This study examines whether pre-decision electroencephalographic (EEG) activity provides incremental information for explaining and predicting herd-consistent investment choices when social and fundamental signals conflict. A controlled 2 × 2 × 2 × 2 within-participant factorial experiment involving 80 English-Mandarin bilingual Chinese investors who met a predefined English-proficiency threshold equivalent to IELTS 6.5 or TOEFL iBT 80 and had prior experience in U.S. equity markets manipulated language, information format, social-media sentiment, and information consistency. Herd-consistent choice was conservatively defined as alignment with the social signal when it contradicted fundamental information. Behavioural and single-trial EEG responses were analysed using mixed-effects models, while machine-learning models were evaluated through nested participant-disjoint validation. The findings indicate that Mandarin-language presentation and short-form financial information are associated with greater conformity to social signals under informational conflict. Conflict between social and fundamental information also elicits stronger frontal-midline theta activity, consistent with heightened demands on cognitive control and conflict monitoring before choice. Pre-decision P300 and theta provide distinct predictive information beyond contextual and participant characteristics, indicating that attentional updating and conflict processing contribute differently to subsequent herd-consistent decisions. These findings support a process-based account of investment conformity in which information architecture, social influence, and pre-decision neurocognitive processing jointly shape herd-consistent choices.

Limiting the expansion of the primary injury after a traumatic spinal cord injury (SCI) can offer improved functional outcomes. Glibenclamide (glyburide) has been shown to limit intraspinal bleeding and promote vascular stability after SCI in rats, but its impact on intraspinal hemodynamics has not been investigated. Here, we hypothesized that acute glibenclamide treatment would improve intraspinal hemodynamics after a cervical contusion SCI in a rat model (200 kdyn). Intravital ultrafast contrast enhanced ultrasound (CEUS) imaging revealed that glibenclamide treatment significantly increased total blood volume (i.e., tissue perfusion) at 72-hours post-injury (hpi) compared to vehicle treated controls (p<0.05, Cohen's d >1.2). Histological data confirmed that glibenclamide treatment significantly lowered caspase-8-positive cells in the white matter at 72-hpi (p<0.05, Cohen's d>1.2). Weekly forelimb locomotor scoring revealed significant functional improvements in animals treated with glibenclamide at 4-weeks post injury (wpi) (p<0.001, Cohen's d>1.2), which continued through to 8-wpi compared to vehicle treated animals (p<0.05, Cohen's d>1.2). Glibenclamide intervention significantly reduced lesion size by 8-wpi compared to controls (p<0.05; Cohen's d>1.2). This study is the first to report in vivo improvements in intraspinal blood volume associated with glibenclamide treatment after acute cervical SCI in rats.

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by neuronal dysfunction and impaired autophagy. Salidroside (SAL), a bioactive component derived from Rhodiola, exhibits neuroprotective activity; however, its effects and mechanisms in ASD remain largely unknown. Here, we examined the effects of SAL on valproic acid (VPA)-induced neuronal injury and ASD-related behaviors and assessed the role of the sirtuin 2 (SIRT2)/forkhead box O1 (FoxO1) pathway. VPA-induced HT22 cell injury models and ASD mouse models were used in this study. HT22 cells were exposed to 2mM VPA and treated with 20μM SAL, with AGK2 applied for SIRT2 inhibition. ASD mice received SAL administration from postnatal day 21 for 14 days, and AK-7 was used to further evaluate SIRT2 involvement. VPA exposure decreased HT22 cell viability, caused neuronal damage, increased autophagosome accumulation, and induced ASD-like behaviors in mice, including impaired social interaction, enhanced repetitive grooming, and reduced exploratory activity. SAL treatment improved cell viability, alleviated neuronal damage, attenuated autophagy-related changes, and improved behavioral abnormalities, whereas these effects were partially blocked by AGK2 or AK-7. Furthermore, SAL reversed VPA-induced alterations in autophagy-related proteins, including decreased Beclin-1 and LC3 expression and increased p62 expression, while restoring SIRT2, FoxO1, NeuN, and MAP2 levels and reducing the Ac-FoxO1/FoxO1 ratio in HT22 cells and hippocampal tissues. These findings indicate that SAL protects against VPA-induced neuronal injury and ASD-related behavioral deficits, which are associated with changes in the SIRT2/FoxO1 pathway and autophagy-related processes.

Ferroptosis plays a crucial role in the pathological process of cerebral ischemia-reperfusion (I/R) injury, but the specific regulatory mechanism of Clusterin in this process remains unclear. This study aims to investigate whether interfering with Clusterin can alleviate cerebral I/R injury by regulating neuronal ferroptosis. A cerebral I/R injury mouse model was established and the adeno-associated virus (AAV-sh-Clusterin) was stereotactically injected into the brain. Brain tissue damage was evaluated using TTC and HE staining. The expressions of blood-brain barrier proteins (Occludin, ZO-1) and inflammatory factors (IL-1β, TNF-α, IL-6) were detected. Downstream differentially expressed genes were analyzed through mRNA transcriptome sequencing. The expression changes of iron death-related indicators (Fe2+, MDA, GSH, NRF2, GPX4, ACSL4, SLC7A11) were evaluated by means of biochemical methods and WB/qPCR. Subsequently, an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model of HT22 cells was constructed to analyze the effects of Clusterin interference on the proliferation and ferroptosis of HT22 cells. The interaction between Clusterin and TFR1 was detected, and a rescue experiment was carried out by overexpressing TFR1. Clusterin was significantly upregulated in both in vitro and in vivo models. Interference with Clusterin effectively reduced the volume of cerebral infarction, upregulated the expressions of Occludin and ZO-1, and inhibited the inflammatory response. Besides, interference with Clusterin significantly decreased the ferroptosis level in mouse brain tissue. There is a protein interaction between Clusterin and TFR1, and the rescue experiment indicated that overexpression of TFR1 could counteract the inhibitory effect of sh-Clusterin on ferroptosis and the proliferation protection effect of HT22 cells. In summary, interfering with Clusterin by inhibiting TFR1-dependent neuronal ferroptosis significantly mitigates neuronal damage and inflammatory responses induced by cerebral I/R.

Structural magnetic resonance imaging reveals lateral ventricular enlargement as a prominent structural change in normal aging, with accelerated expansion in Alzheimer's disease and related dementias. In this study, we characterize ventricular shape changes and corresponding mechanical loading in cognitively normal (CN), mild cognitive impairment (MCI), and Alzheimer's disease (AD) subjects in their seventies, using longitudinal magnetic resonance images over a two-year interval. Surface-based deformation metrics were computed to capture localized displacement magnitude, curvature changes, surface area stretch, and maximum principal wall strain, both relative to the population average at baseline and relative to each subject's baseline over the two-year follow-up. Longitudinal displacement over two years increased markedly with disease progression, rising 114 ± 15% from CN to AD. Area stretch exhibited a more modest 6 ± 1% increase, while maximum principal wall strain nearly doubled, increasing 110 ± 16% from CN to AD. Curvature change remained minimal when averaged globally, although localized deformations along ventricular edges suggest subtle region-specific alterations. The significant differences between mechanics-related features for individual disease groups highlight the value of deformation-derived mechanomarkers that go beyond the more commonly reported volumetric analyses. As such, our mechanomarkers demonstrated a predictive value for disease classification, especially in the direct comparison of CN and AD. Our results highlight the potential of ventricular mechanomarkers as non-invasive, MRI-derived biomarkers for early detection and monitoring of neurodegenerative progression, providing insight into the mechanical loading resulting from structural brain shape changes.

Ischemic and haemorrhagic strokes together constitute the leading cause of death and disability worldwide, and their pathological mechanisms involve an imbalance in mitochondrial dynamics. Dynamin-related protein 1 (Drp1), a key GTPase driving mitochondrial fission, is overexpressed in response to post-stroke pathological signals (calcium overload, oxidative stress, and inflammatory factors), leading to fragmentation of the mitochondrial network and subsequently triggering energy depletion, reactive oxygen species (ROS) bursts, and various forms of programmed cell death. This article provides a comprehensive review of the molecular regulatory networks and cell-type-specific effects of Drp1 in ischemic and haemorrhagic stroke, covering key processes such as neuronal apoptosis, inflammatory polarisation of glial cells, and disruption of the vascular endothelial barrier. The literature was synthesized based on a thematic rather than a formal systematic approach, with emphasis on high-quality mechanistic studies and preclinical evidence published over the past decade. Building upon a summary of preclinical evidence for the protective effects of pharmacological inhibitors such as Mdivi-1, P110 and Drpitor1, the paper provides an in-depth analysis of the bottlenecks currently facing translation, including core challenges such as the narrow therapeutic time window, insufficient blood-brain barrier permeability, the need to strike a balance between physiological and pathological fission, and the lack of biomarkers. Finally, this paper outlines next-generation intervention strategies based on nanodelivery systems, precise temporal regulation and multi-omics integration, emphasising a paradigm shift from 'complete blockade' to 'fine-tuning', thereby providing a theoretical basis for the development of innovative Drp1-targeted therapies for stroke.

Neurological disorders pose a major global health challenge for complicated pathogenesis and a lack of effective curative treatments. As a post-translational modification, glycosylation has emerged as a multifunctional regulator in the nervous system, influencing key processes including receptor activation, cell adhesion, and immune surveillance. Its dysfunction is increasingly recognized as a shared mechanism across various neurological disorders. This review synthesizes the molecular mechanisms of glycosylation within a novel framework of four neurological disorder categories: neurodevelopmental disorders, proteostasis disorders, neuroimmunological disorders, and acute nerve injuries. Furthermore, we advance the concept of glycosylation as an integrator of mechanistic crosstalk and demonstrate its pivotal role in bridging and amplifying intertwined pathological cascades. This integrative perspective aims to reframe the understanding of disease pathogenesis and inspire innovative diagnostic paradigms and therapeutic strategies.

Portable functional near-infrared spectroscopy (fNIRS) may support brain-based monitoring around local anesthesia, but between-patient variability and patient-overlapping validation can limit generalization. We examined affected-tooth classification before versus after anesthesia, exploratory Pre-session affected-versus-healthy classification using both resting-state and held-out healthy-tooth reference schemes, and validation inflation. We analyzed fNIRS data from 25 patients during percussion before ("Pre") and after ("Post") anesthesia. The primary cohort comprised 13 patients with complete pain abolition; 156 affected-tooth epochs were classified using Pre-session healthy-tooth responses as patient-specific references. Leave-one-subject-out (LOSO) validation tested each patient using models trained on the others. A random forest using a fixed, data-informed three-feature oxyhemoglobin (HbO) panel achieved mean area under the receiver operating characteristic curve (AUC) = 0.752 (95% confidence interval [CI], 0.624-0.865; one-sided exact conditional p = 0.0057). Fold-nested selection yielded AUC = 0.740. Referencing improved estimates for two of four classifiers. In Pre-session analyses, resting-state and split-half referencing increased affected-versus-healthy AUC from matched raw values of 0.513 and 0.524-0.731 (12 patients) and 0.782 (21 patients); both gains survived eight-comparison adjustment. Because tooth blocks followed a fixed order, these pain-related estimates may include block-position effects. Across 32 feature-based configurations, pooled-epoch cross-validation exceeded LOSO by a mean of 0.159 AUC (95% CI 0.078-0.252); inflation was also positive in all three aligned waveform models. These results support proof-of-concept held-out-patient classification of pain-related affected-tooth responses before versus after anesthesia, exploratory referenced affected-versus-healthy classification before anesthesia, and patient-disjoint validation for estimating performance in new patients.