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1837965</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1837965</link>
        <title><![CDATA[α-Lipoic acid suppresses p53 by preventing annexin A2 degradation to protect dopaminergic neurons in a Parkinson's disease model]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ying Liu</author><author>WenPing Sun</author>
        <description><![CDATA[Objectivep53 plays a critical role in Parkinson's disease (PD) pathogenesis. p53 activation induces mitochondrial dysfunction and reactive oxygen species (ROS) production, contributing to progressive dopaminergic neuron degeneration. Although α-lipoic acid (ALA) exhibits neuroprotective effects in neurodegeneration, its underlying mechanisms remain unclear. This study investigated the neuroprotective role and molecular mechanism of ALA in 1-methyl-4-phenylpyridinium (MPP+)- treated PC12 cells, a cellular model of dopaminergic toxicity.MethodsNeuroprotective effects of ALA on dopaminergic neurons were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay for cell viability, Hoechst 33258 staining and flow cytometry to detect cellular apoptosis, and western blot analysis.ResultsALA treatment significantly inhibited p53 expression and attenuated MPP+-induced apoptosis in dopaminergic neurons. ALA also prevented annexin A2 degradation and protected PC12 cells from MPP+-induced toxicity.ConclusionsALA downregulates p53 expression by preventing annexin A2 degradation, thereby reducing p53 protein levels and providing neuroprotection under neurodegenerative conditions. This suggests the potential of ALA in modulating p53 pathways for PD therapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnins.2026.1816455</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnins.2026.1816455</link>
        <title><![CDATA[Distributed cortico-subcortical networks enable robust speech state detection from sparse intracranial recordings]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Chen Feng</author><author>En Zhang</author><author>Yifei Jia</author><author>Zhoule Zhu</author><author>Junming Zhu</author><author>Di Wu</author><author>Kedi Xu</author>
        <description><![CDATA[IntroductionAccurate and reliable detection of speech state transitions is a prerequisite for practical speech brain–computer interfaces (BCIs). While cortical language areas have been extensively studied, it remains unclear whether speech onset information is exclusively localized to these regions or distributed across a broader cortico-subcortical network. Here, we investigated the feasibility of decoding speech state transitions using sparse stereo-electroencephalography (SEEG) recordings that sample both cortical and subcortical structures.MethodsFour Mandarin-speaking epilepsy patients undergoing clinical SEEG monitoring performed a sentence-reading task. Neural signals were segmented and labeled as rest or speech based on acoustic onset. A convolutional neural network was trained to classify speech states using broadband or high-gamma features derived from different anatomical channel subsets. We further evaluated continuous decoding performance, model robustness to channel dropout, and the specific contributions of different brain regions.ResultsSpeech state decoding accuracy exceeded chance level (50%) in all participants, with peak single-participant accuracies surpassing 90%. Models integrating both cortical and subcortical signals generally outperformed those restricted to a single anatomical domain. Notably, broadband signals yielded higher classification accuracy than high-gamma features. In continuous decoding simulations, performance remained above chance, although reduced relative to discretized evaluation. Crucially, decoding accuracy was robust to random channel reduction (up to 50%) and remained above 70% even after excluding classical speech-related cortical regions. Contribution analyses indicated participant-specific patterns of model sensitivity, with relatively higher contributions observed in frontal regions and the thalamus in multiple participants.DiscussionThese findings support the hypothesis that speech state information is represented in a distributed cortico-subcortical network rather than being confined to canonical language areas. The robustness of decoding performance despite channel reduction and regional exclusion suggests that sparsely sampled SEEG data can effectively drive speech detection modules. This study demonstrates the feasibility of utilizing deep brain recordings for speech BCIs, offering a pathway toward more stable and generalized implantable systems. Moreover, such autonomous speech state detection may also serve as an ethical safeguard, ensuring that neural language decoding is activated only during intended communicative acts.]]></description>
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