Severe premenstrual symptoms (PS) have been linked to emotional eating (EE) and binge eating. The purpose of this study was to examine whether EE, dietary restraint, and/or food addiction (FA) mediated the relationship between PS and the odds of screening positive for an eating disorder. The role of irrational beliefs (IB), which can lead to dysfunctional emotional and/or behavioral responses, was examined as a potential moderator. 600 women (mean age = 26.6 ± 0.2 years) who had menstruated at least twice in the previous year completed online questionnaires. Methods to screen out automated ("bot") responses were employed. Through purposive sampling, 25 % of the sample identified primarily as Asian, Black, Latina/Hispanic, White. No significant racial/ethnic identity differences were found for PS or any psychological measures. Results indicated that there was a positive relationship between PS and IB, depression, EE, external eating, dietary restraint, FA, and the odds of screening positive for an eating disorder. PS was weakly negatively associated with age but not with body mass index. EE and FA mediated the positive relationship between PS and the odds of having a positive screen for an eating disorder (controlling for depression). The association between PS and FA was stronger at higher levels of IB. IB also moderated the association between EE and the odds of having a positive screen for an eating disorder. Overall, the results indicate that those who have more severe PS engage in more uncontrolled eating in the form of EE and FA (particularly at higher IB levels for the latter) which are associated with higher odds of having a positive screen for an eating disorder.

The gut microbiota plays a pivotal role in the pathogeneses of Alzheimer's disease (AD), influencing neuroinflammation and disease progression. Understanding the role of the gut microbiota in this process is critical for uncovering novel therapeutic avenues and deepening insights into AD pathogenesis. Nevertheless, the specific gut microbiota alterations under pathogenetic stress in AD remain unclear. In this study, immunofluorescence was performed to detect β-amyloid (Aβ) deposition, hyperphosphorylated tau proteins (P-tau), and the activation of microglia in the brains of APPswe/PSEN1dE9 transgenic (APP/PS1) mice and C57BL/6 J wild-type (WT) mice. Congo red staining and thioflavin-S staining were used to detect Aβ plaques accumulation in the hippocampus and cortex. 16S rRNA sequencing was used to elucidated the bacteria changes between the APP/PS1 and WT mice. The results of immunofluorescence and pathological stainings exhibited that the APP/PS1 mice showed significant increase of Aβ deposition and P-tau, and greater activation of microglia in the hippocampus and cortex, compared with WT mice. 16S rRNA sequencing identified increased abundance of Muribaculaceae, Ligilactobacillus, Dubosiella, Limosilactobacillus, Alistipes, Lactobacillus, and Enterorhabdus, and decreased abundance of Lachnospiraceae_NK4A136_group, Clostridia_UCG-014, and Lachnospiraceae _UCG-006 in APP/PS1 mice, revealing distinct hub bacteria with AD under pathogenetic pressure.

Gonadotropin-inhibitory hormone (GnIH) is a neuropeptide pivotal in reproduction, which has recently been implicated in appetite-driven obesity among mammals. Yet, its functions in metabolic homeostasis and sex-specific lipid regulation remain largely underexplored. In this study, we found that GnIH administration initially caused weight gain and increased food intake in both male and female rats within 2 weeks. However, at week 6, male rats receiving high-dose (10 μg/100 μL) GnIH gained weight, while female rats receiving low-dose (1 μg/100 μL) GnIH lost weight. In addition, high-dose GnIH increased organ weight and glucose levels in male rats, while reduced white adipose tissues (WAT) and raised triglycerides in females. Histologically, GnIH dose-dependently increased hepatic lipid vacuoles in male rats, while female rats exhibited nuclear swelling and cellular damage. Mechanistically, GnIH exhibited sex-specific effects on hepatic lipid metabolism. In male rats, it enhanced lipogenesis through the upregulation of microsomal triglyceride transfer protein (MTP) and CCAAT/enhancer binding protein (c/EBP), while inhibiting lipolysis via reduced peroxisome proliferator-activated receptor γ (PPARγ), Adiponectin (ADPN), and AMP-activated protein kinase α (AMPKα) phosphorylation. Conversely, female rats treated with GnIH displayed diminished MTP expression alongside elevated lipolysis. In WAT, GnIH promoted lipogenesis in male rats, evidenced by increased fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), and c/EBP levels. However, it suppressed this process in females even though lipolytic markers such as ADPN and PPARγ were elevated in both sexes. Overall, GnIH exerts distinct sex-specific effects on lipid metabolism, promoting anabolic pathways in males while triggering catabolic responses in females. These findings highlight the complex role of GnIH in energy homeostasis and underscore its potential as a target for sex-specific therapeutic interventions in metabolic disorders.

It is known that Total cholesterol (TC) and Triglycerides (TG) levels can increase by up to 50 % during late pregnancy, conserving glucose and amino acids for the fetus while enabling the mother to derive energy from elevated lipids. However, the impact of aerobic exercise on lipid levels in non-dyslipidemic pregnant women remains unclear. To compare the effects of a structured aerobic exercise program versus usual physical activity on maternal lipid levels in pregnant women during their third trimester.

Cognitive impairment is characterized by reduced cognitive abilities in one or more areas such as language, memory, and reasoning. It is a common problem in various neurological diseases and the aging process, seriously affecting people's quality of life and overall health. Fibroblast growth factor 21 (FGF21), a hormone regulating glucose/lipid metabolism and energy homeostasis, exhibits neuroprotective properties. To investigate the impact and mechanism of endogenous deletion of FGF21 on cognitive function, FGF21 knockout mice and wild-type mice were used. Different behavioral paradigms were used to study the effects of FGF21 on the cognitive behavior of mice. Morphological changes were observed by Nissl and HE staining, and RNA sequencing was performed to explore potential links between FGF21 and cognitive impairment-related diseases. Behavioral and morphological analyses demonstrated that FGF21 knockout mice exhibited deficits in learning and memory, anxiety-like behaviors, and neuronal degeneration. Transcriptomic profiling revealed that FGF21 deficiency altered multiple neuroprotective processes, including metabolism and synaptic transmission. These deficits may be mediated through downregulation of the PPAR signaling pathway, thereby affecting cognitive function. This research indicates that endogenous FGF21 deletion disrupts basic cognitive and emotional behaviors of mice, which may accelerate the development of cognitive impairment-related diseases (including Alzheimer's disease, vascular cognitive impairment, frontotemporal dementia, dementia with Lewy bodies), and suggests FGF21 as a potential therapeutic target for these diseases.

Gut microbiota has been implicated in influencing various health-related behaviors, including physical activity. This study aimed to investigate the causal relationship between gut microbiota and physical activity in individuals of European ancestry.

Making decisions is a vital part of life for all beings. Impaired decision-making can lead to various neuropsychiatric diseases and problems, such as drug addiction and gambling. Therefore, it is essential to identify the causes of these disorders and seek effective treatments. Rodents play a key role in studying the brain's neural mechanisms of emotional and cognitive control.

Circadian rhythms regulate fundamental physiological and behavioral functions, yet are increasingly disrupted by contemporary environmental stressors such as rotating shift work and social isolation. Although each disruptor independently compromises circadian homeostasis, their interactive effects remain insufficiently characterized. Given the role of social cues as non-photic zeitgebers, we investigated whether social isolation exacerbates behavioral and molecular circadian disruption induced by repeated light-dark phase shifts, and whether social interaction confers resilience. Male AKR mice were assigned to six experimental groups defined by housing condition (grouped or isolated) and lighting regimen, comprising a stable 12-hour light-dark cycle, successive delays, or successive advances, with 8-hour phase shifts imposed every fourth day across six cycles. Locomotor activity was assessed using wheel-running, and transcript levels of Per1, Cry1, Bmal1, and Clock were quantified in the prefrontal cortex and hippocampus by RT-qPCR. Both phase delay and advance protocols disrupted behavioral rhythms and dampened circadian amplitude, with successive advances producing more pronounced desynchronization than delays. These effects were significantly amplified by social isolation, which led to marked rhythm fragmentation, phase misalignment, and delayed re-entrainment. At the molecular level, isolated mice displayed downregulation of Per1 and Cry1, and upregulation of Bmal1, most prominently in the hippocampus. Notably, group housing preserved circadian stability across behavioral and transcriptional domains, implicating social cues as modulators of internal synchrony. These findings demonstrate that social isolation potentiates the circadian desynchrony elicited by rotating shift paradigms and identify social interaction as a non-photic signal capable of partially restoring rhythm coherence and clock gene expression.

Cognitive deficits are common in primates, particularly in memory and emotional processes. Rhesus monkey (Macaca mulatta), widely used in cognitive and behavioral research, are central to memory studies. The relationship between recognition memory performance and pupillary dynamics in rhesus monkeys remains underexplored. This study investigated pupil dynamics during recognition memory tasks and their physiological correlates in five sexually mature male rhesus monkeys. We measured pupil diameter and oscillatory features during tasks and analyzed the relationship between behavioral performance and physiological indicators. We found that the average correct response rate exceeded the random success level, and reaction times were significantly shorter during successful recognition than failures, highlighting their cognitive efficiency. During recognition of familiar scenes, average pupil diameter increased, while maximum change in pupil size decreased, indicating reduced cognitive load. Both the frequency and amplitude of pupillary oscillation were lower during successful trials, reflecting decreased cognitive conflict and effective processing. This change reflects a decrease in cognitive conflict and suggests that information processing was more effective. The absolute value of the pupil peak slop decreased during successful recognition, indicating more stable cognitive state. These results support that pupillary dynamics can serve as physiological markers of cognitive effort in rhesus monkeys. Future studies should investigate how stimulus characteristics influence recognition and incorporate measures, such as intracranial EEG and fMRI, to enhance our understanding of their neural mechanisms. This research supports the rhesus monkey model in cognitive neuroscience and contributes to understanding primate cognition and its physiological foundations, with implications for clinical and translational research.

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects 38% of adults globally and has been identified as a significant and increasing contributor to global health and economic burdens. Obesity is significantly associated with MASLD. Eating behaviours may represent an underexplored shared risk factor for these adverse physiological outcomes. Here, we tested a novel mediation model and hypothesised that emotional and uncontrolled eating would be positively associated with liver fibrosis (kilopascals; kPa) and steatosis (controlled attenuation parameter; CAP) via body mass index. 129 UK clinical patients undergoing a fibroscan, completed validated questionnaires on eating behaviours, snack and alcohol consumption. We confirmed an indirect relationship between emotional eating and steatosis mediated by BMI (P=0.002), but not for liver fibrosis (P=0.1). A direct relationship between unhealthy snack consumption and steatosis (P=0.04) was also shown. We failed to show any direct or indirect relationships between uncontrolled eating and either fibrosis or steatosis. In an exploratory analysis, we also used separate logistic regressions to examine whether emotional eating and BMI were predictive of MASLD, alcohol related liver disease (ArLD) and other causes of deranged liver function tests (binary status). MASLD status was significantly positively predicted by both emotional eating (P=0.003) and BMI (P=0.024). By contrast, lower emotional eating scores predicted a higher likelihood that someone would have ArLD (P=0.035) and emotional eating scores were not a significant predictor of other causes of deranged liver function ('other group', P=0.398). Our findings indicate that psychological therapy focusing on emotional eating may represent a fruitful intervention target for MASLD.

Prolonged exposure to vibration and noisy environments has been shown to contribute to the development of anxiety disorders. Pharmacological interventions are typically not administered during the early stages, which may lead to the uncontrolled progression of anxiety symptoms. In this study, we found that daily exposure to low-frequency vibration for 1 hour significantly increased anxiety-like behavior in zebrafish, with the most pronounced effects observed at 100 Hz. Behavioral analyses demonstrated that exposure to blue light significantly alleviated vibration-induced anxiety. Further physiological measurements showed that vibration and noise exposure markedly elevated cortisol and norepinephrine levels in zebrafish. In contrast, prolonged exposure to 455 nm blue light significantly increased serotonin levels and decreased norepinephrine concentrations, thereby counteracting the anxiety-like state. These findings suggest that 455 nm blue light may serve as an effective, simple, adaptable, and relatively safe strategy for preventing or alleviating anxiety induced by long-term exposure to vibration and noise.

Mice exposed to intermittent social defeat (ISD) stress in late adolescence exhibit short-term anxiety- and depression-like behaviours and demonstrate greater sensitivity to the rewarding effects of cocaine in adulthood. Furthermore, the development of depression-like symptoms predicts subsequent enhanced vulnerability to cocaine reward. The aim of this study was to investigate whether ketamine, a non-competitive glutamate N-methyl-D-aspartate (NMDA) receptor antagonist with antidepressant properties, could prevent the short-term effects of ISD on anxiety- and depression-like behaviours and the long-term effects of ISD on the cocaine-induced conditioned place preference. Four groups of late adolescent C57BL/6 male mice were used. One non-stressed group (control) and three ISD-exposed groups treated with ketamine (0, 10 or 30 mg/kg). After the last defeat episode, the mice were tested in the elevated plus maze, social interaction, splash and tail suspension tests. Three weeks later, the mice were conditioned with cocaine (1 mg/kg). Stressed mice showed anxiety, displayed a deficit in social interaction, spent less time immobile in the tail suspension test and developed a cocaine place preference. Ketamine attenuated ISD-induced anxiety, social avoidance and cocaine reward potentiation. These results support the usefulness of ketamine in preventing some effects of social stress.

Chronic pain profoundly impacts mental health, and the social environment significantly modulates pain perception and emotional states. Recognizing the influence of biological sex on pain modulation, basic pain research increasingly investigates sex differences. The hyperalgesic priming protocol effectively models the neuroplastic mechanisms underlying the transition from acute to chronic pain in male and female rodents. Furthermore, accumulating evidence implicates specific hormones, including oxytocin, vasopressin, and corticosterone, in the pathophysiology of pain. This study aimed to determine the interactive influence of sex and social isolation on pain-related behaviors and plasma levels of oxytocin, vasopressin, and corticosterone in mice subjected to hyperalgesic priming. Two experiments were conducted using adult male and female mice (60-63 postnatal days). Experiment 1 assessed mechanical hypersensitivity, facial expression, and anxiety- and depression-like behaviors. In Experiment 2, following a period of social isolation, mice were euthanized, and blood samples were collected via cardiac puncture for plasma hormone analysis. Our results revealed that social isolation impaired recovery from mechanical hypersensitivity and increased facial expressions of pain, specifically in female mice. Independent of sex and hyperalgesic priming, isolation produced heightened anxiety- and depression-like behaviors. Hormonal analyses demonstrated sex-specific effects of isolation. Plasma oxytocin levels decreased upon isolation in both male and female mice. Curiously, primed isolated males showed a recovery of oxytocin levels similar to naïve mice, whereas primed isolated females maintained significantly lower oxytocin levels. Social isolation, coupled with hyperalgesic priming, also decreased vasopressin levels in females. While males displayed higher baseline vasopressin levels, isolation and/or hyperalgesic priming led to a reduction in their plasma vasopressin compared to naïve groups. Curiously, social isolation decreased of corticosterone levels in both males and females. In conclusion, our findings demonstrate that social isolation differentially modulates behavioral and hormonal responses to hyperalgesic priming in a sex-dependent manner, highlighting the complex interplay between social environment, sex, and pain chronification.

Reduced social interactions negatively impact adolescents. However, underlying mechanisms of social isolation (SI) stress and interventions remain unclear. Therefore, we investigated the effects of an exercise intervention on SI stress-induced behavioral abnormalities and the underlying mechanisms. We used male mice: Ctrl (N = 32), SI (N = 33), SI + voluntary wheel running (VWR) (N = 14), and SI + lurasidone (N = 7), and assessed emotion, anxiety, depression, social interactions, and cognitive functions using behavioral tests. In addition, we measured plasma corticosterone and performed immunohistochemical staining for ΔFosB, a marker of repeatedly activated neurons, to assess the stress response and identify brain regions associated with SI stress. Interventions lasted for 3 weeks, and behavioral assessments were initiated 2 weeks after the intervention initiation. The SI mice exhibited significant hyperactivity, reduced self-care and motivation, impaired recognition, excessive sniffing toward strangers and aggressive but avoidant social behaviors. We observed significant improvements in recognition impairments and excessive sniffing behavior after VWR. In addition, there was a trend toward reduced flight behavior. However, VWR did not induce a significant change in the number of attacks and the ΔFosB expression in the ventral tegmental area (VTA). Lurasidone administration significantly reduced sniffing and aggressive behavior and increased ΔFosB-positive cells in VTA. Our results suggest that, while VWR and lurasidone both mitigate some aspects of SI-induced behavioral deficits, they likely act independent or only partially overlapping neurobiological pathways. Thus, VWR may act through broader neuroadaptive processes, potentially involving serotonergic modulation, neurotrophic factors, or stress regulatory circuits.

Social stress is a critical risk factor for depression, impacting millions of individuals globally. This study investigated the behavioral and cardiovascular effects of a chronic social defeat model in male Wistar rats, focusing on identifying cardiovascular markers associated with depressive-like phenotypes. Male Wistar rats were subjected to a 7-day resident-intruder social defeat paradigm, followed by behavioral assessments (open field test, novel object recognition test, and forced swimming test) and cardiovascular recordings (mean arterial pressure, heart rate, and heart rate variability). Socially defeated rats exhibited increased immobility in the forced swimming test, indicative of depressive-like behavior. While locomotion and anxiety-like behaviors in the open field were unchanged, both defeated and isolated groups showed impaired short-term memory. Cardiovascular analysis revealed that defeated animals had a significantly elevated basal heart rate and a reduced high-frequency (HF) component of heart rate variability, suggesting decreased parasympathetic activity. No significant changes were observed in blood pressure or baroreflex sensitivity across groups. Correlation analysis highlighted a strong positive correlation between short-term memory and HF power in the control group, a relationship that was disrupted in both isolated and defeated groups. These findings suggest that chronic social defeat induces specific behavioral alterations, such as increased immobility and impaired memory, coupled with cardiovascular dysregulation characterized by basal tachycardia and reduced parasympathetic tone. This study underscores the potential of heart rate variability as a physiological marker for stress-induced depressive phenotypes and emphasizes the association between behavioral and cardiovascular systems under social stress.

Observing others' suffering and being observed during stress may differentially influence behavioral patterns and brain functions such as learning, memory, and mood. This study investigated the effects of prolonged social equality and inequality on spatial learning and memory deficits, as well as obsessive-compulsive disorder (OCD)-like behaviors in rats.

Aging and stress are major risk factors for impaired neural plasticity and maladaptive behavior, and their interaction is shaped by genetic predispositions. We examined how aging and prior stress affect behavior, molecular markers of apoptosis and neuroplasticity, neuroinflammation, and the gut microbiota in rat strains selectively bred for contrasting nervous system excitability: high-threshold (HT, low-excitability) and low-threshold (LT, high-excitability). Adult (5-month-old) and middle-aged (14-month-old) males were studied with or without chronic emotional-pain stress in adulthood. Aging induced strain-specific behavioral and molecular profiles: in HT rats, reduced locomotion and increased freezing in the open field were accompanied by a lower amygdalar Bcl2/Bax ratio and higher Map2 expression, whereas LT rats presented fewer behavioral changes but increased Bax. Prior stress produced long-term, opposite effects: in HT rats it changed the gut microbiota composition, attenuated anxiety-like behavior and decreased amygdalar Bax, whereas in LT rats it increased anxiety with minor microbiota alterations. Overall, aging and stress produced distinct, strain-dependent signatures across behavior, gene expression, and microbiota composition. HT rats exhibit plasticity and microbiota remodeling consistent with resilience, whereas LT rats show limited behavioral flexibility and microbiota stability, a pattern potentially modeling vulnerability to stress-related aging. The use of contrasting excitability rat strains underscores the importance of genetic background for understanding individual variability in resilience and vulnerability to aging and stress.

Rodent maternal separation (MS) models have been widely used to investigate the effects of early life stress (ELS) on neural development. However, the presence of sex differences in timing-dependent specificity has yet to be confirmed. The objective of this was to elucidate the timing-dependent specificity of MS in female rats and compare it with that previously reported using male rats. Female Long-Evans rat pups were randomly divided into three groups: early MS (Early-MS: postnatal day [PND] 1‒9); late MS (Late-MS: PND 10‒20); and control (CTL). All groups were evaluated for psychiatric disorder-like behaviours using several behavioural tests, and Drebrin and Golgi-Cox staining were performed to assess changes in dendritic spines immunohistochemically. Both Early- and Late-MS groups exhibited learned helplessness-like behaviour, as shown by increased immobility in the forced swim test. However, only the Early-MS group demonstrated reduced active coping behaviour, as measured by climbing. Only the Late-MS group exhibited obsessive-compulsive-like behaviour, as reflected by increased marble burying. Neuroanatomically, spine density in the hippocampal CA1 region increased in the Early-MS group in the basal dendrites, whereas it decreased in the Late-MS group in the apical dendrites. These behavioural and neuroanatomical alterations suggest that ELS affects female rats depending on the timing of exposure. These patterns differ partially from those reported in males, contributing to our understanding of sex-specific mechanisms underlying the impact of ELS on brain plasticity and behaviour.

Heart rate variability (HRV) coherence near 0.1 Hz has been proposed as a sensitive marker of autonomic regulation and stress resilience. Slow-tempo music has been associated with enhanced parasympathetic activity, and the stochastic resonance framework suggests that controlled noise may optimize weak physiological signals. This study examined whether embedding auditory noise into slow-tempo music could enhance HRV coherence.

Taste and olfactory dysfunctions significantly impair flavor perception, reduce eating pleasure, and affect emotional well-being. Existing interventions primarily focus on restoring sensory function, with limited attention to the potential of sound as a cross-modal pathway for flavor reconstruction. As a multimodal stimulus, food-related sound shows compensatory potential in evoking flavor associations and triggering emotional memory. This study investigates whether real-world food sounds can effectively elicit flavor-related associations and memories, and aims to establish a symbolic mapping model between auditory cues and flavor perception. Forty participants (including 20 clinically diagnosed with taste or smell disorders) were exposed to 15 real food sound clips. They rated each clip across dimensions including flavor association strength, emotional arousal, image clarity, and memory activation. Open-ended responses were also collected for semantic analysis. Results showed that participants with sensory impairments scored significantly higher across all perceptual dimensions compared to controls (p< 0.01), indicating a stronger compensatory response to sound. Specific sounds, such as stir-frying and hotpot boiling, exhibited particularly strong evocative effects. Semantic analysis revealed that auditory associations were closely linked to specific foods and culturally familiar scenarios, highlighting the emotional embeddedness of these cues. This study suggests that real food sounds may serve as effective substitutes for flavor perception, offering a context-rich and emotionally resonant compensatory pathway. The findings provide theoretical support for the development of "sound-flavor training sets," with potential applications in inclusive eating design and sensory rehabilitation.

Recent studies have found that aerobic exercise improves sensorimotor adaptation. For instance, adaptation to an abruptly-presented 45° visuomotor rotation is improved if preceded by an acute bout of exercise. Still, it is known that adaptation is driven both by an explicit (cognitive) process as well as an implicit process. Given that exercise is known to benefit cognitive function, it remains an open question whether exercise selectively improves implicit adaptation. Here we tested this hypothesis, using a paradigm known to isolate implicit adaptation. In a within-participant design, participants (n = 26) had to reach toward a target, while being pseudo randomly exposed to CW or CCW 30° visuomotor rotations. Implicit adaptation was assessed by the involuntary bias in hand direction that follows a rotated trial, called post rotation bias (PRB). On separate days, participants performed 180 trials before (PRE) and after (POST) a period of exercise, or a period of rest. The exercise bout consisted of 20 min of moderate intensity cycling, which has previously been shown to benefit performance in cognitive and adaptation tasks. Results revealed robust PRBs in both conditions and phases, but critically there was an interaction: the magnitude of PRBs was significantly attenuated following rest, but not following exercise. Further analyses revealed that movements were produced significantly faster following exercise, confirming that exercise impacted motor vigor. By showing that an acute bout of exercise prevents the attenuation of implicit adaptation that is observed following rest, these results indirectly suggest that exercise has a positive effect on implicit adaptation.