Brain Research最新文献

{"title":"The effects of 15-day complete fasting on the attentional network: An ERP study","authors":"Chao Wang ,&nbsp;Ziqing Cao ,&nbsp;Haibo Qin ,&nbsp;Liping Tian ,&nbsp;Yuan Jiang ,&nbsp;Zhongquan Dai ,&nbsp;Lizhong Chi ,&nbsp;Bin Wu","doi":"10.1016/j.brainres.2024.149343","DOIUrl":"10.1016/j.brainres.2024.149343","url":null,"abstract":"<div><div>This study examined whether and how a 15-day complete fast affects attentional network function. During a 15-day complete fasting, 17 healthy participants completed an attentional network test, while behavioral and EEG data were obtained. EEG results were marginally significant for the interaction between fasting stages and cue hints on the N1 amplitude of the altering network (F _{(3, 48)} = 2.57, <em>p</em> = 0.065, <em>η²_p</em> = 0.14). The interaction between fasting stages and cue hints was marginally significant on the N1 amplitude of the orienting network (F _{(3, 48)} = 2.71, <em>p</em> = 0.056, <em>η²_p</em> = 0.15). The interaction between fasting stages and target types was significant on the N2 amplitude of the executive control network (F _{(3, 48)} = 2.86, <em>p</em> = 0.047, <em>η²_p</em> = 0.15). The main effect of target types was significant on the P3 amplitude (F _{(1, 16)} = 4.71, <em>p</em> = 0.045, <em>η²_p</em> = 0.23). This suggests that participants’ allocation of attentional resources to the three sub-networks of the attentional network was not significantly affected during the 15 days of complete fasting. These study results help further understand the relationship between complete fasting and attentional networks and provide theoretical support and reference for the survival and work of astronauts actively in complete fasting during future near-Earth planet landings or even deep space exploration.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1849 ","pages":"Article 149343"},"PeriodicalIF":2.7,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuronal PLPP/CIN exaggerates the immune response of hippocampal microglia to LPS challenge dependent on PAK1-NF-κB-COX-2 signaling pathway","authors":"Ji-Eun Kim,&nbsp;Su Hyeon Wang,&nbsp;Duk-Shin Lee,&nbsp;Tae-Hyun Kim,&nbsp;Tae-Cheon Kang","doi":"10.1016/j.brainres.2024.149345","DOIUrl":"10.1016/j.brainres.2024.149345","url":null,"abstract":"<div><div>Recently, we have reported that pyridoxal-5′-phosphate phosphatase/chronophin (PLPP/CIN) selectively dephosphorylates neurofibromin 2 (NF2, also known as merlin) at serine (S) 10 site. Since NF2 inhibits p21-activated kinase 1 (PAK1)-mediated nuclear factor-κB (NF-κB) activation, in the present study, we investigated the role of PLPP/CIN-mediated NF2 S10 dephosphorylation in lipopolysaccharide (LPS)-induced neuroinflammation and explored its related signaling pathways in the mouse hippocampus. <em>PLPP/CIN</em> overexpression increased NF2 S10 dephosphorylation and PAK1 S204 autophosphorylation under physiological condition, which were reversed by <em>PLPP/CIN</em> deletion. Following LPS injection, <em>PLPP/CIN</em> overexpression exacerbated microglial activation, although microglial PLPP/CIN expression was undetectable. In addition, <em>PLPP/CIN</em> overexpression enhanced PAK1 and NF-κB phosphorylations, and upregulated cyclooxygenase-2 (COX-2) and prostaglandin E synthase 2 (PTGES2) expressions in CA1 neurons. <em>PLPP/CIN</em> overexpression also augmented microglial interleukin-1β induction. <em>PLPP/CIN</em> ablation and 1,1′-dithiodi-2-naphthtol (IPA-3, a PAK1 inhibitor) pretreatment ameliorated these LPS-induced neuroinflammatory responses. These findings indicate that PLPP/CIN-mediated NF2 S10 dephosphorylation may facilitate PAK1-NF-κB-COX-2-PTGES2 signaling pathway in CA1 neurons, which would subsequently exaggerate immune response of microglia following LPS treatment. Therefore, our findings suggest that this PLPP/CIN-mediated neuron-microglia interaction may play an important role in the pathogenesis of inflammation-related neurological diseases.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1849 ","pages":"Article 149345"},"PeriodicalIF":2.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142703274","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted downregulation of insulin signaling restricts human tau pathogenesis by reinstating the aberrant heterochromatin loss and mTOR/4EBP/S6K pathway in Drosophila","authors":"Pragati ,&nbsp;Surajit Sarkar","doi":"10.1016/j.brainres.2024.149347","DOIUrl":"10.1016/j.brainres.2024.149347","url":null,"abstract":"<div><div>Tauopathies are a group of neurodegenerative diseases characterized by the accumulation of paired helical filaments (PHFs)/or neurofibrillary tangles (NFTs) in neuronal/glial cells. Besides hyperphosphorylation of tau protein, aberrant heterochromatin loss and translation dysfunction have emerged as other important aspects contributing to the disease pathogenesis. We have recently reported that tissue-specific downregulation of insulin signaling or its growth-promoting downstream sub-branch effectively reinstates the tau-mediated overactivated insulin pathway, and restricts pathogenic tau hyperphosphorylation and aggregate formation. We next investigated if the downregulation of the insulin pathway or its growth-promoting downstream sub-branch makes any impact on tau-mediated aberrant heterochromatin loss and translation dysfunction. For the first time, we demonstrate that tissue-specific downregulation of insulin signaling or its growth-promoting branch effectively restricts the pathogenic tau-induced heterochromatin loss. We further report that expression of human tau in <em>Drosophila</em> causes induction of the mTOR/4EBP/S6K pathway and energy disbalance which gets effectively balanced upon downregulation of insulin signaling. Our findings establish an imperative role of insulin signaling in effectively mitigating various aspects of tau etiology in <em>Drosophila</em> ranging from hyperphosphorylation, chromatin relaxation, and translational upsurge. Our findings could be beneficial in establishing novel therapeutic options against tauopathies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1849 ","pages":"Article 149347"},"PeriodicalIF":2.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Apoptosis and long non-coding RNAs: Focus on their roles in ischemic stroke","authors":"Jia Min Ding ,&nbsp;Hui Min Zhong ,&nbsp;Kuan Huang ,&nbsp;Wen Zeng ,&nbsp;Li Chen","doi":"10.1016/j.brainres.2024.149346","DOIUrl":"10.1016/j.brainres.2024.149346","url":null,"abstract":"<div><div>Ischemic stroke (IS) is a severe and sudden cerebrovascular event, associated with notably high rates of mortality and morbidity. The process of apoptosis, a genetically orchestrated form of programmed cell death, is divided into two pathways: intrinsic and extrinsic. The intricate involvement of long non-coding RNA (lncRNA) in the pathobiology of IS, particularly in modulating neuronal apoptosis, is a burgeoning area of research. This review synthesizes the current understanding of the regulatory mechanisms of lncRNA on neuronal apoptosis in the context of ischemic stroke. Specifically, we highlight the roles of lncRNA such as ANRIL, C2dat1/2, H19, TUG1, MEG3, SNHG, and GAS5, which have been implicated in the facilitation of neuronal apoptosis. Conversely, the lncRNA N1LR has been shown to exert an inhibitory effect on this process. The role of MALAT1 in neuronal apoptosis remains a subject of ongoing debate, as its function oscillates between pro-apoptotic and anti-apoptotic roles, thus highlighting the need for further elucidation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1849 ","pages":"Article 149346"},"PeriodicalIF":2.7,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring DPP IV inhibitors for Alzheimer’s disease: Bridging diabetes and neurodegeneration","authors":"Swagata Pattanaik,&nbsp;Shakti Ketan Prusty,&nbsp;Pratap Kumar Sahu","doi":"10.1016/j.brainres.2024.149342","DOIUrl":"10.1016/j.brainres.2024.149342","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by neurofibrillary tangles (NFTs), senile plaques from Aβ deposits, neuronal inflammation, oxidative stress, and impaired neuronal transmission involving acetylcholine and glutamate. Diabetes patients are at a higher risk of developing AD-like pathology due to shared pathological and molecular mechanisms, including insulin resistance, oxidative stress, formation of advanced glycation end products (AGEs), and overactive immune systems. Current treatments of AD typically address only one aspect of the disease, rather than treating it as a multifactorial process. Targeting cerebral glucose-insulin metabolism has emerged as a promising strategy for AD management. Numerous studies show positive correlations between anti-diabetic drugs and AD management. Among these, DPP IV inhibitors have demonstrated significant therapeutic benefits against AD in experimental settings. DPP IV inhibitors have been shown to significantly reduce Aβ oligomerization, phosphorylated tau (p-tau), oxidative stress, and inflammatory markers, presenting a potentially effective approach for targeting AD-like pathology. Although preclinical data are promising, clinical trials are needed to validate these findings and establish the safety and efficacy of DPP IV inhibitors as a therapeutic intervention for AD. This could represent a novel approach for addressing both the metabolic and neurodegenerative aspects of AD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149342"},"PeriodicalIF":2.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reward processing dominates the brain during feedback evaluation: Electrophysiological evidence","authors":"Wenqi Song ,&nbsp;Rixin Qi ,&nbsp;Lingyao Tong ,&nbsp;Congcong Qi ,&nbsp;Li Li ,&nbsp;Shiwei Jia","doi":"10.1016/j.brainres.2024.149337","DOIUrl":"10.1016/j.brainres.2024.149337","url":null,"abstract":"<div><div>During reinforcement learning, people learn based on both positive and negative feedback. Researchers have revealed the reward positivity (RewP) that reflects positive feedback evaluation, however, no electrophysiological indicator has been found to explain negative feedback processing. In reinforcement learning, people would like to expect the positive feedback after a choice, which might explain why previous studies usually found neural responses for reward processing, while the negative feedback processing seems absent. However, no study has designed a task to separate positive and negative feedback processing to measure the corresponding electrophysiological responses. Thus, the present study designed gain processing-advantaged (GA) and loss processing-advantaged (LA) contexts using a modified gambling task to measure specific neural responses to gain processing and loss processing. Electroencephalography (EEG) data were processed using time-domain and time–frequency analyses. The results revealed the RewP and delta oscillation following gain feedback in the GA context, while no negativity or other components specific to loss processing was found, even in the loss condition of LA context. The current results indicate that reward processing dominates the brain during feedback evaluation, whereas loss processing can’t be captured by electrophysiological signal.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149337"},"PeriodicalIF":2.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nrf2 activator tertiary butylhydroquinone enhances neural stem cell differentiation and implantation in Alzheimer’s disease by boosting mitochondrial function","authors":"Long Lin,&nbsp;Jiameng Li,&nbsp;Zhengtao Yu,&nbsp;Jun He,&nbsp;You Li,&nbsp;Junwen Jiang,&nbsp;Ying Xia","doi":"10.1016/j.brainres.2024.149341","DOIUrl":"10.1016/j.brainres.2024.149341","url":null,"abstract":"<div><h3>Aims</h3><div>To investigate the effects of Nrf2 agonist tertiary butylhydroquinone (TBHQ)-stimulated neural stem cells (NSCs) transplantation (NSC(TBHQ)) on neuronal damage and cognitive deficits in an AD model and its underlying principles.</div></div><div><h3>Methods</h3><div>BHQ-treated NSCs were examined with or without Aβ1-42 to investigate the effects of TBHQ on the proliferation and differentiation functions. The mitophagy inhibitor Cyclosporine A (CSA) was used to explore the regulation of mitophagy by TBHQ. The no-, ethanol-, and TBHQ-treated NSCs were transplanted into the bilateral hippocampal region of model mice to explore the effects of NSC(TBHQ) on neuronal, cognitive, and mitochondrial functional impairments in mice.</div></div><div><h3>Results</h3><div>TBHQ reversed the Aβ1-42-caused inhibition on NSC proliferation and differentiation, as well as on levels of mitochondrial membrane potential, adenosine triphosphate (ATP), and mitochondrial fusion-associated proteins. TBHQ alleviated the Aβ1-42-induced increase in apoptosis, mitochondrial damage, mitochondria-derived reactive oxygen species (mtROS), and mitochondrial fission-related proteins. TBHQ activated the Parkin, Beclin, LC3II/I, and COXIV expression, while inhibiting the p62 expression. CSA reversed the effects of TBHQ on NSC proliferation and differentiation. After NSC(TBHQ) transplantation, it not only further extended the dwell time in the target quadrant and shorten the time and distance for finding the hidden platform, but also further decreased the Aβ and p-Tau/Tau levels, while increasing the expression of NeuN. The effects of NSC(TBHQ) transplantation on mitochondrial function were consistent with the <em>in vitro</em> experiments.</div></div><div><h3>Conclusions</h3><div>The study shows that NSC(TBHQ) intensifies the beneficial impact of NSCs transplantation on cognitive impairment and neuronal damage in AD models, likely due to TBHQ’s role in promoting NSCs growth and differentiation via mitophagy, thus laying a theoretical foundation for improving NSCs transplantation for AD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1849 ","pages":"Article 149341"},"PeriodicalIF":2.7,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142680837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Memory is improved and reflex maturation accelerated in the progeny of rat dams that consumed pequi (Caryocar Brasiliense)","authors":"Suedna da Costa Silva Kindelan ,&nbsp;Michelly Pires Queiroz ,&nbsp;Jany Jacielly Dos Santos ,&nbsp;Maria Lucia de Azevedo Oliveira ,&nbsp;Paloma Cristina Milhomens Ferreira Melo ,&nbsp;Camila Carolina de Menezes Santos Bertozzo ,&nbsp;Juliano Carlo Rufino Freitas ,&nbsp;Natália Dantas de Oliveira ,&nbsp;Raphaela Veloso Rodrigues Dantas ,&nbsp;Marta Suely Madruga ,&nbsp;Juliana Késsia Barbosa Soares","doi":"10.1016/j.brainres.2024.149318","DOIUrl":"10.1016/j.brainres.2024.149318","url":null,"abstract":"<div><div>This study evaluated the influence of maternal consumption of pequi pulp and nuts during pregnancy and lactation on reflex and somatic maturation and memory performance in rat offspring. The pups were divided into three groups: Control, treated with distilled water; a Pulp group and a Nuts group, treated with 2000 mg/kg of body weight of pequi pulp and nuts, respectively. Reflex and somatic maturation of the offspring were evaluated during lactation. Short and long-term memory consolidation in adolescent offspring were measured by evaluating habituation to the open field and object recognition. Data showed an acceleration of reflex maturation in three of the seven parameters evaluated in the Nuts group and four parameters in the Pulp group compared to the control. There was an acceleration in the appearance of somatic maturation in one parameter in the Nuts group and three in the pulp group compared to the control. The long-term object recognition rate was higher in the Nuts group compared to the control and highest in the Pulp group. Maternal levels of malonaldehyde in the brain were measured and their levels in the Pulp and Nuts groups were lower than those in the Control group. We can conclude that consumption of both pulp and pequi nuts promoted a reduction in oxidative stress in the maternal brain, promoted acceleration of reflex and somatic maturation, and improved long-term memory in the offspring, with these effects being more intense in the Pulp group.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149318"},"PeriodicalIF":2.7,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DLGAP3 suppresses malignant behaviors of glioma cells via inhibiting RGS12-mediated MAPK/ERK signaling","authors":"Jing Wei ,&nbsp;Yuan Li ,&nbsp;Fangzheng Jiao ,&nbsp;Xiaoya Wang ,&nbsp;Han Zhou ,&nbsp;Yifan Qiao ,&nbsp;Zihan Yuan ,&nbsp;Chao Qian ,&nbsp;Yanlong Tian ,&nbsp;Yan Fang","doi":"10.1016/j.brainres.2024.149334","DOIUrl":"10.1016/j.brainres.2024.149334","url":null,"abstract":"<div><h3>Background</h3><div>Glioma is the most common malignant tumor of the central nervous system, and is characterized by high recurrence, poor prognosis and especially complex pathogenesis. The synaptic plasticity-related protein DLGAP3 is mainly involved in the assembly and function of postsynaptic density complex. It’s widely known that DLGAP3 participating in the occurrence of various neuropsychiatric diseases, but its role in glioma tumorigenesis remains largely unclear.</div></div><div><h3>Methods</h3><div>We ectopically expressed and knocked down DLGAP3 in glioma cells to perform a series of functional studies in vitro. Meanwhile, western blot analysis, co-immunoprecipitation, enrichment analysis and dual-luciferase reporter system assays were performed to explore the mechanism of DLGAP3 suppressing glioma tumorigenesis and progression.</div></div><div><h3>Results</h3><div>We found that DLGAP3 was low expressed in gliomas, and decreased DLGAP3 expression was strongly correlated with poor survival of glioma patients. Ectopic expression of DLGAP3 in glioma cell lines dramatically inhibited cell proliferation, invasion and migration. In addition, our data also showed that DLGAP3 can tightly connected with RGS12, and DLGAP3 overexpression significantly increased the expression of RGS12 and inhibited the phosphorylation levels of MEK and ERK. Furthermore, the RGS12 inhibited transcription and translation of <em>BRAF</em>, which further decreased the activity of MAPK/ERK signaling pathway. This suggests that DLGAP3 may act as a tumor suppressor in gliomas and inhibits glioma tumorigenesis by regulating RGS12 and the downstream MAPK/ERK signals axis.</div></div><div><h3>Conclusion</h3><div>Our data indicates that DLGAP3 is a potential tumor suppressor and valuable prognostic biomarker in gliomas.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149334"},"PeriodicalIF":2.7,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142646852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-gamma frequency flash stimulation as a possible cognitive facilitator in rat pups","authors":"Yu Fu ,&nbsp;Qingfeng Zhai","doi":"10.1016/j.brainres.2024.149314","DOIUrl":"10.1016/j.brainres.2024.149314","url":null,"abstract":"<div><div>High-gamma frequency flashes can enhance cognition by synchronizing neural oscillations in mammals. Early flash treatment promotes the development of improved cognitive functions in young children. However, it is unclear whether exposure to high-gamma frequency flashes in preschool-aged individuals affects cognition in preadolescents by regulating neural oscillations in the brain. Here, we aimed to investigate the effects of gamma-frequency flashes on cognitive ability. In this study, the effect of high-frequency flicker on cognitive performance was verified by behavioural experiments such as the open-field test and the water maze, but also proteomics. We found that external 40 Hz and 70 Hz frequency flashes synchronized neural oscillations at the corresponding frequencies in the primary visual cortex (V1) of rats. Rats that underwent 70 Hz flash intervention had better cognitive behavioural performance in the early stages of training. The 70 Hz flash frequency upregulated proteins associated with neuronal growth and differentiation, such as Snapin, FoxO3, Hspa12a, and Penk, and activated the MAPK signalling pathway, signalling pathway regulating stem cell pluripotency, and the neuroactive ligand-receptor interaction pathway. These proteins and pathways play important roles in cognitive functions. Our study revealed that 70 Hz flashes received by young children early in their development substantially promote the growth of cognitive capabilities in the brain. Exposure to 70 Hz flashes may be a new intervention method and a new strategy for improving cognition.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149314"},"PeriodicalIF":2.7,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}