Behavioral and Brain Functions最新文献

{"title":"FTO (fat-mass and obesity-associated protein) deficiency aggravates age-dependent depression-like behaviors and cognitive impairment.","authors":"Mengdie Li, Yating Yang, Tangcong Chen, Yueyang Luo, Yingqian Zhang, Huanzhong Liu, Michael Maes","doi":"10.1186/s12993-025-00280-3","DOIUrl":"10.1186/s12993-025-00280-3","url":null,"abstract":"<p><strong>Background: </strong>The demethylase fat mass and obesity-related associated protein (FTO) is strongly associated with depression. Aging is a risk factor for synaptic plasticity damage in the brain and leads to neurocognitive dysfunctions. FTO-dependent m6A modification plays an important role in neurodevelopment and cognitive function. However, whether FTO is associated with susceptibility to depression in different age groups remains unknown.</p><p><strong>Methods: </strong>We subjected 3-and 12-month-old C57BL/6J male mice to chronic unpredictable mild stress (CUMS) for 6 weeks, of which 3 weeks were used for hippocampal injection of FTO knockdown adeno-associated virus 9 shRNA (FTO-KD AAV9). Finally, 36 male mice in each 3-month-old and 12-month-old groups were divided into three groups (n = 12): Sham, CUMS, and FTO-KD. After 6 weeks, we assessed behavioral deficits (depressive and anxiety-like behaviors and cognitive impairment) by behavioral tests and hippocampal neuronal damage (dendritic spine density, neuronal atrophy, and expression of proteins associated with synaptic plasticity) by molecular biochemical experiments.</p><p><strong>Results: </strong>The results showed that 12-month-old C57BL/6J mice were more likely to develop depression-like behavior and spatial learning and memory impairment induced by CUMS than 3-month-old mice. Chronic stress-induced depression-like behavior and cognitive impairment worsened after the FTO-KD intervention. In the hippocampus of 3- and 12-month-old mice, CUMS induced the downregulation of FTO, nerve growth factor (NGF), reelin, and synaptic plasticity-related proteins. It also caused abnormal brain-derived neurotrophic factor (BDNF)- the tropomyosin-related kinase B (TrkB) signaling, reduced density of dendritic spines, and an increased number of neuronal pyknotic nuclei, leading to neuronal disarray, which was more significant in 12-month-old animals. FTO deficiency accelerated neuronal damage in the hippocampus of 12-month-old CUMS mice.</p><p><strong>Conclusions: </strong>This study provides rodent evidence that FTO deficiency may increase the susceptibility to depression in older adults by impairing hippocampal neuronal function and neuronal synaptic plasticity in an age-dependent manner. This suggests that the development of FTO activators may be an effective treatment for depression in older adults.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"18"},"PeriodicalIF":4.7,"publicationDate":"2025-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12167586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144301115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The gut microbiome and metabolomic alterations underlying colitis-induced encephalopathy in mice: mechanistic insight.","authors":"Aimin Cai, Dingchao Shen, Qiushuang Xiong, Shize Li, Chenyu Qiu, Lele Li, Zhiwei Chen, Xinlu Lin, Qing Yao, Youting Zhang, Ruijie Chen, Longfa Kou","doi":"10.1186/s12993-025-00283-0","DOIUrl":"10.1186/s12993-025-00283-0","url":null,"abstract":"<p><strong>Background: </strong>In addition to classical gastrointestinal symptoms, patients with inflammatory bowel disease (IBD) often exhibit neurological manifestations, such as mood disorders and cognitive dysfunctions, which are frequently overlooked. However, the potential pathogenesis of IBD-related encephalopathy remains unclear, and few studies have explored the influence of interactions between the gut microbiota and the host gut-brain metabolome on the emergence of brain diseases in IBD mice. In this study, we conducted a comprehensive analysis of gut microbiome and metabolome alterations in dextran sulfate sodium salt (DSS)-induced IBD mice compared to control mice, focusing on colonic contents and hippocampal tissue. Our aim was to investigate the putative mechanisms underlying the microbiota-gut-brain axis in IBD-induced encephalopathy.</p><p><strong>Results: </strong>IBD mice showed depression-like behaviors and cognitive deficits. Metabolic profiling revealed distinct patterns in the colonic contents and hippocampal areas of IBD mice, marked by decreased energy metabolism, amino acid levels, short-chain fatty acids (SCFAs), and choline metabolism. These metabolic changes were negatively associated with the abundance of Bacteroides, Turicibacter, Ruminococcus, and Akkermansia, while Desulfovibrio and Lactobacillus showed positive correlations.</p><p><strong>Conclusions: </strong>This study identifies unique microbial and gut-brain metabolite signatures associated with DSS-induced changes and offers new metabolic insights into the microbiota-gut-brain axis in IBD-related brain disorders. It highlights the potential of targeting gut microbiota to modulate host metabolism as a therapeutic approach for IBD-related neurological complications.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"17"},"PeriodicalIF":4.7,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160427/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144282314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined enriched environment and fluoxetine enhance myelin protein expression in the prefrontal cortex of a chronic unpredictable stress depression model.","authors":"Jingyang Gu, Cong Liu, Yan Li, Laipeng Feng, Mengjun Geng, Jiao Dong, Jinhong Han, Liqin Zhao, Qiujing Shao, Hui-Ying Wang, Chang-Hong Wang","doi":"10.1186/s12993-025-00282-1","DOIUrl":"10.1186/s12993-025-00282-1","url":null,"abstract":"<p><strong>Background: </strong>The primary protein components of white matter include myelin basic protein (MBP) and 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP). Alterations in their expression are significantly implicated in depression. This study investigated changes in MBP and CNP expression associated with depressive-like behaviors induced by chronic unpredictable stress (CUS) and evaluated therapeutic interventions using fluoxetine (FLU), an enriched environment (EE), or their combination.</p><p><strong>Methods: </strong>Male Sprague Dawley rats were randomly assigned to a control group and four CUS-exposed groups undergoing 6 weeks of stress. During the final 3 weeks of CUS, rats received daily fluoxetine (CUS + FLU group), were housed in EE (CUS + EE group), or received combined EE and fluoxetine (CUS + FLU + EE group). Depression-like behaviors were assessed through sucrose preference, forced swimming, and open field tests after CUS completion and at the end of weeks 4-6. Protein and mRNA expression levels of MBP and CNP in the prefrontal cortex were quantified via immunohistochemistry, western blot, and qRT-PCR.</p><p><strong>Results: </strong>Three weeks following CUS exposure, rats demonstrated significant depression-like behavioral phenotypes. By the fifth week, these behavioral deficits were ameliorated in the CUS + FLU + EE, whereas the CUS + FLU and CUS + EE groups exhibited comparable behavioral recovery by week 6. Parallel molecular analyses revealed diminished protein and mRNA expression levels of MBP and CNP in the prefrontal cortex of CUS-exposed animals, accompanied by a pronounced elevation in IL-1β expression. Therapeutic interventions with FLU, EE, or their combination significantly attenuated these CUS-induced molecular alterations.</p><p><strong>Conclusions: </strong>The antidepressant effects correlated with restored MBP, CNP, and IL-1β expression levels, suggesting that MBP/CNP deficiencies in depression may involve IL-1β elevation. In particular, combined enriched environment and fluoxetine accelerated behavioral recovery.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"16"},"PeriodicalIF":4.7,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12160429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144274128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling genetic risk contributions to nonverbal status in autism spectrum disorder probands.","authors":"Huan Liu, Shenghan Wang, Binbin Cao, Jijun Zhu, Zhifang Huang, Pan Li, Shunjie Zhang, Xian Liu, Jing Yu, Zhongting Huang, Linzhuo Lv, Fuqiang Cai, Weixin Liu, Zhijian Song, Yuxin Liu, Tao Pang, Suhua Chang, Ying Chen, Junfang Chen, Wen-Xiong Chen","doi":"10.1186/s12993-025-00278-x","DOIUrl":"10.1186/s12993-025-00278-x","url":null,"abstract":"<p><p>Autism spectrum disorder (ASD) presents a wide range of cognitive and language impairments. In this study, we investigated the genetic basis of non-verbal status in ASD using a comprehensive genomic approach. We identified a novel common variant, rs1944180 in CNTN5, significantly associated with non-verbal status through family-based Transmission Disequilibrium Testing. Polygenic risk score (PRS) analysis further showed that higher ASD PRS was significantly linked to non-verbal status (p = 0.034), specific to ASD and not related to other conditions such as bipolar disorder, schizophrenia and three language-related traits. Using structural equation modeling (SEM), we found two causal SNPs, rs1247761 located in KCNMA1 and rs2524290 in RAB3IL1, linking ASD with language traits. The model indicated a unidirectional effect, with ASD driving language impairments. Additionally, de novo mutations (DNMs) were found to be related with ASD and interaction between common variants and DNMs significantly impacted non-verbal status (p = 0.038). Our findings also identified 5 high-risk ASD genes, and DNMs were enriched in glycosylation-related pathways. These results offer new insights into the genetic mechanisms underlying language deficits in ASD.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"15"},"PeriodicalIF":4.7,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144246214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurodegeneration models in Parkinson's disease: cellular and molecular paths to neuron death.","authors":"Diana D Álvarez-Luquín, Rubén R González-Fernández, Martin E Torres-Velasco, Eduardo Ichikawa-Escamilla, Asiel Arce-Sillas, Eduardo Martínez-Martínez, Clara L Miranda-Narvaez, Juan F Rodríguez-Ramírez, Laura Adalid-Peralta","doi":"10.1186/s12993-025-00279-w","DOIUrl":"10.1186/s12993-025-00279-w","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects dopaminergic neurons in the substantia nigra pars compacta. It is a complex disease that is strongly influenced by environmental and genetic factors. While the exact causes of PD are not well understood, research on the effects of toxic substances that induce neuronal death has shed some light on the etiology of the disease. In addition, studies have implicated protein aggregation and impaired mitochondrial, endoplasmic reticulum (ER), proteasome, and/or lysosomal function in the pathogenesis of PD. This review focuses on the alterations in intraneuronal organelles and the role of toxic agents that lead to organelle damage and neurodegeneration that characterize PD. We describe in vivo and in vitro models that have been used to elucidate the factors that lead to the death of dopaminergic neurons and summarize the molecular mechanisms that may underlie the changes that promote neurodegeneration. A deeper understanding of the mechanisms of neuronal death may help us to develop new therapies and interventions to delay or prevent the progression of PD.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"14"},"PeriodicalIF":4.7,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125839/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144191428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential neuronal functions of LNX1 and LNX2 revealed by behavioural analysis in single and double knockout mice.","authors":"Laura Cioccarelli, Joan A Lenihan, Leah G Erwin, Paul W Young","doi":"10.1186/s12993-025-00276-z","DOIUrl":"https://doi.org/10.1186/s12993-025-00276-z","url":null,"abstract":"<p><strong>Background: </strong>Ligand of NUMB protein-X 1 (LNX1) and LNX2 proteins are closely related PDZ domain-containing E3 ubiquitin ligases that interact with and potentially modulate numerous synaptic and neurodevelopmentally important proteins. While both LNX1 and LNX2 are expressed in neurons, it is noteworthy that neuronal LNX1 isoforms lack the catalytic domain responsible for ubiquitination of substrates. Thus, the shared interaction partners of LNX1 and LNX2 might be differentially regulated by these proteins, with LNX1 acting as a stabilizing scaffold while LNX2 may promote their ubiquitination and degradation. Despite the identification of many LNX interacting proteins and substrates, our understanding of the distinct in vivo functions of LNX1 and LNX2 remains very incomplete.</p><p><strong>Results: </strong>We previously reported that mice lacking both LNX1 in the central nervous system and LNX2 globally exhibit decreased anxiety-related behaviour. Here we significantly extend this work by examining anxiety-related and risk-taking behaviours in Lnx1^-/- and Lnx2^-/- single knockout animals for the first time and by analysing previously unexplored aspects of behaviour in both single and double knockout animals. While the absence of both LNX1 and LNX2 contributes to the decreased anxiety-related behaviour of double knockout animals in the open field and elevated plus maze tests, the elimination of LNX2 plays a more prominent role in altered behaviour in the dark-light emergence test and wire beam bridge risk-taking paradigms. By contrast, Lnx knockout mice of all genotypes were indistinguishable from wildtype animals in the marble burying, stress-induced hyperthermia and novel object recognition tests. Analysis of the ultrasonic vocalizations of pups following maternal separation revealed significant differences in call properties and vocal repertoire for Lnx1^-/- and Lnx1^-/-;Lnx2^-/- double knockout animals. Finally, decreased body weight previously noted in double knockout animals could be attributed largely to Lnx1 gene knockout.</p><p><strong>Conclusions: </strong>These results identify specific roles of LNX1 and LNX2 proteins in modulating distinct aspects of anxiety and risk-taking behaviour and social communication in mice. They also reveal an unexpected role for neuronally expressed LNX1 isoforms in determining body weight. These novel insights into the differential neuronal functions of LNX1 and LNX2 proteins provide a foundation for mechanistic studies of these phenomena.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"13"},"PeriodicalIF":4.7,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12020136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imaging-validated correlates and implications of the pathophysiologic mechanisms of ageing-related cerebral large artery and small vessel diseases: a systematic review and meta-analysis.","authors":"Joseph A Ackah, Xuelong Li, Huixing Zeng, Xiangyan Chen","doi":"10.1186/s12993-025-00274-1","DOIUrl":"https://doi.org/10.1186/s12993-025-00274-1","url":null,"abstract":"<p><strong>Background: </strong>Cerebral large artery and small vessel diseases are considered substrates of neurological disorders. We explored how the mechanisms of neurovascular uncoupling, dysfunctional blood-brain-barrier (BBB), compromised glymphatic pathway, and impaired cerebrovascular reactivity (CVR) and autoregulation, identified through diverse neuroimaging techniques, impact cerebral large artery and small vessel diseases.</p><p><strong>Methods: </strong>Studies (1990-2024) that reported on neuroradiological findings on ageing-related cerebral large artery and small vessel diseases were reviewed. Fifty-two studies involving 23,693 participants explored the disease mechanisms, 9 studies (sample size = 3,729) of which compared metrics of cerebrovascular functions (CF) between participants with cerebral large artery and small vessel diseases (target group) and controls with no vascular disease. Measures of CF included CVR, cerebral blood flow (CBF), blood pressure and arterial stiffness.</p><p><strong>Results: </strong>The findings from 9 studies (sample size = 3,729, mean age = 60.2 ± 11.5 years), revealed negative effect sizes of CVR [SMD = - 1.86 (95% CI - 2.80, - 0.92)] and CBF [SMD = - 2.26 (95% CI - 4.16, - 0.35)], respectively indicating a reduction in cerebrovascular functions in the target group compared to their controls. Conversely, there were significant increases in the measures of blood pressure [SMD = 0.32 (95% CI 0.18, 0.46)] and arterial stiffness [SMD = 0.87 (95% CI 0.77, 0.98)], which signified poor cerebrovascular functions in the target group. In the combined model the overall average effect size was negative [SMD = - 0.81 (95% CI - 1.53 to - 0.08), p < 0.001]. Comparatively, this suggests that the negative impacts of CVR and CBF reductions significantly outweighed the effects of blood pressure and arterial stiffness, thereby predominantly shaping the overall model. Against their controls, trends of reduction in CF were observed exclusively among participants with cerebral large artery disease (SMD = - 2.09 [95% CI: - 3.57, - 0.62]), as well as those with small vessel diseases (SMD = - 0.85 [95% CI - 1.34, - 0.36]). We further delineated the underlying mechanisms and discussed their interconnectedness with cognitive impairments.</p><p><strong>Conclusion: </strong>In a vicious cycle, dysfunctional mechanisms in the glymphatic system, neurovascular unit, BBB, autoregulation, and reactivity play distinct roles that contribute to reduced CF and cognitive risk among individuals with cerebral large artery and/or small vessel diseases. Reduction in CVR and CBF points to reductions in CF, which is associated with increased risk of cognitive impairment among ageing populations ≥ 60 years.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"12"},"PeriodicalIF":4.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12016073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143968539","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute high-intensity noise exposure exacerbates anxiety-like behavior via neuroinflammation and blood brain barrier disruption of hippocampus in male rats.","authors":"Yifei Song, Haoyu Zhang, Xiaoni Wang, Lei Huang, Yiting Kang, Zeguo Feng, Fadong Zhao, Hongwei Zhuang, Jianbao Zhang","doi":"10.1186/s12993-025-00275-0","DOIUrl":"https://doi.org/10.1186/s12993-025-00275-0","url":null,"abstract":"<p><p>The health risks associated with acute noise exposure are increasing, particularly the risk of mental health. This study aims to identify the association between acute high-intensity noise exposure and anxiety behavior in male rats, and to explore the associated neurobiological mechanisms. Male rats were subjected to different levels of acute high-intensity noise to determine the intensity that causes long-lasting anxiety-like behaviors. Anxiety-like behaviors were evaluated using the open field test (OFT) and the elevated plus maze test (EPMT) on the third day and 1month post-exposure, respectively. A range of techniques, including immunofluorescence staining, western blot, ELISA, and real-time quantitative PCR, were used to investigate neuronal apoptosis, glial cell activation, neuroinflammation, and blood-brain barrier (BBB) disruption in the hippocampus. Upon exposure to 135 dB of acute noise, male rats exhibited enduring anxiety-like behaviors. Subsequent investigations discovered that this noise intensity not only activated glial cells and triggered neuroinflammation within the hippocampus but also decreased the expression levels of ZO-1, claudin-5, and occludin, suggesting a disruption of the BBB. Additionally, this exposure was associated with the induction of neuronal apoptosis in the hippocampal region. In conclusion, acute exposure to 135 dB noise may cause persistent anxiety in male rats through a cyclical interaction between neuroinflammation and BBB disruption, potentially leading to neuronal apoptosis.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"11"},"PeriodicalIF":4.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12016381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comprehensive review on the impact of polyphenol supplementation and exercise on depression and brain function parameters.","authors":"Shihong Jie, Aili Fu, Chuan Wang, Sogand Rajabi","doi":"10.1186/s12993-025-00273-2","DOIUrl":"10.1186/s12993-025-00273-2","url":null,"abstract":"<p><p>The objective of this review study is to examine the combined antidepressant effects of exercise and polyphenol supplementation, with a focus on specific polyphenolic compounds such as crocin, curcumin, and quercetin, as well as different forms of physical exercise, including aerobic and resistance training. The research examines how these interventions influence depressive-like behaviors, cognitive function, and neurochemical markers in animal models and human participants. The findings demonstrate that both exercise and polyphenols independently contribute to mood enhancement, reduced anxiety, and improved cognitive function through mechanisms such as neurogenesis, neurotransmitter modulation, and anti-inflammatory effects. Notably, the combined interventions showed a synergistic effect, providing more significant benefits in reducing symptoms of depression and anxiety, enhancing cognitive performance, and supporting overall mental well-being. These results suggest that integrating exercise and polyphenol supplementation could be a promising non-pharmacological approach to managing depression and related disorders.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"10"},"PeriodicalIF":4.7,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143717888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of cerebellar-cortical connectivity in modulating attentional abilities: insight from football athletes.","authors":"Jian Wang, Siyu Gao, Junfu Tian, Hao Hong, Chenglin Zhou","doi":"10.1186/s12993-025-00272-3","DOIUrl":"10.1186/s12993-025-00272-3","url":null,"abstract":"<p><p>Neuroplasticity, a phenomenon present throughout the lifespan, is thought to be influenced by physical training. However, the relationship between neuroplastic differences and attentional abilities remains unclear. This study explored the differences in brain function and attentional abilities between professional football athletes and novices, and further investigated the relationship between the two. To address this question, we included 49 football athletes and 63 novices in our study, collecting data on resting-state functional connectivity and Attention Network Test (ANT). Behavioral results from the ANT indicated that football experts had superior orienting attention but weaker alerting functions compared to novices, with no difference in executive control attention. fMRI results revealed that football experts exhibited higher fractional Amplitude of Low-Frequency Fluctuations (fALFF) values in the bilateral anterior cerebellar lobes, bilateral insula, and left superior temporal gyrus. Functional connectivity analysis showed increased connectivity between the left anterior cerebellar lobe and various cortical regions, including the right supramarginal gyrus, left precuneus, left superior frontal gyrus, bilateral posterior cerebellar lobes, and bilateral precentral gyri in experts compared to novices. More importantly, in the expert group but not in novice group, functional connectivity differences significantly predicted attentional orienting scores. Graph theoretical analysis showed that experts exhibited higher betweenness centrality and node efficiency in the right cerebellar lobule III (Cerebelum_3_R) node. Our findings demonstrate that long-term professional football training may significantly affect neuroplasticity and attentional functions. Importantly, our analysis reveals a substantive connection between these two aspects, suggesting that the integration of neuroplastic and attentional changes is likely mediated by cerebellar-cortical connectivity.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"9"},"PeriodicalIF":4.7,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11934456/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143699598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}