Neuroscience最新文献_第7页

From plate to brain: benefits, deficiencies, and research needs of plant-based diets 从盘子到大脑：植物性饮食的好处、不足和研究需求。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-10 DOI: 10.1016/j.neuroscience.2025.09.005

Humberto Peña-Jorquera , Valeska Cid-Jofré

{"title":"From plate to brain: benefits, deficiencies, and research needs of plant-based diets","authors":"Humberto Peña-Jorquera , Valeska Cid-Jofré","doi":"10.1016/j.neuroscience.2025.09.005","DOIUrl":"10.1016/j.neuroscience.2025.09.005","url":null,"abstract":"<div><div>In recent years, plant-based diets and their specific components have gained popularity across all age groups and have attracted growing interest in the scientific community due to their potential health benefits. While these benefits have been extensively studied concerning overall health, their impact on cognitive performance and brain structure remains less understood. At the same time, concerns have been raised about the potential risk of nutritional deficiencies associated with plant-based diets. Given these uncertainties and gaps in the literature, it is crucial not only to recognize the potential benefits but also to address the possible drawbacks of plant-based eating. Moreover, little is known about the role of specific plant-derived components in brain function and structure, as well as the most effective strategies to mitigate potential risks.</div><div>Special attention is given to the modulatory role of the gut microbiota, short-chain fatty acids, and neuroinflammation. Moreover, this review identifies critical gaps in research involving younger individuals and populations from low- and middle-income countries, where dietary transitions and nutritional deficiencies pose unique risks.</div><div>Therefore, this review provides a novel perspective by critically integrating evidence on the benefits and risks of plant-based diets, encompassing brain structure, cognitive function, and potential bidirectional neurochemical pathways via the gut-brain axis, while highlighting implications across different life stages and underrepresented populations.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 335-350"},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Functional characterization and in vitro pharmacological rescue of a novel KCNA2 variant associated with developmental and epileptic encephalopathy 一种与发育性和癫痫性脑病相关的新型KCNA2变异的功能表征和体外药理学救援。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-10 DOI: 10.1016/j.neuroscience.2025.09.014

Changning Xie , Miriam Kessi , Fang He , Fei Yin , Jing Peng

{"title":"Functional characterization and in vitro pharmacological rescue of a novel KCNA2 variant associated with developmental and epileptic encephalopathy","authors":"Changning Xie , Miriam Kessi , Fang He , Fei Yin , Jing Peng","doi":"10.1016/j.neuroscience.2025.09.014","DOIUrl":"10.1016/j.neuroscience.2025.09.014","url":null,"abstract":"<div><div>Mutations in <em>KCNA2</em>, which encodes Kv1.2, have been reported to be associated with developmental and epileptic encephalopathy (DEE), however, little is known about the underlying mechanisms. Herein, we identified a novel <em>KCNA2</em> mutation (c.1175C > T, p.S392F) in two unrelated patients with DEE. We further investigated the functional consequences of this mutation by western-blotting, immunocytochemistry, cell death assay, staining as well as patch clamp, and assessed its sensitivity to 4-aminopyridine (4-AP) in the Chinese hamster ovary cells and cortical neurons. Our findings revealed that the p.S392F induced a hyperpolarizing shift both in inactivation and inactivation curves relative to wild-type (WT) channels suggesting it to be a mixed GOF and LOF variant, and was partly rescued by 4- AP. It also induced cell death of which was rescued by 4-AP. Moreover, primary neurons expressing the p.S392F mutation showed a reduction in neuronal firing. The application of 4-AP decreased neuronal firing in S392F transfected neurons. Besides, analysis of the clinical features of eleven patients with mixed GOF and LOF variants from our hospital and literature revealed epilepsy in 100.00 % of the cases, developmental delay/intellectual disability in 100.00 %, speech delay in 100.00 %, and ataxia in 36.36 %, of whom three patients could be partly improved by 4-AP. Thus, this study adds a novel recurrent mixed GOF and LOF variant, new underlying mechanisms and unique genotype-phenotype associations. Moreover, it highlights the therapeutic role of 4-AP.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"586 ","pages":"Pages 88-99"},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145054785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SELENOPROTEIN T deficiency alters projection neuron migration during corticogenesis in mice 硒蛋白T缺乏改变小鼠皮质发生过程中投射神经元的迁移

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-10 DOI: 10.1016/j.neuroscience.2025.09.015

Emmanuelle Carpentier , Anthony Falluel-Morel , Lisa Brunet , Magalie Bénard , David Alexandre , David Godefroy , Ben Yamine Mallouki , Loubna Boukhzar , Arnaud Arabo , Youssef Anouar

{"title":"SELENOPROTEIN T deficiency alters projection neuron migration during corticogenesis in mice","authors":"Emmanuelle Carpentier , Anthony Falluel-Morel , Lisa Brunet , Magalie Bénard , David Alexandre , David Godefroy , Ben Yamine Mallouki , Loubna Boukhzar , Arnaud Arabo , Youssef Anouar","doi":"10.1016/j.neuroscience.2025.09.015","DOIUrl":"10.1016/j.neuroscience.2025.09.015","url":null,"abstract":"<div><div>During corticogenesis, projection neurons migrate along the radial glial axis to form cortical layers, the alteration of which is associated with functional deficits in adulthood. As byproducts of cell metabolism, reactive oxygen species act as second messengers to contribute to neurodevelopment; however, free radical excess may impede this process. Selenoprotein T (SELENOT) is a newly identified thioredoxin-like enzyme of the endoplasmic reticulum abundantly expressed during embryogenesis whose gene disruption in the brain leads to neuroblast cell demise and neuromorphological alterations due to increased free radical levels. To determine the potential contribution of SELENOT to the establishment of cortical networks, we first analyzed its expression profile in the neocortex at different stages of development using RNA scope <em>in situ</em> hybridization. These studies revealed the expression of SELENOT in different cortical layers, and its localization in glutamatergic and GABAergic neurons. Targeted SELENOT gene knockout in the cortex using <em>in utero</em> electroporation-mediated gene disruption or Nes-Cre/loxP transgenesis system resulted in an alteration of neuroblast migration polarity, at the level of radial scaffolding, and projection neuron positioning. These results indicate that SELENOT which is highly expressed in the cortex during neurodevelopment plays a crucial role in corticogenesis by promoting projection neuron migration.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 323-334"},"PeriodicalIF":2.8,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145046488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of electro-acupuncture on motor dysfunction in middle cerebral artery occlusion/reperfusion rats though cortex-striatum somatostatin neural circuit 电针通过皮层-纹状体生长抑素神经回路对大脑中动脉闭塞/再灌注大鼠运动功能障碍的影响。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-09 DOI: 10.1016/j.neuroscience.2025.09.012

Yi Zheng , Wenju Wang , Sijia Xia , Tao Jiang , Rui Li , Minguang Yang , Weilin Liu , Lidian Chen , Jing Tao

{"title":"Effect of electro-acupuncture on motor dysfunction in middle cerebral artery occlusion/reperfusion rats though cortex-striatum somatostatin neural circuit","authors":"Yi Zheng , Wenju Wang , Sijia Xia , Tao Jiang , Rui Li , Minguang Yang , Weilin Liu , Lidian Chen , Jing Tao","doi":"10.1016/j.neuroscience.2025.09.012","DOIUrl":"10.1016/j.neuroscience.2025.09.012","url":null,"abstract":"<div><div>Ischemic stroke caused motor dysfunction results poses substantial health burdens and socioeconomic challenges. Electro-acupuncture (EA) at the acupoints of Quchi (LI11) and Zusanli (ST36) has shown positive efficacy in motor dysfunction after stroke. Considering the reported functions of the GABAergic system in locomotion, the present study aims to investigate the detailed mechanism of EA effects on motor regulation, focusing on the neural histological and chemical changes in the GABAergic system. Results demonstrated that EA at LI11 and ST36 improved the modified neurological severity score (mNNS) score and motor function of MCAO/R rats. EA at LI11 and ST36 also prompted γ-aminobutyric acid-ergic (GABAergic) system by the expression of GABA related receptors and GABA interneurons. Here, We have identified long-range projecting GABAergic interneurons, which can be classified into different subtypes based on the molecular markers they express: Parvalbumin (PV+), Somatostatin (SST+), and Vasoactive Intestinal Peptide (VIP+). Additionally, optogenetic stimulation of this projecting neurons can improve the motor dysfunction of MCAO/R rats. Notably, cortex M1-striatum (CS)-SST neural circuit which showed an indescribable role in locomotion improvement under EA intervention. The downregulation of the type II dopamine receptor in medium-sized spiny neurons (DR2-MSNs) and the upregulation of Synaptophysin (SYN) and Postsynaptic Density-95 (PSD95) suggest that MSNs and synaptic plasticity might be the downstream mechanisms of EA treatment at LI11 and ST36. To conclude, EA at LI11 and ST36 can promote synaptic plasticity and improve motor function by targeting and regulate downregulated DR2-MSNs neurons through the CS-SST neural circuit.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 262-278"},"PeriodicalIF":2.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evaluating the stress system of the grieving brain: corticotropin-releasing factor receptors and partner loss in coyotes (Canis latrans) 评估悲伤大脑的应激系统：促肾上腺皮质激素释放因子受体和土狼的伴侣损失。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-09 DOI: 10.1016/j.neuroscience.2025.07.049

Rachel Tong , Sara M. Freeman

{"title":"Evaluating the stress system of the grieving brain: corticotropin-releasing factor receptors and partner loss in coyotes (Canis latrans)","authors":"Rachel Tong , Sara M. Freeman","doi":"10.1016/j.neuroscience.2025.07.049","DOIUrl":"10.1016/j.neuroscience.2025.07.049","url":null,"abstract":"<div><div>Forming social bonds is fundamental in helping us foster connections with others. The loss of a loved one often results in grief, stress, and loneliness, and the stress response system of the body has been implicated in the physiological symptoms associated with grieving. Corticotropin releasing factor (CRF) is the hormone that initiates the stress response in the body and acts at two different receptor subtypes CRF receptor (CRFR)1 and CRFR2. Many studies on CRF and social loss have been conducted in monogamous prairie voles, but studies in longer-lived monogamous mammals could improve understanding of the effects of losing pair bonds. A monogamous mating system and stable pair bonding behavior exhibited by coyotes (<em>Canis latrans</em>) make them an appropriate animal model to study social bonds and social loss. Our goal of this larger study was to map CRFR1 and CRFR2 in the coyote brain using a competitive binding approach and to quantify CRFR levels in both widowed and paired female coyotes, allowing us to determine if CRFRs densities changed in response to partner loss. The results of our mapping study showed that the olfactory system, hippocampus, and amygdala were sites of action of CRFRs. Region-specific differences in CRFR1 and CRFR2 binding were observed after partner loss. Specifically, elevated CRFR1 and CRFR2 binding were detected in widows in the olfactory bulb and olfactory tubercle respectively, suggesting a potential role of the olfactory system in regulating the brain’s response to social loss in coyotes.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"584 ","pages":"Pages 412-417"},"PeriodicalIF":2.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033705","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reinforcement learning at the interface of artificial intelligence and cognitive science 强化学习在人工智能和认知科学的接口。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-09 DOI: 10.1016/j.neuroscience.2025.09.004

Tursun Alkam, Ebrahim Tarshizi, Andrew H. Van Benschoten

{"title":"Reinforcement learning at the interface of artificial intelligence and cognitive science","authors":"Tursun Alkam, Ebrahim Tarshizi, Andrew H. Van Benschoten","doi":"10.1016/j.neuroscience.2025.09.004","DOIUrl":"10.1016/j.neuroscience.2025.09.004","url":null,"abstract":"<div><div>Reinforcement learning (RL) is a computational framework that models how agents learn from trial and error to make sequential decisions. Rooted in behavioural psychology, RL has become central to artificial intelligence and is increasingly applied in healthcare to personalize treatment strategies, optimize clinical workflows, guide robotic surgery, and adapt neurorehabilitation. These same properties, learning from outcomes in dynamic and uncertain environments, make RL a powerful lens for modelling human cognition. This review introduces RL to neuroscientists, clinicians, and psychologists, aiming to bridge artificial intelligence and brain science through accessible terminology and clinical analogies. We first outline foundational RL concepts and explain key algorithms such as temporal-difference learning, Q-learning, and policy gradient methods. We then connect RL mechanisms to neurobiological processes, including dopaminergic reward prediction errors, hippocampal replay, and frontostriatal loops, which support learning, planning, and habit formation. RL’s incorporation into cognitive architectures such as ACT-R, SOAR, and CLARION further demonstrates its utility in modelling attention, memory, decision-making, and language. Beyond these foundations, we critically examine RL’s capacity to explain human behaviour, from developmental changes to cognitive biases, and discuss emerging applications of deep RL in simulating complex cognitive tasks. Importantly, we argue that RL should be viewed not only as a modelling tool but as a unifying framework that highlights limitations in current methods and points toward new directions. Our perspective emphasizes hybrid symbolic–subsymbolic models, multi-agent RL for social cognition, and adaptive healthcare applications, offering a roadmap for interdisciplinary research that integrates computation, neuroscience, and clinical practice.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 289-312"},"PeriodicalIF":2.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endocrine circuitry in autism spectrum disorders: A systematic review of mechanistic insights and clinical implications 自闭症谱系障碍的内分泌回路：机制见解和临床意义的系统综述。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-09 DOI: 10.1016/j.neuroscience.2025.09.009

Maria Angelopoulou , Panayiotis Siaperas , Sarantis Livadas , Elina Karantana , Dimitrios T. Papadimitriou , Nikolaos Angelopoulos

{"title":"Endocrine circuitry in autism spectrum disorders: A systematic review of mechanistic insights and clinical implications","authors":"Maria Angelopoulou , Panayiotis Siaperas , Sarantis Livadas , Elina Karantana , Dimitrios T. Papadimitriou , Nikolaos Angelopoulos","doi":"10.1016/j.neuroscience.2025.09.009","DOIUrl":"10.1016/j.neuroscience.2025.09.009","url":null,"abstract":"<div><div>The increasing global prevalence of Autism Spectrum Disorder (ASD) diagnoses—largely driven by heightened awareness, evolving diagnostic criteria, and improved detection—has intensified efforts to elucidate its complex neurobiological underpinnings, although the true change in occurrence remains uncertain.</div><div>While much attention has been paid to genetic and neurodevelopmental factors, emerging evidence highlights the crucial role of the endocrine system in modulating social, cognitive, and behavioral outcomes associated with ASD.</div><div>To systematically review the existing literature on endocrine dysfunction and hormonal signaling pathways implicated in ASD, with the aim of identifying common mechanistic links and evaluating their clinical relevance.A comprehensive literature search was conducted across PubMed, Scopus, and Google Scholar for studies published between 1980 and 2024.</div><div>The review included 183 human studies evaluating associations between ASD and hormonal alterations, encompassing thyroid function, HPA axis dysregulation, growth hormone signaling, sex hormones, obesity, melatonin, oxytocin, vitamin D status, and exposure to endocrine-disrupting chemicals.</div><div>Alterations in multiple endocrine axes were consistently associated with ASD, including prenatal thyroid imbalances, cortisol rhythm dysregulation, aberrant IGF-1 levels, elevated fetal steroidogenic activity, and impaired oxytocin signaling.</div><div>Endocrine disruptors such as phthalates and pesticides were also linked to increased ASD risk in susceptible populations.</div><div>Endocrine dysfunctions are frequently associated with ASD, with multiple hormonal axes potentially influencing its pathophysiology, although causality remains unconfirmed. Understanding hormonal influences across developmental stages could inform early detection strategies and novel therapeutic approaches.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 351-366"},"PeriodicalIF":2.8,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145040885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The untapped potential of opportunistic neuroscience models (Invited commentary on “Evaluating the stress system of the grieving brain: corticotropin-releasing factor receptors and partner loss in coyotes (Canis latrans)) 机会主义神经科学模型尚未开发的潜力（特邀评论“评估悲伤大脑的压力系统：促肾上腺皮质激素释放因子受体和土狼（Canis latrans）的伴侣损失”）。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-09 DOI: 10.1016/j.neuroscience.2025.08.036

Peter F. Cook

引用次数: 0

Prediction of microRNAs targeting oestrogen receptor beta: implications for emotional disorders 预测靶向雌激素受体的microrna：对情绪障碍的影响

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-08 DOI: 10.1016/j.neuroscience.2025.09.011

Daniel Kalinowski, Magdalena Zielińska

{"title":"Prediction of microRNAs targeting oestrogen receptor beta: implications for emotional disorders","authors":"Daniel Kalinowski, Magdalena Zielińska","doi":"10.1016/j.neuroscience.2025.09.011","DOIUrl":"10.1016/j.neuroscience.2025.09.011","url":null,"abstract":"<div><div>This review consolidates the most recent information regarding the role of microRNAs (miRNAs) that target the oestrogen receptor beta (<em>ESR2</em>/ERβ) gene in the pathophysiology of emotional disorders, with a particular emphasis on stress-related conditions and anxiety. Since in silico predictions frequently precede experimental validation and algorithms such as TargetScan and DIANA-microT identified possible miRNA binding sites on <em>ESR2</em> based on sequence complementarity, we demonstrate a high degree of accuracy in predicting functional interactions. Parallel evidence unrelated to the studied biological contexts supports the idea that miRNAs may regulate ERβ signalling in emotional disorders, thereby further supporting miRNA-<em>ESR2</em> interactions. Moreover, the differential expression of circulating miRNAs in clinical conditions has the potential to elucidate underlying mechanisms and serve as biomarkers for anxiety and stress-related disorders, despite scarce studies directly identifying circulating miRNAs targeting ERβ. This review compiles the available data on emotional disorders, miRNAs, and <em>ESR2</em>, highlighting their potential interactions and advocating for the expansion of research to uncover new insights into the molecular underpinnings of these conditions.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 213-221"},"PeriodicalIF":2.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145020231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

10-Hz tACS counteracts PASAT-related suppression of alpha power: A pilot study 10hz tACS抵消pasat相关的α功率抑制：一项试点研究。

IF 2.8 3区医学

Neuroscience Pub Date : 2025-09-08 DOI: 10.1016/j.neuroscience.2025.09.006

Anai Gonzalez-Ramirez , Jorge Gutierrez , Jörn Rickert , Elias Manjarrez

{"title":"10-Hz tACS counteracts PASAT-related suppression of alpha power: A pilot study","authors":"Anai Gonzalez-Ramirez , Jorge Gutierrez , Jörn Rickert , Elias Manjarrez","doi":"10.1016/j.neuroscience.2025.09.006","DOIUrl":"10.1016/j.neuroscience.2025.09.006","url":null,"abstract":"<div><div>Although it is well known that the amplitude of electroencephalographic (EEG) alpha waves typically decreases during cognitive tasks, no studies have examined whether this attenuation can be modulated with external interventions. In this pilot study, we investigated whether transcranial alternating current stimulation (tACS) at a fixed frequency of 10 Hz could counteract task-related alpha suppression in 10 participants receiving experimental (verum) stimulation and 8 participants receiving sham stimulation. As expected, a mental task involving the Paced Auditory Serial Addition Test (PASAT) significantly reduced alpha power. However, after 10 min of 1 mA 10 Hz tACS, we observed a significant partial reversal of this attenuation (Group × Time: F(1,14) = 8.06, p = 0.013, η<sup>2</sup>p = 0.37), even as participants continued the task. In contrast, the sham control group showed no significant change. Consistently, PASAT behavioral accuracy improved after 10 Hz tACS (t(9) = 4.89, p = 0.0009, dz = 1.55), but not in the sham condition. In conclusion, these pilot findings demonstrate that 10 Hz tACS can counteract alpha power suppression and enhance cognitive performance during a demanding arithmetic task, warranting replication in larger and more diverse samples to confirm generalizability and clinical potential</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"585 ","pages":"Pages 279-288"},"PeriodicalIF":2.8,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0