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        <title>Frontiers in Behavioral Neuroscience | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/behavioral-neuroscience</link>
        <description>RSS Feed for Frontiers in Behavioral Neuroscience | New and Recent Articles</description>
        <language>en-us</language>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-05-13T18:10:25.461+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1833021</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1833021</link>
        <title><![CDATA[Cannabinoids in Alzheimer’s disease: animal–human evidence and clinical pharmacology challenges]]></title>
        <pubdate>2026-05-13T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Maria Komedera</author><author>Urszula Wojda</author><author>Anna Kiryk</author>
        <description><![CDATA[Cannabinoids have emerged as potential modulators of pathological processes in Alzheimer’s disease (AD), including neuroinflammation, synaptic dysfunction, and protein aggregation. Cannabidiol (CBD) and Δ9-tetrahydrocannabinol (THC), the main phytocannabinoids from Cannabis sativa, interact with the endocannabinoid system and may influence neuronal and glial signaling pathways relevant to AD pathology. This mini review summarizes evidence from transgenic animal models and clinical studies evaluating CBD, THC, and their combination in AD. Preclinical studies show that CBD and THC reduce β-amyloid accumulation, attenuate tau phosphorylation, and regulate neuroinflammatory responses, often associated with improvements in learning and memory. Cognitive outcomes appear to depend on cannabinoid composition, with CBD or THC administered individually showing more consistent effects, while combined CBD + THC effects appear dose- and ratio-dependent. Clinical evidence in AD patients remains limited and primarily reports improvements in neuropsychiatric symptoms, such as reductions in agitation, nighttime activity, and behavioral disturbances, whereas cognitive improvements are modest. Cannabinoid-based treatments are generally well tolerated, with mild sedation, somnolence, or disorientation as the most reported adverse effects. Overall, current data support the biological plausibility of cannabinoids as modulators of neuroinflammatory and synaptic processes in AD. However, heterogeneity in formulations, dosing, and study design limits firm conclusions. Future research should focus on dose optimization, biomarker-guided clinical trials, and long-term safety assessments to better define their therapeutic potential in AD.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1768582</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1768582</link>
        <title><![CDATA[Gardenoside restores blood–brain barrier integrity following ischemic stroke via AMPK-dependent ZO-1 preservation]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Rongze Jia</author>
        <description><![CDATA[BackgroundBlood-brain barrier (BBB) disruption is a critical pathological feature of ischemic stroke, yet effective therapies targeting BBB repair remain limited. Gardenoside, an iridoid glycoside from Gardenia jasminoides Ellis, has shown neuroprotective properties, but its role in post-stroke BBB restoration is unclear. This study investigated whether Gardenoside preserves BBB integrity after ischemic stroke via AMPK-dependent regulation of the tight junction protein ZO-1.MethodsMale and female C57BL/6 mice (8–10 weeks) underwent transient middle cerebral artery occlusion (MCAO; 60 min ischemia, 24 h reperfusion). Gardenoside (20 mg/kg/day, i.p.) was administered for 21 days pre-MCAO and continued post-reperfusion. Neurological deficits, BBB permeability (sodium fluorescein, Evans blue), infarct volume (TTC), endothelial activation markers (ICAM-1, VCAM-1), ZO-1 expression (qPCR, western blot, immunofluorescence), and AMPK phosphorylation were assessed. In parallel, human brain microvascular endothelial cells (HBMVECs) were subjected to oxygen-glucose deprivation/reperfusion (OGD/R; 6 h OGD, 24 h reoxygenation) with Gardenoside (5–10 μM) ± the AMPK inhibitor compound C. Outcomes included cell viability (CCK-8), LDH release, permeability (FITC-dextran, TEER), and ZO-1/AMPK signaling.ResultsIn MCAO mice, Gardenoside significantly reduced neurological deficit scores (by ~50%), BBB permeability (28–32% reduction), and infarct volume (45% reduction) compared to vehicle-treated controls. It suppressed ICAM-1 and VCAM-1 expression (mRNA: 43–52%; protein: 30–34%) and restored ZO-1 levels to near-sham values. Gardenoside increased AMPK phosphorylation (p-AMPK/AMPK ratio: 2.1-fold). Co-administration of compound C (10 mg/kg) abolished these protective effects, reversing infarct volume, BBB leakage, neurological scores, and ZO-1 restoration. In vitro, Gardenoside (5–10 μM) dose-dependently improved HBMVEC viability (from 42% to 68–88% of control), reduced LDH release (27–47%), decreased permeability (25–40%), and restored TEER (40–66%) and ZO-1 expression (50–98%) following OGD/R. These effects were associated with enhanced AMPK phosphorylation and were completely reversed by compound C (10 μM). Comparable efficacy was observed in female mice.ConclusionGardenoside preserves BBB integrity and improves neurological outcomes after ischemic stroke through AMPK-dependent restoration of ZO-1. These findings identify AMPK-mediated tight junction preservation as a previously unrecognized mechanism of Gardenoside, supporting its potential as a vascular-targeted therapy for ischemic stroke.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1863849</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1863849</link>
        <title><![CDATA[Editorial: Methodological innovations and translational insights in Early Life Adversity studies]]></title>
        <pubdate>2026-05-12T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Gonzalo Viana Di Prisco</author><author>Paul Ruiz</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1819512</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1819512</link>
        <title><![CDATA[iMOSS: an integrated open-source tail suspension test platform for high-resolution immobility scoring and synchronization with neural activity]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Zengyou Ye</author><author>Xia Min</author><author>Sarah T. Johnson</author><author>Xuehong Cao</author><author>Satoshi Ikemoto</author>
        <description><![CDATA[The tail suspension test (TST) is widely used to assess stress-coping behavior in rodents, characterized by alternating periods of active (struggling) and passive (immobile) responses. Immobility in the TST is interpreted as behavioral despair and serves as a key measure for screening antidepressant compounds. Traditional manual scoring is labor-intensive and temporally imprecise, while existing automated systems often misclassify behaviors and have not shown the capacity to integrate behavioral data with neural recording methods. Here, we improved upon the traditional TST with our new developed iMOSS (Immobility/Mobility Optimized Scoring System)—two open-source, low-cost, and scalable tools for high-resolution quantification of mobility and immobility: (1) iMOSS-MV, a video-based frame-by-frame manual-scoring software instrument designed to precisely annotate the exact onset frame for each binary event, and (2) iMOSS-AS, a sensor-based automated instrument detecting immobility/mobility bouts from the sensor-signal using a machine-learning optimized detection threshold. The output from iMOSS-AS closely matched that from iMOSS-MV and outperformed other publicly available tools. Moreover, both systems reliably detected changes in mobility and immobility induced by imipramine treatment, demonstrating sensitivity to pharmacological manipulation. Finally, both iMOSS tools readily integrated with neural data, as shown by simultaneous analysis of medial septal glutamatergic calcium activity via fiber photometry. Thus, either iMOSS-MV or iMOSS-AS alone offers an efficient, user-friendly, and bias-minimized platform for high-throughput behavioral analysis, enabling seamless integration of behavioral and neural data in systems neuroscience research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1766772</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1766772</link>
        <title><![CDATA[Sex-specific hippocampal microstructural alterations in 11–12-year-old adolescents with a history of mild traumatic brain injury]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiyoung Ma</author><author>Deborah A. Yurgelun-Todd</author><author>Erin C. McGlade</author>
        <description><![CDATA[IntroductionMild traumatic brain injury (mTBI) is common in children and adolescents and frequently accompanied by transient cognitive and emotional disturbances. While pediatric mTBI can shape subsequent brain maturation, its impact on neurodevelopmental trajectories remains poorly understood, particularly regarding hippocampal microstructure, a region critical for memory and highly vulnerable to brain injury.MethodsUsing restriction spectrum imaging (RSI) data from the Adolescent Brain Cognitive Development Study (ABCD Study®; n = 4,399), this study aimed to characterize hippocampal microstructural alterations in adolescents (aged 11–12 years) with a history of mTBI and to examine their associations with verbal learning and memory performance on the Rey Auditory Verbal Learning Test (RAVLT). Sex-stratified analyses were performed considering potential sex differences in vulnerability and responses to brain injury. History of mTBI was assessed using the modified Ohio State University TBI Screen-Short Version, a retrospective parent report.ResultsMale adolescents with a history of mTBI exhibited higher hippocampal restricted normalized diffusion (RND) than their peers without mTBI (Bonferroni-corrected p = 0.02), whereas no group differences were observed in females. Within the male mTBI group, higher hippocampal RND was positively associated with both immediate (p = 0.01) and delayed (p = 0.04) recall scores on the RAVLT, suggesting potential adaptive or reparative neuroplastic processes following injury.DiscussionThese findings demonstrate sex-specific hippocampal microstructural alterations in young adolescents with a history of mTBI, highlighting potential neuroplastic adaptations during development. Although causal inference is limited given the cross-sectional design of the analysis, and mTBI history was based on retrospective parent report, the results underscore the importance of considering sex differences in recovery mechanisms and may inform future efforts to identify neuroimaging biomarkers that predict recovery trajectories and guide targeted interventions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1805594</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1805594</link>
        <title><![CDATA[From use to abuse: psychological, neurobiological, and spiritual pathways in relational harm and recovery]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Shilpa Bhardwaj</author><author>Arif Ali</author><author>Fayaz Ahmad Paul</author>
        <description><![CDATA[This viewpoint examines the distinction between relational “use” and “abuse” through psychological, neurobiological, relational, and spiritual lenses. It conceptualizes use as a form of mutual and ethical interdependence, whereas abuse is understood as a persistent pattern of control that undermines an individual’s autonomy and self-worth. The paper highlights the profound impact of chronic emotional abuse on both mind and body, including dysregulation of stress-response systems, alterations in brain functioning, increased inflammation, and accelerated biological aging. It further emphasizes that the experience and impact of abuse vary across gender, age, and sociocultural contexts, often remaining unrecognized due to prevailing cultural norms. Additionally, the paper explores the role of spirituality in recovery, suggesting that it can facilitate meaning-making, enhance emotional regulation, and foster resilience, while acknowledging that its effectiveness is not universal. Ultimately, the paper positions relational abuse as a significant public health concern that requires nuanced, interdisciplinary, and culturally sensitive responses.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1775487</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1775487</link>
        <title><![CDATA[Eye-movement signatures of syntactic development: real-time mapping of passive sentence comprehension in children aged 6–10]]></title>
        <pubdate>2026-05-08T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Olga V. Kruchinina</author><author>Daria W. Lundina</author><author>Tatyana A. Balabanova</author><author>Nataliya V. Makurina</author><author>Elizaveta I. Galperina</author>
        <description><![CDATA[IntroductionThe ability to understand complex sentences, such as passives, improves during middle childhood. However, it remains unknown when children transition from a “wait-and-listen” strategy to incremental, word-by-word revision of interpretive hypotheses, and whether behavioral accuracy reflects mature online processing.MethodsUsing eye-tracking in a sentence-picture matching task, we examined how Russian-speaking children aged 6–7 years (n = 16), 8–10 years (n = 16), and adults (n = 35) process four sentence types (active/passive, direct/reversed word order). Semantic cues were minimized, forcing reliance on morphosyntactic markers. Linear mixed models treated age as a continuous variable to capture fine-grained trajectories.ResultsAccuracy improved sharply between ages 7 and 8, with 8–10-year-olds performing at adult levels. However, oculomotor patterns revealed a clear dissociation: at the critical second word in passive direct sentences—where the participle signals thematic role revision—adults and 8–10-year-olds showed a distinct signature (decreased fixation time, increased gaze returns), indicating rapid incremental revision. This signature was absent in 6–7-year-olds, who delayed engagement until the third word. Linear mixed models confirmed that age-related increases in fixation duration were specifically tied to this revision point, extending previous ERP findings that localized revision effects only to the third word.DiscussionAdult-like behavioral accuracy by age 8–10 masks continued immaturity of incremental revision mechanisms. Eye-tracking captures this dissociation, positioning it as a sensitive marker of syntactic development and revealing that the ability to use morphosyntactic cues for real-time revision continues to develop beyond middle childhood.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1767175</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1767175</link>
        <title><![CDATA[The magic of mushrooms: psilocybin influences behavior in the mangrove rivulus fish, Kryptolebias marmoratus]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Dayna Forsyth</author><author>Nicoletta Faraone</author><author>Simon G. Lamarre</author><author>Suzanne Currie</author>
        <description><![CDATA[Non-human models, including fish, are increasingly important for investigating how pharmacological agents such as hallucinogens influence behavior, physiology, and cellular processes. These models help to reveal underlying mechanisms and to support assessments of toxicological impact, efficacy, and safety. In this study, we used isogenic lineages of the amphibious mangrove rivulus (Kryptolebias marmoratus), an emerging model fish known for high activity and socially dynamic interactions. This species often display aggression towards conspecifics making it well-suited to study behavioral effects of low doses of the psychoactive compound, psilocybin. We determined whether psilocybin could induce calming effects and reduce social aggression and activity. We socially stimulated fish using pairs of size-matched fish from different isogenic lineages and compared baseline social behavior following a waterborne dose of psilocybin. Waterborne psilocybin treatment resulted in a significant decrease in activity levels and in the frequency of swimming bursts (an aggressive behavior) towards a conspecific fish from a different lineage, with modest alterations on other behaviors. Our results also revealed considerable intraspecific variation in the behavioral response of these homozygous fish, suggesting the effects of psilocybin were largely independent of genotype. This study demonstrates that psilocybin reduces aggression and activity in an emerging fish model, adding to the evidence supporting its potential as a therapeutic agent for future clinical translation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1843064</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1843064</link>
        <title><![CDATA[Editorial: Between emotional regulation and dysregulation: perspectives, interventions, tools and technologies for psychological well-being]]></title>
        <pubdate>2026-05-07T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Luigia Simona Sica</author><author>Michela Ponticorvo</author><author>Alessandro Frolli</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1802923</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1802923</link>
        <title><![CDATA[Salidroside mitigates cognitive deficits in AlCl3 exposed aging mouse by modulating APP processing and mitochondrial dysfunction]]></title>
        <pubdate>2026-05-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yiru Dong</author><author>Huiling Jin</author><author>Shengmin Wang</author><author>Yanji Xu</author>
        <description><![CDATA[Background and objectivesMitochondrial dysfunction and oxidative stress are key contributors to the progression of Alzheimer’s disease (AD). Salidroside, a bioactive glycoside derived from Rhodiola rosea, exhibits neuroprotective and antioxidative properties; however, its effects on mitochondrial dysfunction and APP processing in AD remain to be fully elucidated.Methods and study designWe employed both in vivo and in vitro models to evaluate the neuroprotective potential of salidroside. D-galactose-induced AlCl3 exposed aging mouse model was used for behavioral assessments, biochemical analyses of brain tissue biomarkers, and evaluation of mitochondrial dysfunction-related proteins and functions. In vitro experiments with HT-22 hippocampal neurons assessed the effects of salidroside on oxidative stress, mitochondrial integrity, apoptosis, and amyloid precursor protein (APP) processing.ResultsSalidroside significantly improved cognitive performance and reduced Aβ deposition in the AlCl3 exposed aging mouse by modulating APP processing, characterized by downregulation of β- and γ-secretase activities and enhancement of α-secretase activity. These changes coincided with decreased mitochondrial protein aggregation and restored mitochondrial function and redox balance. In vitro, salidroside attenuated reactive oxygen species (ROS) generation, inhibited neuronal apoptosis, and suppressed Aβ production, demonstrating broad neuroprotective effects relevant to AD pathology.ConclusionOur results suggest that salidroside may alleviate mitochondrial dysfunction and reduce mitochondrial protein aggregation by modulating APP processing, promoting sAPPα production while decreasing β-CTF and Aβ levels. These findings provide preliminary evidence supporting the neuroprotective potential of salidroside in ameliorating mitochondrial impairment and cognitive deficits associated with Alzheimer’s disease, warranting further investigation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1815692</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1815692</link>
        <title><![CDATA[Long-term consequences of prenatal saccharin exposure: evidence of sex-specific molecular programing in the prefrontal cortex and behavior of adolescent rats]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Beatriz Pacheco-Sánchez</author><author>Raquel López-Merchán</author><author>Pablo Rubio</author><author>Pilar García-Martos</author><author>Juan Suárez</author><author>Carlos Sanjuan</author><author>Leticia Rubio</author><author>Stella Martín-de-Las-Heras</author><author>Fernando Rodríguez de Fonseca</author><author>Francisco Alén</author><author>Marialuisa de Ceglia</author><author>Patricia Rivera</author>
        <description><![CDATA[IntroductionCertain events that occur in early life, such as changes in nutrition, can induce structural and functional modifications in brain development, leading to behavioral programing in the offspring. These effects depend on the timing, intensity, and duration of exposure, and may contribute to chronic disorders in adulthood. Artificial non-nutritive sweeteners (NNS), such as saccharin, have recently been proposed as potential developmental disruptors. Saccharin consumption during pregnancy is discouraged, as it can cross the placenta and accumulate in the fetus.MethodsIn this study, pregnant rats were administered 0.1% saccharin in drinking water throughout gestation. On postnatal day 21, offspring were assessed for behavioral outcomes using the open field and elevated plus maze tests. During sacrifice, the prefrontal cortex of the animals was collected.ResultsGestational saccharin exposure induced sex-specific behavioral changes: offspring of saccharin-consuming mothers spent more time in the center of the arena, while only females showed increased open-arm entries. These alterations were coupled with changes in prefrontal endocannabinoid, glutamatergic, and GABAergic gene expression. Only saccharin-exposed male pups showed significant alterations in Dagla, Daglb and Gpr55 along with increased expression of glutamatergic receptors (Grin1, Grin2a, Grin2c, Gria1, Grm3). Females exhibited reduced expression of GABAergic receptor genes (Gabrg2, Gabbr2), and significant changes in the phosphorylated expression of proteins involved in the insulin pathway (IRS-1, PI3K, AKT, GSK3b).DiscussionThese findings suggest that developmental NNS exposure produces long-lasting behavioral outcomes in offspring, which are linked to alterations in multiple signaling pathways within the prefrontal cortex.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1839983</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1839983</link>
        <title><![CDATA[Excitability-margin narrowing as a candidate gating mechanism for maladaptive circuit reactivation: a ventral CA1-centered model]]></title>
        <pubdate>2026-04-30T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Patryk Rosa</author>
        <description><![CDATA[We propose that the excitability margin (ΔVmargin), defined as the difference between spike threshold and resting membrane potential, may function as a quantitative gating variable linking chronic stress, inflammatory load, and transient increases in excitability associated with reactivation to emotionally polarized replay or other maladaptive forms of circuit reactivation. Based on a conceptually guided integration of published electrophysiological data, we modeled how chronic restraint stress, a conservatively parameterized stress-associated inflammatory component, and a transient state of increased engram reactivity may jointly reduce the excitability reserve of ventral CA1 (vCA1) pyramidal neurons. In the main scenario, the model-derived effective margin decreased from 18.4 mV to approximately 6.0 mV, corresponding to a 67.5% reduction. Additional illustrative pro-excitatory scenarios further reduced the margin to approximately 4.3 mV, 3.7 mV, or 1.7 mV. These values fall within the range of physiologically reported amplitudes of transient depolarizing events, including local NMDA spikes, sharp wave–associated depolarizations, intracellular ripples, and larger subthreshold burst-related events. This suggests that in circuits where analogous transient depolarizing events occur, narrowing of ΔVmargin may increase the likelihood that otherwise subthreshold network activity contributes to threshold crossing and maladaptive reactivation. We therefore hypothesize that progressive narrowing of ΔVmargin may act as a gating mechanism for preferential reactivation of vulnerable neuronal ensembles, increasing the probability of repetitive, emotionally polarized replay or other maladaptive forms of circuit reactivation and secondary circuit destabilization. This framework may provide a unifying excitability-based mechanistic hypothesis and a hypothesis-generating transdiagnostic framework relevant to schizophrenia-, depression-, and trauma-related phenotypes, while remaining potentially informative for other conditions characterized by excitability instability. The model generates clear, falsifiable predictions: interventions that widen ΔVmargin or reduce trigger efficacy should attenuate hyperreactivity in the vCA1/vHipp system analyzed here and limit secondary markers of network dysregulation, while also providing a transferable framework for testing analogous low-margin dynamics in other phenotype-relevant circuit nodes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1774848</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1774848</link>
        <title><![CDATA[Unbiased autoantibody screening using nucleic acid protein programmable array in pediatric autoimmune neuropsychiatric disorder associated with streptococcal infections]]></title>
        <pubdate>2026-04-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jelena Eremija</author><author>Michael Daines</author><author>Sydney Rice</author><author>Juliette C. Madan</author><author>Susan Swedo</author><author>Fayez K. Ghishan</author><author>Pawel R. Kiela</author>
        <description><![CDATA[IntroductionPediatric autoimmune neuropsychiatric disorder associated with streptococcal infections (PANDAS) is characterized by the abrupt onset of obsessive-compulsive disorder and/or tics, along with other neuropsychiatric symptoms in children, in the setting of Group A beta-hemolytic streptococcus infection and presumed immune dysregulation. Current diagnostic testing has limited utility in diagnosis of PANDAS.MethodsThe Nucleic Acid Protein Programmable Array (NAPPA) is a protein expression system that enables the study of protein-autoantibody interactions. We employed this system for unbiased screening of potential autoimmune targets in PANDAS.ResultsInitially, we compared children with PANDAS to patients with autism spectrum disorder (ASD) and identified 1,235 non-overlapping protein targets. These targets were subsequently used to re-screen samples from PANDAS, ASD and healthy controls (HC). In the secondary screen, 117 autoantibody targets were exclusively detected in PANDAS and absent from both ASD and HC groups. However, autoantibody profiles were highly heterogeneous: 67.5% of PANDAS-positive targets were reactive in only a single patient, and no individual protein or multi-protein panel classifier achieved reliable diagnostic discrimination under proper cross-validation. Targets that discriminated PANDAS from HC largely failed to discriminate PANDAS from ASD, and vice versa, indicating that autoantibody-based diagnosis is confounded by reactivity shared across neuropsychiatric conditions. Despite poor diagnostic performance, functional enrichment analysis revealed that PANDAS-specific targets were significantly overrepresented among transcription factors, apoptosis regulators, chromatin/epigenetic modifiers, neural development proteins, and immune-regulatory molecules, with the majority being intracellular proteins enriched for intrinsically disordered regions.DiscussionThese findings support the hypothesis of autoimmunity and epitope spreading as features of PANDAS but indicate that the heterogeneity of the humoral response represents a fundamental challenge for serological diagnosis. Future studies with larger cohorts and complementary approaches are necessary to determine whether autoantibody signatures can be leveraged for clinical utility.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1808641</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1808641</link>
        <title><![CDATA[Acute changes in postural stability during Instagram Reels viewing using virtual reality–based posturography]]></title>
        <pubdate>2026-04-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hanifi Korkmaz</author><author>Yasin Tok</author><author>Rania Alkahtani</author><author>Hadeel Alsaleh</author><author>Reem Elbeltagy</author>
        <description><![CDATA[Short-form video platforms such as Instagram Reels deliver continuous high–visual-flow stimulation that imposes substantial visual–cognitive load even in the absence of active motor interaction, yet their impact on postural control remains largely unexplored. This study examined whether passive Instagram Reels viewing acutely alters postural stability in healthy adolescents and young adults, and whether addiction severity and habitual use patterns modulate this effect. Regular Instagram users aged 16–21 years completed virtual reality–based static posturography before and during passive Instagram Reels viewing (i.e., viewing short-form, algorithm-driven video content without active user interaction such as scrolling or screen contact). Instagram addiction severity and usage habits were assessed, and their associations with viewing-related postural changes were evaluated. Vestibular-related postural stability decreased during Reels viewing. Higher Instagram addiction severity and longer daily Instagram use were associated with smaller reductions in vestibular-related postural stability between pre- and during-viewing conditions, a pattern compatible with partial habituation and/or compensatory postural control strategies. The purpose of Instagram use was not meaningfully associated with the magnitude of change. Passive short-video exposure can acutely compromise vestibular-related postural stability even during quiet standing, while habitual exposure appears to attenuate the immediate destabilizing effect. These findings extend smartphone–balance research toward a more ecologically relevant exposure model and provide a reference framework for future studies in clinically vulnerable populations, future studies in clinically vulnerable populations, such as individuals with vestibular disorders, neurological conditions, or balance impairments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1682995</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1682995</link>
        <title><![CDATA[The influence of trait anxiety on performance in the CatWalk test]]></title>
        <pubdate>2026-04-28T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Edoardo Parrella</author><author>Valentina Salari</author><author>Yasamin Meamarzadegan</author><author>Lorena Torroni</author><author>Vivekanand Jha</author><author>Giulia Spagnoli</author><author>Ali Jafari Fereidouni</author><author>Andrea Lazzarin</author><author>Vittoria Giuliari</author><author>Giuseppe Bertini</author><author>Paolo Francesco Fabene</author>
        <description><![CDATA[IntroductionTrait anxiety refers to the individual variability in the predisposition to respond anxiously to stimuli. Anxiety has been shown to affect several physiological processes, including fine motor tasks, both in humans and in rodents. Therefore, trait anxiety may be a confounder factor in behavioral studies assessing motor functions in preclinical animal models. Among the tools employed to investigate motor functions in rodents, CatWalk XT is one of the most used. CatWalk XT is a computer-assisted apparatus that allows rapid and objective quantification of both static and dynamic gait parameters in rodents. The test consists of a training period in which the mouse learns to cross a platform and a test day in which the mouse footprints are recorded and analyzed.MethodsHere, we investigated whether trait anxiety, assessed with the Elevated Plus Maze (EPM) test, influences mice performance on CatWalk XT.ResultsThe results showed a correlation between anxiety levels as measured by the EPM and CatWalk test, with trait anxiety affecting the CatWalk learning and gait parameters. Indeed, mice with higher degrees of anxiety displayed a higher number of noncompliant runs during the training, ultimately protracting the time required by the experimenter to perform the CatWalk test. In addition, mice displaying fewer total entries in the EPM exhibited increased print lengths when assessed with the CatWalk system.DiscussionIn conclusion, our findings indicate that individual differences in trait anxiety must be considered when testing mice with the CatWalk XT system. The use of specific anxiety tests before CatWalk testing may be useful to exclude those mice showing the highest levels of anxiety. This strategy would optimize researcher’s time, limit animals’ stress, and avoid errors in the results interpretation.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1729876</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1729876</link>
        <title><![CDATA[Infrasound exposure is linked to aversive responding, negative appraisal, and elevated salivary cortisol in humans]]></title>
        <pubdate>2026-04-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kale R. Scatterty</author><author>Dawson VonStein</author><author>Lisa B. Prichard</author><author>Brian C. Franczak</author><author>Trevor J. Hamilton</author><author>Rodney M. Schmaltz</author>
        <description><![CDATA[IntroductionInfrasound describes sound wave frequencies below 20 Hz, which are typically imperceptible to humans. Some animals perceive and demonstrate aversion to infrasound, raising concerns about its potential adverse effects as an anthropogenic pollutant. Recent research suggests humans may also respond to infrasound, despite being below the conventional limit of human hearing. This study explored the non-auditory impact of infrasound on human mood and stress responding.MethodsParticipants (n = 36) were exposed to calming or unsettling music with infrasound (~18 Hz) present or absent in a 2 × 2 between-subjects design (calming vs. unsettling, infrasound on vs. off). Self-report measures were collected immediately post-exposure, and saliva was collected immediately pre-exposure and 20 min post-onset for cortisol assay.ResultsParticipants did not detect infrasound above chance (p = 0.241). Infrasound was associated with elevated salivary cortisol (p = 0.022, rrb = 0.390) and higher self-reported irritability (p = 0.049, η2 = 0.096), disinterest (p = 0.044, η2 = 0.121; p = 0.047, η2 = 0.118), and sadness appraisal (p = 0.002, η2 = 0.253) across both music conditions, with no expectancy effects. Interest, irritability, sadness appraisal, and cortisol were also identified as important predictors of infrasound exposure via random-forest modeling.DiscussionWithout auditory detection nor expectancy effects, infrasound exposure was linked to elevated cortisol and more negative affective self-reporting. These findings align with previous animal studies and suggest infrasound may be aversive to humans, acting as a potential environmental irritant and contributing to more negative subjective experience.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1793337</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1793337</link>
        <title><![CDATA[Association of simultaneous sour taste stimulation with prefrontal cortex activation during stroop task performance in healthy adults: a fNIRS study]]></title>
        <pubdate>2026-04-23T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xiao Juan Li</author><author>Ji Liang Kang</author><author>Fei Fei Ge</author><author>Tingting Ying</author><author>Shuang Liang Li</author><author>Yu Jin</author><author>Xiaobo Chen</author><author>Min Tang</author>
        <description><![CDATA[BackgroundThe prefrontal cortex (PFC) plays a central role in executive functions, particularly during cognitive conflict tasks. Sour taste is a salient oral sensory stimulus and may be associated with changes in behavioral performance and prefrontal activation during cognitive tasks. This study examined whether simultaneous sour taste stimulation was associated with behavioral and prefrontal hemodynamic changes during Stroop task performance in healthy adults using functional near-infrared spectroscopy (fNIRS).MethodsTwenty-six right-handed healthy adults were randomly assigned to either the sour taste group (0.1 M citric acid, n = 13) or the water control group (n = 13). Participants completed a simplified color-word Stroop task in a between-subject block design while receiving simultaneous oral stimulation through cotton swabs placed on the anterior-lateral surface of the tongue. A 52-channel fNIRS system recorded changes in oxygenated and deoxygenated hemoglobin concentrations in the frontal cortex, while behavioral data (reaction time, accuracy) were collected concurrently. Behavioral data were analyzed using mixed-design analysis of variance and interference-score comparisons. Task-related Oxy-Hb responses were analyzed using a general linear model with false discovery rate correction, whereas Deoxy-Hb signals were reviewed descriptively only.ResultsThe sour taste group showed faster overall reaction times and higher overall accuracy than the water control group during Stroop task performance. However, no significant between-group differences were observed in Stroop interference scores for reaction time or accuracy. At the neural level, both groups showed task-related frontal activation, while the sour taste group exhibited higher Oxy-Hb β values in several channels, particularly in the left dorsolateral prefrontal cortex and frontopolar region.ConclusionSimultaneous sour taste stimulation was associated with better overall task performance and stronger task-related prefrontal hemodynamic responses in healthy adults during the Stroop task. These findings support an association between sour taste stimulation, broader behavioral facilitation, and altered prefrontal recruitment, but do not provide clear evidence for a conflict-specific enhancement of Stroop interference control.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1681619</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1681619</link>
        <title><![CDATA[A panel of medaka isogenic lines suggests individual, seasonal, and sexual genetic variation of bdnf gene expression in the brain]]></title>
        <pubdate>2026-04-22T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Eleonora Rovegno</author><author>Christina Vasilopoulou</author><author>Saul Pierotti</author><author>Tomas Fitzgerald</author><author>Joachim Wittbrodt</author><author>Ewan Birney</author><author>Daniela Vallone</author><author>Felix Loosli</author><author>Cristiano Bertolucci</author><author>Nicholas S. Foulkes</author><author>Tyrone Lucon-Xiccato</author>
        <description><![CDATA[IntroductionOnce recognized only in humans, variance in the cognitive phenotype is now acknowledged in a range of vertebrate species. However, our understanding of its underlying causes is still incomplete. Brain-derived neurotrophic factor (BDNF) is an essential protein for brain functioning and plays a key role in cognitive processes such as learning and memory, including interindividual variation. Environmental factors influence BDNF abundance in the brain, and so do genetic polymorphisms in humans and mice.MethodsUsing the Medaka Inbred Kiyosu-Karlsruhe (MIKK) panel of near-isogenic medaka lines, which captures a wide range of natural genetic variation in this species, we investigated the potential quantitative genetic variation in bdnf gene expression in the brain.ResultsOur findings show significant variation in bdnf mRNA expression levels across MIKK lines, with a two-fold difference between the lines exhibiting lower and higher expression. Seasonal variation was also observed, with higher average bdnf levels in summer. However, a tentative analysis suggested that this average effect was not consistent across the lines, with some lines even showing significantly greater expression in winter. Similarly, across the entire sample, males and females did not differ in bdnf expression overall, although some lines displayed sex differences greater than expected by chance.DiscussionThese results suggest that quantitative genetic differences, in concert with environmental influences, contribute to bdnf expression variability.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1819151</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1819151</link>
        <title><![CDATA[Establishment and preliminary application of object recognition system based on DeepLabCut]]></title>
        <pubdate>2026-04-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Cenfei Zhou</author><author>Yihua Sheng</author><author>Jing Xu</author><author>Xiaorui Peng</author><author>Zhujun Jia</author><author>Jianfei Wang</author><author>Yuanyun Zheng</author><author>Sidi Li</author>
        <description><![CDATA[This study aimed to develop a DeepLabCut (DLC)-based object recognition analysis system for assessing rodent cognitive function and validate its application in natural aging and elderly periodontitis mouse models. The system’s hardware was constructed with a custom arena and high-definition industrial camera, and the DLC deep learning algorithm was trained to track five mouse body landmarks, enabling automatic quantification of 36 indicators across three categories: sniffing frequency, exploration duration, and novelty preference. The system subdivided exploratory behaviors by calibrating nose tip and body center, and set dynamic distance thresholds (1 cm, 1.5 cm, 2 cm) for the nose tip to capture fine-grained exploration. In the novel object recognition (NOR) and object location recognition (OLR) paradigms, traditional visual inspection failed to detect significant cognitive differences between young and aged mice, while the DLC system identified marked reductions in aged mice in the frequency and duration of body center and combined nose tip-body center exploration of the new object (2 cm away from the object), as well as corresponding novelty preference indices. In the elderly periodontitis models, traditional metrics showed increased nose tip exploration of the old object (2 cm away from the object) and reduced novelty preference in model mice; the DLC system further detected significantly elevated nose tip exploration frequency toward the old object (1.5 cm away from the object), accompanied by decreased frequency preference for exploration (1 cm away from the object). Collectively, this DLC-based system achieves sensitive, precise, and multidimensional quantification of mouse exploratory behavior, effectively distinguishing cognitive characteristics of aged and disease model mice. By overcoming the limitations of traditional methods, it captures subtle cognitive changes in aging and periodontitis models, screens key indicators for cognitive decline, and provides comprehensive behavioral evidence for elucidating the neural mechanisms underlying aging- and inflammation-associated cognitive impairment.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1785573</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnbeh.2026.1785573</link>
        <title><![CDATA[Tannic acid attenuates glyphosate-based herbicide-induced dopaminergic neurotoxicity associated with motor dysfunction in mice]]></title>
        <pubdate>2026-04-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Patrick Oluwole Abolarin</author><author>Bamidele Victor Owoyele</author>
        <description><![CDATA[IntroductionGlyphosate, a widely used herbicide, has gained attention due to its potential link to neurobehavioral and dopaminergic dysfunctions. Data on interventions against glyphosate-induced neurotoxicity are limited. Hence, the neuroprotective role of tannic acid (TA), a polyphenolic anti-inflammatory and antioxidant agent, was investigated in mice chronically exposed to glyphosate-based herbicide (GBH).MethodsMale Swiss mice were randomly allocated into six groups (n = 8) and received daily oral gavages of specific solutions that were prepared daily: Control (distilled water 1 mL/kg body weight), GBH (500 mg/kg body weight), Pre-TA + GBH (TA 50 mg/kg body weight, pre-treated, then GBH-exposed), TA + GBH (TA 50 mg/kg body weight and GBH-co-treatment), Pre-AA + GBH [ascorbic acid (AA) 100 mg/ kg body weight, pre-treated, then GBH-exposed], and AA + GBH (AA 100 mg/ kg body weight and GBH-co-treatment). Motor function tests, biochemical, and histological analyses of the midbrain were performed 6 weeks post-treatment.ResultsTA significantly inhibited GBH-induced motor dysfunction. As compared to the GBH group, TA treatments significantly (p < 0.0001) decreased midbrain malondialdehyde (MDA), TNF-α, IL-1β, and IL-6 levels. TA treatments increased significantly (p < 0.0001) the concentrations of dopamine, the activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) enzymes in the midbrain relative to the GBH group. These effects were similar to those of the control and AA-treated mice. Conclusively, TA ameliorated GBH-induced motor dysfunction in mice and attenuated associated midbrain oxidative stress, inflammatory responses, and dopaminergic alterations.DiscussionThese findings are suggestive of the neuroprotective effects of TA against environmental toxicant-induced neurotoxicity.]]></description>
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