{"title":"Improving effects of melatonin on memory and synaptic potentiation in a mouse model of Alzheimer's-like disease: the involvement of glutamate homeostasis and mGluRs receptors.","authors":"Narjes Khatoun Shabani Sadr, Fatemeh Bakhtiarzadeh, Koorosh Shahpasand, Javad Mirnajafi-Zadeh, Mehrdad Behmanesh","doi":"10.1186/s12993-025-00271-4","DOIUrl":"https://doi.org/10.1186/s12993-025-00271-4","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is characterized by progressive cognitive decline and synaptic dysfunction, largely driven by amyloid plaques and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau. These pathological hallmarks disrupt glutamate signaling, which is essential for synaptic plasticity and memory consolidation. This study investigates the therapeutic potential of melatonin on memory and synaptic plasticity in an AD-like mouse model, with a focus on its regulatory effects on glutamate homeostasis and metabotropic glutamate receptors (mGluRs).</p><p><strong>Methods: </strong>The study began with an in-silico bioinformatics analysis of RNA-seq datasets from hippocampal tissues of AD patients to identify differentially expressed genes (DEGs) related to glutamate signaling and tau pathology. An AD-like model was induced via intra-hippocampal injection of cis-phospho tau in C57BL/6 mice. Memory function was assessed using behavioral tests. Synaptic plasticity was evaluated using in vitro field potential recording of hippocampal slices. Histological analyses included Nissl staining for neuronal density, Luxol Fast Blue for myelin integrity, and immunofluorescence for tau hyperphosphorylation. Molecular studies employed qPCR and Western blot to assess glutamate-related markers and tau phosphorylation. Melatonin (10 mg/kg) was administered intraperitoneally, starting either two weeks (early intervention) or four weeks (late intervention) post-induction.</p><p><strong>Results: </strong>Key molecular targets in glutamate signaling pathways were identified using bioinformatics. AD-like mice displayed memory deficits and synaptic dysfunction. Melatonin improved cognitive function, especially with early intervention, as confirmed by behavioral tests. Histological studies revealed reduced neuronal loss, improved myelin integrity, and decreased tau hyperphosphorylation. Molecular findings showed restored mGluR expression and reduced GSK3 activity. Early intervention yielded superior outcomes, with partial restoration of synaptic plasticity observed in LTP recordings.</p><p><strong>Conclusions: </strong>These findings underscore the neuroprotective properties of melatonin, mediated by its ability to modulate glutamate signaling and mGluR activity, offering new insights into its potential as a therapeutic agent for AD. Additionally, the results suggest that earlier administration of melatonin may significantly enhance its efficacy, highlighting the importance of timely intervention in neurodegenerative diseases.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"7"},"PeriodicalIF":4.7,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dopamine D1 receptor agonist alleviates post-weaning isolation-induced neuroinflammation and depression-like behaviors in female mice.","authors":"Zi-Wei Zhao, Yun-Chen Wang, Pei-Chun Chen, Shun-Fen Tzeng, Po-See Chen, Yu-Min Kuo","doi":"10.1186/s12993-025-00269-y","DOIUrl":"10.1186/s12993-025-00269-y","url":null,"abstract":"<p><strong>Background: </strong>Major depressive disorder is a significant global cause of disability, particularly among adolescents. The dopamine system and nearby neuroinflammation, crucial for regulating mood and processing rewards, are central to the frontostriatal circuit, which is linked to depression. This study aimed to investigate the effect of post-weaning isolation (PWI) on depression in adolescent mice, with a focus on exploring the involvement of microglia and dopamine D1 receptor (D1R) in the frontostriatal circuit due to their known links with mood disorders.</p><p><strong>Results: </strong>Adolescent mice underwent 8 weeks of PWI before evaluating their depression-like behaviors and the activation status of microglia in the frontostriatal regions. Selective D1-like dopamine receptor agonist SKF-81,297 was administered into the medial prefrontal cortex (mPFC) of PWI mice to assess its antidepressant and anti-microglial activation properties. The effects of SKF-81,297 on inflammatory signaling pathways were examined in BV2 microglial cells. After 8 weeks of PWI, female mice exhibited more severe depression-like behaviors than males, with greater microglial activation in the frontostriatal regions. Microglial activation in mPFC was the most prominent among the three frontostriatal regions examined, and it was positively correlated with the severity of depression-like behaviors. Female PWI mice exhibited increased expression of dopamine D2 receptors (D2R). SKF-81,297 treatment alleviated depression-like behaviors and local microglial activation induced by PWI; however, SKF-81,297 induced these alterations in naïve mice. In vitro, SKF-81,297 decreased pro-inflammatory cytokine release and phosphorylations of JNK and ERK induced by lipopolysaccharide, while in untreated BV2 cells, SKF-81,297 elicited inflammation.</p><p><strong>Conclusions: </strong>This study highlights a sex-specific susceptibility to PWI-induced neuroinflammation and depression. While targeting the D1R shows potential in alleviating PWI-induced changes, further investigation is required to evaluate potential adverse effects under normal conditions.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"6"},"PeriodicalIF":4.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11895232/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596199","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}
Lauren P Giesler, William T O'Brien, Jesse Bain, Gershon Spitz, Emily J Jaehne, Maarten van den Buuse, Sandy R Shultz, Richelle Mychasiuk, Stuart J McDonald
{"title":"Investigating the role of the brain-derived neurotrophic factor Val66Met polymorphism in repetitive mild traumatic brain injury outcomes in rats.","authors":"Lauren P Giesler, William T O'Brien, Jesse Bain, Gershon Spitz, Emily J Jaehne, Maarten van den Buuse, Sandy R Shultz, Richelle Mychasiuk, Stuart J McDonald","doi":"10.1186/s12993-025-00270-5","DOIUrl":"10.1186/s12993-025-00270-5","url":null,"abstract":"<p><strong>Background: </strong>Mild traumatic brain injury (mTBI) poses a significant public health concern, particularly regarding repetitive injury, with outcomes ranging from acute neurobehavioral deficits to long-term impairments. While demographic factors like age and sex influence outcomes, the understanding of genetic contributions, particularly the role of the brain-derived neurotrophic factor (BDNF) Val66Met polymorphism, remains limited. This study aimed to characterize acute effects of repetitive mTBI (rmTBI) in rats with the Val68Met SNP, the rodent equivalent of the human Val66Met, focusing on behavioral, fluid biomarker, and histological changes.</p><p><strong>Methods: </strong>Using a closed-head injury model, rats underwent five mTBIs over consecutive days. Behavioral assessments included sensorimotor function, anxiety-like behavior, spatial learning and memory, and nociceptive response. Plasma neurofilament light (NfL) levels served as a biomarker of axonal injury and immunohistochemistry evaluated microglial activation.</p><p><strong>Results: </strong>Sensorimotor deficits and increased anxiety-like behavior were found in rats with rmTBI, but these changes were not affected by sex or genotype. Plasma NfL levels were higher in rmTBI compared with sham rats, with levels greater in female rmTBI when compared with male rmTBI rats. Microglial activation was observed in the hypothalamus of injured rats, but was not influenced by genotype or sex.</p><p><strong>Conclusions: </strong>While the Val68Met SNP did not significantly influence acute responses to rmTBI in this study, further investigation into alternative functional and pathophysiological outcomes, as well as long-term effects, is required.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"5"},"PeriodicalIF":4.7,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884142/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565997","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":"Effects of TrkB-related induced metaplasticity within the BLA on anxiety, extinction learning, and plasticity in BLA-modulated brain regions.","authors":"Joyeeta Dutta Hazra, Kuldeep Shrivastava, Lisa-Sophie Wüstner, Rachel Anunu, Erez Chervinsky, Somoday Hazra, Simone Beuter, Martin Kriebel, Mouna Maroun, Hansjuergen Volkmer, Gal Richter-Levin","doi":"10.1186/s12993-025-00267-0","DOIUrl":"10.1186/s12993-025-00267-0","url":null,"abstract":"<p><strong>Background: </strong>Neuronal plasticity within the basolateral amygdala (BLA) is fundamental for fear learning. Metaplasticity, the regulation of plasticity states, has emerged as a key mechanism mediating the subsequent impact of emotional and stressful experiences. After mRNA knockdown of synaptic plasticity-related TrkB, we examined the impact of chronically altered activity in the rat BLA (induced metaplasticity) on anxiety-like behavior, fear memory-related behaviors, and neural plasticity in brain regions modulated by the BLA. These effects were investigated under both basal conditions and following exposure to acute trauma (UWT).</p><p><strong>Results: </strong>Under basal conditions, TrkB knockdown increased anxiety-like behavior and impaired extinction learning. TrkBKD also reduced LTP in the vSub-mPFC pathway but not in the dentate gyrus. Compared with those of control animals, acute trauma exposure led to increased anxiety-like behavior and impaired extinction learning in both the trauma-exposed group (CTR-UWT) and the trauma-exposed group on the background of TrkB knockdown (TrkBKD-UWT). However, the deficit in extinction learning was more pronounced in the TrkBKD-UWT group than in the CTR-UWT group. Accordingly, TrkBKD-UWT, but not CTR-UWT, resulted in impaired LTP in the vSub- mPFC pathway. Since LTP in this pathway is independent of BLA involvement, this result suggests that lasting intra-BLA-induced metaplasticity may also lead to transregional metaplasticity within the mPFC, as suggested previously.</p><p><strong>Conclusions: </strong>Taken together, these findings reveal the dissociative involvement of BLA function, on the one hand, in anxiety, which is affected by the knockdown of TrkB, and, on the other hand, in extinction learning, which is more significantly affected by the combination of intra-BLA-induced metaplasticity and exposure to emotional trauma.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"4"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11874401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540002","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}
Yiwen Zhang, Fang Chen, Mubiao Yu, Yinghui Li, Shanguang Chen, Muhammad Iqbal Choudhary, Xinmin Liu, Ning Jiang
{"title":"Sex differences in reward-based operant conditioning performance and neurotransmitter changes following chronic sleep restriction stress in rats.","authors":"Yiwen Zhang, Fang Chen, Mubiao Yu, Yinghui Li, Shanguang Chen, Muhammad Iqbal Choudhary, Xinmin Liu, Ning Jiang","doi":"10.1186/s12993-025-00268-z","DOIUrl":"10.1186/s12993-025-00268-z","url":null,"abstract":"<p><strong>Background: </strong>Sleep deprivation significantly impairs cognitive function, which disrupts daily life. However, sex differences in these impairments are not well understood, as most preclinical studies primarily use male animals, neglecting potential differences between sexes. This study aims to investigate sex-specific differences in cognitive function under sleep deprivation using reward-based operant conditioning tasks.</p><p><strong>Results: </strong>Sprague-Dawley rats were pre-trained on a lever-press task and subsequently divided into control and chronic sleep restriction (CSR) groups. The CSR group underwent 14 days of sleep restriction. After CSR modeling, rats were assessed using the open field test, retraining on the lever-pressing task, signal discrimination task, and extinction task to evaluate motor abilities, memory formation, learning, and cognitive flexibility. CSR significantly impaired task performance in both sexes, with rats requiring more time and exhibiting lower accuracy. In the signal discrimination task, male rats showed longer feeding latency and lower accuracy compared to females. CSR also specifically increased the frequency of operant responses in male rats. In the extinction task, CSR enhanced exploration time and frequency in both sexes, with females exhibiting significantly higher exploration frequencies than males. Biochemically, CSR induced sex-specific alterations, including elevated serum MDA and MAO levels in males and increased serotonin, dopamine, and epinephrine in both sexes. Although activation was observed in metabolites of the tryptophan-kynurenine pathway, sex differences were evident in the kynurenic acid metabolism levels in the prefrontal cortex.</p><p><strong>Conclusions: </strong>CSR impairs cognitive function in both male and female rats, with significant sex differences observed. Male CSR rats exhibited impaired signal discrimination, while CSR impaired extinction learning in female rats. These impairments are accompanied by CSR-induced oxidative stress, neurotransmitter dysregulation, and disturbances in the tryptophan metabolic pathway. These findings underscore the importance of considering sex differences in understanding the effects of sleep deprivation on cognitive function and developing targeted intervention strategies.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"3"},"PeriodicalIF":4.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11871611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531030","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":"Fecal microbiota transplantation attenuates Alzheimer's disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation.","authors":"Xiang Li, Qingyong Ding, Xinxin Wan, Qilong Wu, Shiqing Ye, Yongliang Lou","doi":"10.1186/s12993-024-00265-8","DOIUrl":"10.1186/s12993-024-00265-8","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD. Additionally, disruption of the gut microbiota has been found to be associated with AD, and fecal microbiota transplantation (FMT) has emerged as a potential therapeutic approach. However, the precise mechanism of FMT in the treatment of AD remains elusive. In this study, FMT was performed by transplanting fecal microbiota from healthy wild-type mice into APP/PS1 mice (APPswe, PSEN1dE9) to assess the effectiveness of FMT in mitigating AD-associated inflammation and to reveal its precise mechanism of action. The results demonstrated that FMT treatment improved cognitive function and reduced the expression levels of inflammatory factors by regulating the TLR4/MyD88/NF-κB signaling pathway in mice, which was accompanied by the restoration of gut microbial dysbiosis. These findings suggest that FMT has the potential to ameliorate AD symptoms and delay the disease progression in APP/PS1 mice.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"2"},"PeriodicalIF":4.7,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11715513/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142942873","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}
Sarah Asbury, Jonathan K Y Lai, Kelly C Rilett, Zeeshan Haqqee, Benjamin C Darwin, Jacob Ellegood, Jason P Lerch, Jane A Foster
{"title":"Host genetics maps to behaviour and brain structure in developmental mice.","authors":"Sarah Asbury, Jonathan K Y Lai, Kelly C Rilett, Zeeshan Haqqee, Benjamin C Darwin, Jacob Ellegood, Jason P Lerch, Jane A Foster","doi":"10.1186/s12993-024-00261-y","DOIUrl":"10.1186/s12993-024-00261-y","url":null,"abstract":"<p><p>Gene-environment interactions in the postnatal period have a long-term impact on neurodevelopment. To effectively assess neurodevelopment in the mouse, we developed a behavioural pipeline that incorporates several validated behavioural tests to measure translationally relevant milestones of behaviour in mice. The behavioral phenotype of 1060 wild type and genetically-modified mice was examined followed by structural brain imaging at 4 weeks of age. The influence of genetics, sex, and early life stress on behaviour and neuroanatomy was determined using traditional statistical and machine learning methods. Analytical results demonstrated that neuroanatomical diversity was primarily associated with genotype whereas behavioural phenotypic diversity was observed to be more susceptible to gene-environment variation. We describe a standardized mouse phenotyping pipeline, termed the Developmental Behavioural Milestones (DBM) Pipeline released alongside the 1000 Mouse Developmental Behavioural Milestones (1000 Mouse DBM) database to institute a novel framework for reproducible interventional neuroscience research.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"21 1","pages":"1"},"PeriodicalIF":4.7,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11697848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142920533","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":"Can rewards enhance creativity? Exploring the effects of real and hypothetical rewards on creative problem solving and neural mechanisms.","authors":"Can Cui, Yuan Yuan, Yingjie Jiang","doi":"10.1186/s12993-024-00264-9","DOIUrl":"10.1186/s12993-024-00264-9","url":null,"abstract":"<p><p>Reward cues have long been considered to enhance creative performance; however, little is known about whether rewards can affect creative problem solving by manipulating states of flexibility and persistence. This study sought to elucidate the differential impacts of real versus hypothetical rewards on the creative process utilizing the Chinese compound remote association task. Behavioral analysis revealed a significantly enhanced solution rate and response times in scenarios involving real rewards, in contrast to those observed with hypothetical rewards. Electrophysiological findings indicated that hypothetical rewards led to more positive P200-600 amplitudes, in stark contrast to the amplitudes observed in the context of real rewards. These findings indicate a positive impact of real rewards on creative remote associations and contribute new insights into the relationship between rewards and creative problem solving, highlighting the crucial role of persistence/flexibility in the formation of creativity.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"20 1","pages":"37"},"PeriodicalIF":4.7,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891724","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}
Hiroyuki Ohta, Takashi Nozawa, Kohki Higuchi, Andrea L Meredith, Yuji Morimoto, Yasushi Satoh, Toshiaki Ishizuka
{"title":"Altered trial-to-trial responses to reward outcomes in KCNMA1 knockout mice during probabilistic learning tasks.","authors":"Hiroyuki Ohta, Takashi Nozawa, Kohki Higuchi, Andrea L Meredith, Yuji Morimoto, Yasushi Satoh, Toshiaki Ishizuka","doi":"10.1186/s12993-024-00262-x","DOIUrl":"10.1186/s12993-024-00262-x","url":null,"abstract":"<p><p>The large-conductance calcium- and voltage-activated potassium (BK) channels, encoded by the KCNMA1 gene, play important roles in neuronal function. Mutations in KCNMA1 have been found in patients with various neurodevelopmental features, including intellectual disability, autism spectrum disorder (ASD), or attention deficit hyperactivity disorder (ADHD). Previous studies of KCNMA1 knockout mice have suggested altered activity patterns and behavioral flexibility, but it remained unclear whether these changes primarily affect immediate behavioral adaptation or longer-term learning processes. Using a 5-armed bandit task (5-ABT) and a novel Δrepeat rate analysis method that considers individual baseline choice tendencies, we investigated immediate trial-by-trial Win-Stay-Lose-Shift (WSLS) strategies and learning rates across multiple trials in KCNMA1 knockout (KCNMA1<sup>-/-</sup>) mice. Three key findings emerged: (1) Unlike wildtype mice, which showed increased Δrepeat rates after rewards and decreased rates after losses, KCNMA1<sup>-/-</sup> mice exhibited impaired WSLS behavior, (2) KCNMA1<sup>-/-</sup> mice displayed shortened response intervals after unrewarded trials, and (3) despite these short-term behavioral impairments, their learning rates and task accuracy remained comparable to wildtype mice, with significantly shorter task completion times. These results suggest that BK channel dysfunction primarily alters immediate behavioral responses to outcomes in the next trial rather than affecting long-term learning capabilities. These findings and our analytical method may help identify behavioral phenotypes in animal models of both BK channel-related and other neurodevelopmental disorders.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"20 1","pages":"36"},"PeriodicalIF":4.7,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11681721/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891723","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}
Tina T Vo, Shandell Pahlen, Anqing Zheng, Sian Yu, Emery Lor, Nicholas D Bowman, Robin P Corley, Naomi P Friedman, Sally J Wadsworth, Chandra A Reynolds
{"title":"From controllers to cognition: the importance of selection factors on video game and gameplay mechanic-derived cognitive differences.","authors":"Tina T Vo, Shandell Pahlen, Anqing Zheng, Sian Yu, Emery Lor, Nicholas D Bowman, Robin P Corley, Naomi P Friedman, Sally J Wadsworth, Chandra A Reynolds","doi":"10.1186/s12993-024-00258-7","DOIUrl":"10.1186/s12993-024-00258-7","url":null,"abstract":"<p><p>Playing video games, especially games with action-based mechanics, is correlated with better cognitive performance, yet these performance advantages may originate from intrinsic factors such as earlier life cognitive differences. We investigated whether gaming-cognition associations in a sample past young adulthood remain robust after accounting for adolescent cognitive functioning. Using data from the Colorado Adoption/Twin Study of Lifespan behavioral development and cognitive aging (CATSLife; N = 1241, M<sub>age</sub> = 33.3, %, age range = 28-51, Female = 52.9%), we compared cognitive performance of adult recreational gamers (40.6%) to non-gamers (59.4%) and between different types of gamers. Measures included processing speed, spatial reasoning, and working memory cognitive tasks, gaming status, and gameplay type engagement. The majority of gamer participants reported exclusively playing puzzle/strategy/life simulation games (53.0%) or action type games (33.1%); a smaller proportion reported playing both types of games (10.3%). Overall, gamers significantly outperformed non-gamers across most cognitive tasks (Cohen's d = 0.17-0.25), with limited evidence of a differential gameplay mechanic effect across tasks. Selection effects were evident whereby after adolescent IQ adjustment, gamer cognitive effects diminished by over 35% but persisted for spatial performance. Adolescent IQ predicted puzzle/strategy/life simulation preference but not action-type games, suggesting a selection effect. Our study replicates prior gaming findings and reveals that earlier life functioning contributes to adult gaming-cognition associations. Gamer-spatial associations are not fully attributable to intrinsic factors, and playing video games, regardless of a specific gameplay mechanic or genre, may represent a cognitively engaging lifestyle behavior that may benefit cognitive functioning, with implications for preserved cognition.</p>","PeriodicalId":8729,"journal":{"name":"Behavioral and Brain Functions","volume":"20 1","pages":"35"},"PeriodicalIF":4.7,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142870819","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}