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Pupillometry research has experienced an enormous revival in the last two decades. Here we briefly review the surge of recent studies on task-evoked pupil dilation in the context of cognitive control tasks with the primary aim being to evaluate the feasibility of using pupil dilation as an index of effort exertion, rather than task demand or difficulty. Our review shows that across the three cognitive control domains of updating, switching, and inhibition, increases in task demands typically leads to increases in pupil dilation. Studies show a diverging pattern with respect to the relationship between pupil dilation and performance and we show how an effort account of pupil dilation can provide an explanation of these findings. We also discuss future directions to further corroborate this account in the context of recent theories on cognitive control and effort and their potential neurobiological substrates.

D-galactose has been widely used in aging research because of its efficacy in inducing senescence and accelerating aging in animal models. The present study investigated the benefits of exercise for preventing neurodegeneration, such as synaptic plasticity, spatial learning and memory abilities, in mouse models of aging. D-galactose-induced aging mice were administered daily subcutaneous injections of D-galactose at the base of the neck for 10 consecutive weeks. Then, the mice were subjected to exercise training by running on a treadmill for 6 days a week. Shortened escape latency in a Morris water maze test indicated that exercise improved learning and memory in aging mice. The ameliorative changes were likely induced by an upregulation of Bcl-2 and brain-derived neurotrophic factor, the repression of apoptosis factors such as Fas and Bax, and an increase in the activity of glucose transporters-1 and 4. The data suggest moderate exercise may retard or inhibit neurodegeneration in D-galactose-induced aging mice.

Assessing drivers’ mental workload is crucial for reducing road accidents. This study examined drivers’ mental workload in a simulated auditory-based dual-task driving scenario, with driving tasks as the main task, and auditory-based N-back tasks as the secondary task. A total of three levels of mental workload (i.e., low, medium, high) were manipulated by varying the difficulty levels of the secondary task (i.e., no presence of secondary task, 1-back, 2-back). Multimodal measures, including a set of subjective measures, physiological measures, and behavioral performance measures, were collected during the experiment. The results showed that an increase in task difficulty led to increased subjective ratings of mental workload and a decrease in task performance for the secondary N-back tasks. Significant differences were observed across the different levels of mental workload in multimodal physiological measures, such as delta waves in EEG signals, fixation distance in eye movement signals, time- and frequency-domain measures in ECG signals, and skin conductance in EDA signals. In addition, four driving performance measures related to vehicle velocity and the deviation of pedal input and vehicle position also showed sensitivity to the changes in drivers’ mental workload. The findings from this study can contribute to a comprehensive understanding of effective measures for mental workload assessment in driving scenarios and to the development of smart driving systems for the accurate recognition of drivers’ mental states.

Electroencephalography based brain-computer interfaces (BCIs) show promise of providing an alternative communication channel between the brain and an external device. It is well acknowledged that BCI control is a skill and could be improved through practice and training. In this study, we explore the change of BCI behavioral performance as well as the electrophysiological properties across three training sessions in a pool of 42 human subjects. Our results show that the group average of BCI accuracy and the information transfer rate improved significantly in the third session compared to the first session; especially the significance reached in a smaller subset of a low BCI performance group (average accuracy <70%) as well. There was a significant difference of event-related desynchronization (ERD) lateralization for BCI control between the left- and right-hand imagination task in the last two sessions, but this significant difference was not revealed in the first training sessions. No significant change of value or event-related desynchronization and synchronization (ERD/ERS) for either channel C3 or channel C4, which were used for online control, was found across the training sessions. The change of ERD lateralization was also not significant across the training sessions. The present results indicate that BCI training could induce a change of behavioral performance and electrophysiological properties quickly, within just a few hours of training, distributed into three sessions. Multiple training sessions might especially be beneficial for the low BCI performers.

Measurement of event-related potentials (ERPs) in simulated and real environments is advantageous for understanding cognition and behavior during practice of goal-directed activities. Recently, instead of using task-irrelevant \"probe stimuli\" to elicit ERPs, extraction of ERPs directly from events that occur in simulated and real environments has drawn increased attention. Among the previous ERP studies using immersive virtual reality, only a few cases elicited ERPs from task-related events in dynamic task settings. Furthermore, as far as we surveyed, there were no studies that examined the source of ERPs or correlation between ERPs and behavioral performance in immersive virtual reality environment. In this study, EEG signals were recorded from 16 participants while they were playing the first-person shooter game with immersive virtual reality environment. Error related negativity (ERN) and correct-(response)-related negativity (CRN) elicited by shooting-related events were successfully extracted. We found the ERN amplitudes to be correlated with the individual shooting performance. Interestingly, the main source of the ERN was the rostral anterior cingulate cortex (ACC), which is different from previous studies where the signal source was often estimated to be the more dorsal part of ACC. The obtained results are expected to contribute to the evaluation of cognitive functions and behavioral performance by ERPs in a simulated environment.

Multiple sclerosis (MS) is the most common demyelinating disease of the central nervous system, especially the cerebellum, with numerous physical and mental symptoms. Oxidative stress caused by inflammation can play a role in the occurrence of this disease. Betaine, a natural methyl donor compound, has potent neuroprotective effects. Here, we investigated the effects of betaine on motor behavior, cerebellar histological changes, oxidative stress response, and endoplasmic reticulum stress in a cuprizone (CPZ)-induced multiple sclerosis model in male rats. Twenty Wistar adult male rats were randomly divided into four groups including control, MS, betaine-treated MS, and betaine groups. MS was induced by feeding animals with rodent chow containing 0.5% CPZ for 12 weeks. Betaine was daily administrated as 1% in drinking water for the last 6 weeks. The motor behavioral performance was evaluated by open field, rotarod, and reverse basket tests. Histological analysis of the cerebellum was performed by hematoxylin and eosin (H&E) and Cresyl violet (Nissl) staining. Oxidative stress factors (GSH, GSSG, GPX, GR, and GT) were assessed in the experimental groups and finally, the expression of ERS-associated proteins was measured using western blot analysis. Data showed that treatment with betaine could effectively prevent and reverse the adverse behavioral manifestation compared with the MS group. Betaine treatment protected cerebellar demyelination and neuron and Purkinje cell degeneration against CPZ-induced demyelination. Betaine attenuated the protein levels of ESR-related proteins in the cerebellum of MS rats and similarly increased the level of enzymes related to antioxidants in the cerebellum. Therefore, our results suggest that oral administration of betaine may be used as a novel adjunct therapy against cerebellar dysfunctions in an animal model of MS.

It is well established that inhalation exposure to xylene causes significant learning impairments and neurobehavioral toxicity by altering lipid environments in nerve membranes and affecting neurotransmitter levels. Royal jelly (RJ) has been shown to exhibit potent antioxidant properties that can protect the hippocampus from oxidative damage. The present research was designed to investigate the neuroprotective potential of RJ in mitigating hippocampal injury induced by short-term and long-term xylene inhalation exposure. In this experiment, 48 male Wistar rats were randomly assigned to short-term and long-term groups, each consisting of control, RJ, xylene, and xylene + RJ treatments. Rats were exposed to xylene via inhalation for 6 h daily at a concentration of 500 ppm, while RJ was administered orally at a dose of 200 mg/kg. After 8 weeks, spatial memory and anxiety level were evaluated. Apoptosis and cell necrosis in the hippocampus were identified using the TUNEL method and hematoxylin-eosin staining. Additionally, oxidative stress biomarkers and the expression of apoptosis-related genes in hippocampal tissue were investigated. The results revealed that xylene exposure caused a significant impairment in spatial working memory performance, as reflected by reductions in arm entries and alternation percentage, along with a significant suppression of antioxidant enzyme activities (CAT, TAC, SOD, and GPx) compared to the control group. Additionally, xylene exposure significantly heightened anxiety-like behaviors, elevated MDA levels, increased the number of TUNEL-positive apoptotic cells in the hippocampus, and upregulated the expression of apoptotic markers including caspase-3, Bax, and p53 genes, alongside promoting necrotic cell death. Co-treatment with RJ significantly improved behavioral alterations, enhanced antioxidant activity, and decreased hippocampal apoptosis/necrosis. In conclusion, RJ mitigates xylene-induced neurotoxicity via antioxidant and anti-apoptotic pathways, suggesting therapeutic potential against xylene-related cognitive and neuronal damage.

Background EEG microstate analysis provides insights into the spatial and temporal dynamics of brain activity during cognitive tasks. The four canonical microstates (classes A, B, C, and D) have been widely reported and associated with various cognitive functions. However, the relationship between microstate parameters and behavioral responses in cognitive functions, such as working memory (WM), has not been sufficiently investigated. This study investigates how microstate dynamics relate to WM performance during a memory‐guided saccade (MGS) task. Methods EEG and Eye‐tracking data were recorded from participants performing an MGS task at two target eccentricities (near and far). Saccade error was used as a behavioral index of WM performance. Microstate parameters (occurrence, coverage, duration, and transition probability) were computed for the four canonical microstates during the trials. Results Our analysis revealed a significant reduction in the coverage of microstate C, often associated with the default mode network, during the memory maintenance interval compared to baseline. Moreover, a notable increase was observed in the duration of microstate D, considering polarity during the memory interval, which could be related to the frontoparietal control network (FPCN). Notably, the transition probability (TP) from D+ to D‐ during the memory duration correlated with saccade errors, indicating a behavioral predictive capacity. Furthermore, we identified distinct patterns of microstate D transitions to other microstates that differed significantly between the near and far target conditions, suggesting a functional role in spatial coding. Conclusion Microstate dynamics, particularly those of microstate D, play a dual role in spatial WM by supporting information coding and predicting behavioral accuracy. The polarity‐specific transitions within microstate D provide a neural signature of WM performance, with implications for understanding network‐level mechanisms underlying spatial memory and saccade control. The schema of the microstate analysis procedure is as follows: (a) For each subject and each trial, a time interval of 500 ms before stimulus onset to 1500 ms after stimulus offset was selected for analysis. The black dashed line indicates stimulus onset, and the red dashed line indicates stimulus offset (300 ms). (b) Global field power (GFP) was calculated for each trial. (c and d) Maps at local maxima of GFP were chosen for clustering analysis; the red asterisks indicate the local maximum. (e) Spatial clustering of topographic maps across trials and subjects.

The present study evaluated the protection of Lactiplantibacillus plantarum CCFM8661, a candidate probiotic with excellent benzopyrene (B[a]P)-binding capacity in vitro , against B[a]P-induced toxicity in the colon and brain of mice. Mice that received B[a]P alone served as the model group. Each mouse in the L. plantarum treatment groups were administered 2×10 9 colony forming unit (CFU) of L. plantarum strains once daily, followed by an oral dose of B[a]P at 50 mg/kg body weight. Behavior, biochemical indicators in the colon and brain tissue, and the gut microbiota composition and short-chain fatty acid (SCFA) levels in the gut were investigated. Compared to the treatment in the model group, CCFM8661 treatment effectively reduced oxidative stress in the brain, improved behavioral performance, increased intestinal barrier integrity, and alleviated histopathological changes in mice. Moreover, CCFM8661 increased the gut microbiota diversity and abundance of Ruminococcus and Lachnospiraceae and reduced the abundance of pro-inflammatory Turicibacter spp. Additionally, the production of SCFAs was significantly increased by L. plantarum CCFM8661. Our results suggest that CCFM8661 is effective against acute B[a]P-induced toxicity in mice and that it can be considered as an effective and easy dietary intervention against B[a]P toxicity.

Motor dysfunction is a hallmark of Parkinson's disease (PD); however, non-motor symptoms such as gastrointestinal dysfunction often arise prior to motor symptoms. Alterations in the gut microbiome have been proposed as the earliest event in PD pathogenesis. PD symptoms often demonstrate sex differences. Glutamatergic neurotransmission has long been linked to PD pathology. Metabotropic glutamate receptors (mGlu), a family of G protein-coupled receptors, are divided into three groups, with group III mGlu receptors mainly localized presynaptically where they can inhibit glutamate release in the CNS as well as in the gut. Additionally, the gut microbiome can communicate with the CNS via the gut-brain axis. Here, we assessed whether deficiency of metabotropic glutamate receptor 8 (mGlu8), group III mGlu, modulates the effects of the neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), on behavioral and cognitive performance in female and male mice. We studied whether these effects are associated with changes in striatal tyrosine hydroxylase (TH) levels and the gut microbiome. Two-week sub-chronic MPTP increased activity of female and male wild-type (WT) and mGlu8 knockout (KO) mice in the open field. MPTP also showed genotype- and sex-dependent effects. MPTP increased the time WT, but not KO, females and males spent exploring objects. In WT mice, MPTP improved sensorimotor function in males but impaired it in females. Further, MPTP impaired cued fear memory in WT, but not KO, male mice. MPTP reduced striatal TH levels in WT and KO mice but these effects were only pronounced in males. MPTP treatment and genotype affected the diversity of the gut microbiome. In addition, there were significant associations between microbiome α-diversity and sensorimotor performance, as well as microbiome composition and fear learning. These results indicate that specific taxa may directly affect motor and fear learning or that the same physiological effects that enhance both forms of learning also alter diversity of the gut microbiome. MPTP's effect on motor and cognitive performance may then be, at least in part, be mediated by the gut microbiome. These data also support mGlu8 as a novel therapeutic target for PD and highlight the importance of including both sexes in preclinical studies.