Behavioural Brain Research最新文献

{"title":"Corrigendum to \"Behavioral characterization of bulbar sensorimotor function in a rat model of Alexander disease\" [Behav. Brain Res. 514 (2026) 116359].","authors":"Jared S Cullen, John A Russell, Cynthia A Kelm-Nelson, John C Szot, Albee Messing, Tracy L Hagemann, Nadine P Connor","doi":"10.1016/j.bbr.2026.116412","DOIUrl":"10.1016/j.bbr.2026.116412","url":null,"abstract":"","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116412"},"PeriodicalIF":2.9,"publicationDate":"2026-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148688467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of Concern: \"Pharmacological activation of the Nrf2 pathway by 3H-1, 2-dithiole-3-thione is neuroprotective in a mouse model of Alzheimer disease'' [BBR, 336 (2018) pp 219-226].","authors":"","doi":"10.1016/j.bbr.2026.116388","DOIUrl":"10.1016/j.bbr.2026.116388","url":null,"abstract":"","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":"514 ","pages":"116388"},"PeriodicalIF":2.9,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148719916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Moderated mediation of cerebrospinal fluid fibroblast growth factor 21 and KLB rs17618244 genotype in the association between educational attainment and cognitive function.","authors":"Jianxia Lin, Lidong Su, Xiaoyu Yang, Danyang Zhao, Xingguang Luo, Lei Hao, Yanlong Liu, Fan Wang","doi":"10.1016/j.bbr.2026.116458","DOIUrl":"https://doi.org/10.1016/j.bbr.2026.116458","url":null,"abstract":"<p><strong>Background: </strong>Although educational attainment influences both cognitive function and metabolic regulation, the biological mechanisms underlying this relationship remain unclear. This study investigated whether cerebrospinal fluid fibroblast growth factor 21 (CSF FGF21) mediates the association between educational attainment and cognitive function, and whether this pathway is moderated by the KLB rs17618244 genotype.</p><p><strong>Methods: </strong>A total of 186 participants were included in this cross-sectional study. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), and CSF FGF21 levels were measured. Genotyping of the KLB rs17618244 variant was performed using MassARRAY single nucleotide polymorphism genotyping technology. Mediation and moderated mediation analyses were conducted using the PROCESS macro.</p><p><strong>Results: </strong>CSF FGF21 significantly mediated the association between educational attainment and cognitive function (β = 0.02, 95% CI: 0.0003 to 0.0526). Moderated mediation analysis further indicated that the KLB rs17618244 genotype significantly moderated this indirect pathway (Index = -0.05, 95% CI: -0.1219 to -0.0002). Specifically, the indirect protective effect of educational attainment on cognitive function through CSF FGF21 was significant only among AA/AG carriers (Effect = 0.05, 95% CI: 0.0060 to 0.1205), but not among GG carriers.</p><p><strong>Conclusion: </strong>In this cross-sectional study, CSF FGF21 statistically accounted for part of the association between educational attainment and cognitive function, particularly among KLB rs17618244 AA/AG carriers.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116458"},"PeriodicalIF":2.9,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From diet to drinking behavior: ketogenic diet decreases ethanol intake in young adult female mice.","authors":"Laura Torres-Rubio, Susana Mellado, Sandra Montagud-Romero, María Pascual, Marta Rodríguez-Arias","doi":"10.1016/j.bbr.2026.116465","DOIUrl":"https://doi.org/10.1016/j.bbr.2026.116465","url":null,"abstract":"<p><p>The normalization of ethanol consumption in Western societies represents a major public health concern, particularly when drinking begins during adolescence. The ketogenic diet (KD) has demonstrated therapeutic potential in various conditions, including substance use disorders. This, together with evidence showing that the diet does not significantly affect locomotor activity or aversive and spatial memory in adolescent male mice, makes it an interesting tool for addressing ethanol consumption during a critical developmental period: the transition from adolescence to young adulthood. However, the lack of evidence in females highlights an important gap in current research. This study aimed to evaluate the effects of a KD during adolescence on behavioral profile and ethanol consumption during young adulthood in female OF1 mice. In Experiment 1, behavioral profile was assessed after administration of a KD or control diet from postnatal day (PND) 25 to PND 48. Motor activity, anxiety-like behavior, memory, and learning were evaluated. In Experiment 2, ethanol consumption was assessed using the Drinking in the Dark and operant self-administration paradigms following dietary intervention from PND 39 to PND 82. The KD did not alter locomotion, anxiety-like behavior, or aversive memory, but enhanced hippocampus-dependent spatial memory. Molecular analyses revealed changes in gene expression, including Adora2a, Opmr1, Drd1, Cnr1, and Il-6. Additionally, KD significantly reduced ethanol consumption, which was associated with altered expression of Crhr1, Drd2, Adora2a, and Adora1. These findings support the potential of KD as a therapeutic strategy for reducing ethanol intake in females without negatively impacting behavioral development during adolescence.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116465"},"PeriodicalIF":2.9,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular Vesicles in Neurodegenerative Diseases: A New Frontier in Diagnosis and Therapy.","authors":"Suleiman Ibrahim Mohammad, Asokan Vasudevan, Ghaleb Oriquat, Tushar B Gajjar, Malathi Hanumanthayya, Sandeep Kumar Shukla, Navin Kumar Tailor, Mirza R Baig, Omar Fadaam, Amir S Abdul","doi":"10.1016/j.bbr.2026.116455","DOIUrl":"https://doi.org/10.1016/j.bbr.2026.116455","url":null,"abstract":"<p><p>Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease are among the progressive disorders of the nervous system that are characterized by the gradual destruction of neurons, the accumulation of misfolded proteins, and the limited effective therapeutic options. In recent years, numerous lines of evidence have emphasized the important role of extracellular vesicles (EVs) in the formation and progression of these diseases. These vesicles are membrane-bound nanoscale structures that are secreted by almost all cell types and play a role in cell-cell communication through the transfer of molecules such as proteins, lipids, and nucleic acids. In neurodegenerative disorders, EVs can facilitate the transport and dissemination of disease-related proteins, including amyloid-β, tau, α-synuclein, mutant huntingtin, SOD1, and TDP-43, thus contributing to the spread of pathological processes in different parts of the nervous system. On the other hand, the ability of these vesicles to cross the blood-brain barrier and reflect molecular changes occurring in the central nervous system makes them valuable candidates for the development of minimally invasive biomarkers. This review reviews the biogenesis, classification, isolation methods, and molecular content of EVs, and analyzes their role in the pathogenesis, diagnosis, and treatment of the most important neurodegenerative diseases. Also, the importance of EV-associated proteins, RNAs, and lipids as emerging diagnostic biomarkers, as well as the therapeutic potential of natural and engineered vesicles as drug delivery systems and regulators of neuroinflammation and neurodegenerative processes, is discussed.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116455"},"PeriodicalIF":2.9,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Levetiracetam in Stroke: A Narrative Review of Neuroprotective Mechanisms and Therapeutic Potential.","authors":"Seyed Hesam Hojjat, Fatemeh Rasouli, Sonia Fathi-Karkan","doi":"10.1016/j.bbr.2026.116454","DOIUrl":"https://doi.org/10.1016/j.bbr.2026.116454","url":null,"abstract":"<p><strong>Background: </strong>Stroke remains of the leading causes of mortality/long-term disability worldwide, with post-stroke seizures and secondary neuronal injury contributing to unfavorable outcomes. Levetiracetam (LEV), the widely used antiepileptic drug in clinical practice, has demonstrated neurobiological effects beyond seizure control in experimental models, raising interest in its potential role in stroke-related neuroprotection and neurological recovery.</p><p><strong>Objective: </strong>To synthesize experimental and clinical evidence on LEV in stroke, focusing on (i) preclinical neuroprotective mechanisms and outcomes and (ii) clinical outcomes in stroke populations, particularly post-stroke seizure management and safety.</p><p><strong>Methods: </strong>We conducted a narrative review informed by a comprehensive literature search of major biomedical databases (PubMed/MEDLINE, Scopus, Web of Science Core Collection, Embase, and Google Scholar) from 2001-2025, and eligible studies included preclinical stroke models evaluating LEV and clinical studies involving LEV use in stroke patients. Study selection and data extraction were performed using predefined criteria and risk of bias was further assessed using standardized tools. Due to heterogeneity in stroke models, patient populations, interventions, and outcomes, findings were synthesized narratively and summarized in structured tables.</p><p><strong>Results: </strong>The preclinical literature suggests that LEV may reduce infarct volume and improve neurological outcomes in several ischemic and hemorrhagic stroke models. Reported mechanisms include modulation of neuroinflammatory signaling, attenuation of apoptosis, reduced oxidative stress, and preservation of blood-brain barrier integrity, although methodological limitations and incomplete reporting contribute to uncertainty across studies. In clinical studies, the most consistent evidence supports LEV use for post-stroke seizure treatment and prevention, with generally favorable tolerability compared with older antiepileptic drugs. However, direct clinical evidence supporting LEV as a neuroprotective therapy to improve stroke lesion outcomes or long-term functional recovery remains limited and indirect.</p><p><strong>Conclusions: </strong>Experimental data support biologically plausible neuroprotective effects of LEV in stroke models, while clinical evidence primarily supports its role in post-stroke seizure management and tolerability. The potential for LEV to modify stroke-related neurological injury in humans remains uncertain and requires well-designed clinical trials with stroke-specific neuroprotection endpoints.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116454"},"PeriodicalIF":2.9,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Buspirone attenuates neuropathic pain and related depression following sciatic nerve injury in mice: Role of opioid receptors.","authors":"Behnam Ghorbanzadeh, Ali Foroughinia, Reza Notash, Amir Mashayekhi, Soheila Alboghobeish, Kosar Gholamiyan","doi":"10.1016/j.bbr.2026.116456","DOIUrl":"10.1016/j.bbr.2026.116456","url":null,"abstract":"<p><p>Patients with neuropathic pain also experience depression. Although they are treated with various therapies, the effectiveness of these medications is unclear. In the present study, the effect of buspirone on allodynia and depressive-like behavior caused by chronic constriction injury (CCI) of the sciatic nerve, as well as the role of opioid pathways, was investigated. Our findings showed that acute and sub-chronic administration of buspirone (0.3-10 mg/kg) attenuated the mechanical and cold allodynia induced by CCI. In addition, a moderate dose of buspirone (1 mg/kg), but not a high dose (10 mg/kg), reduced the depressive-like behavior induced by CCI. Furthermore, pretreatment with naloxone attenuated the effects of buspirone, whereas co-administration with an ineffective dose of morphine potentiated its action. Also, hippocampal μ-opioid receptor mRNA was decreased, whereas κ-opioid receptor mRNA was increased in CCI mice 14 days after surgery. However, repeated buspirone in CCI-mice mitigated the observed alteration in opioid receptors mRNA expression. In addition, unlike morphine, buspirone did not produce tolerance or withdrawal symptoms following repeated administration. Collectively, these data provide evidence that buspirone can effectively alleviate neuropathic pain and exerts antidepressant-like benefits, potentially through modulation of opioid receptors. Moreover, the effects of buspirone may also be associated with changes in mRNA expression of μ-and κ-opioid receptors in the hippocampus.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116456"},"PeriodicalIF":2.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Why the body matters in major depressive disorder: Neuroimaging findings of somatic symptoms and ongoing challenges.","authors":"Weiyan Wang, Xiang Wang","doi":"10.1016/j.bbr.2026.116457","DOIUrl":"10.1016/j.bbr.2026.116457","url":null,"abstract":"<p><p>With growing recognition that somatic symptoms constitute a clinically significant yet underexplored dimension of major depressive disorder (MDD), symptoms including sleep disturbances, gastrointestinal discomfort, pain, appetite changes, and fatigue have attracted increasing research attention. These symptoms are not only highly prevalent but are also closely associated with poor prognosis, treatment resistance, and elevated suicide risk. In this context, neuroimaging studies of the somatic manifestations of MDD have provided critical insights to advance precision diagnosis and individualized intervention. This review comprehensively integrates functional and structural neuroimaging findings on discrete somatic symptoms and somatic symptom clusters in MDD. It identifies the specific neural circuit abnormalities associated with individual symptom domains while elucidating shared pathophysiological mechanisms across symptom types, including disrupted interoceptive processing, pathological default mode network activity, and impaired sensory gating. On this basis, the review discusses the therapeutic and predictive implications of these findings and proposes future research directions oriented toward network-based brain-symptom mapping, transdiagnostic and longitudinal designs, and multimodal multilevel integration. By synthesizing existing evidence, this review provides a framework for understanding the neural substrates of somatic symptoms in MDD, developing somatic phenotype-based biomarkers and targeted neuromodulation therapies, and integrating systems-level neuroimaging into precision psychiatry to advance biologically informed diagnosis/treatment.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116457"},"PeriodicalIF":2.9,"publicationDate":"2026-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manual asymmetries and cortical modulation: relationships between motor control and interhemispheric connectivity.","authors":"Lidiane Aparecida Fernandes, Tércio Apolinário-Souza, Lucas Eduardo Antunes Bicalho, Marco Antonio Cavalcanti Garcia, Guilherme Menezes Lage","doi":"10.1016/j.bbr.2026.116449","DOIUrl":"10.1016/j.bbr.2026.116449","url":null,"abstract":"<p><p>Manual asymmetries in goal-directed aiming have been linked to interhemispheric interactions, yet it remains unclear whether experimentally modulating hemispheric activity alters both motor behavior and interhemispheric functional coupling. We investigated how bilateral transcranial direct current stimulation (tDCS) targeting primary motor cortices modulates manual asymmetries and interhemispheric connectivity during aiming. Twelve healthy right-handed male adults completed a protocol comprising three sessions: dominant hemisphere inhibition (DHI; cathode over C3/anode over C4), non-dominant hemisphere inhibition (NDHI; cathode over C4/anode over C3), and sham stimulation. In each session, participants performed a goal-directed aiming task with both hands before and after 20 min of tDCS. Behavioral outcomes included reaction time, movement time, response time, spatial accuracy (radial error), kinematic (peak velocity; relative time to peak velocity), and online control indices (number of discontinuities and first submovement error). EEG was recorded continuously, and interhemispheric coupling between motor regions was quantified in the high-alpha band during preparation and execution phases. tDCS produced selective behavioral effects, including condition-dependent changes in reaction time and response-time asymmetry, modulation of relative time to peak velocity, and increased movement discontinuities under DHI compared with sham, while movement time and several accuracy metrics showed minimal change. Interhemispheric coupling during preparation was largely unchanged; however, during execution, a robust Condition × Hand interaction emerged, with NDHI increasing coherence changes and coherence asymmetry relative to DHI. These findings suggest that bilateral tDCS can differentially shape interhemispheric functional coupling during movement execution and modulate specific temporal/kinematic components of aiming, with limited impact on overall movement time and endpoint accuracy.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116449"},"PeriodicalIF":2.9,"publicationDate":"2026-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148879126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bovine lactoferrin can reduce Aβ /TAU accumulation in two major pathological Alzheimer's disease rat models.","authors":"Sedanur Kılınç, Şenay Görücü Yılmaz, Ahmet Sarper Bozkurt, Sibel Oğuzkan Balcı","doi":"10.1016/j.bbr.2026.116453","DOIUrl":"10.1016/j.bbr.2026.116453","url":null,"abstract":"<p><strong>Introduction: </strong>Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline. Bovine lactoferrin (bLf) is an iron-binding protein with immunomodulatory effects both in the intestine and throughout the body. In this study, the potential therapeutic effects of bLf were evaluated using two different rat models that mimic key aspects of AD pathology.</p><p><strong>Method: </strong>Forty-two female Wistar albino rats (10-12 weeks old, weighing 200-250 g) were included in the study and randomly assigned to 7 groups of 6 rats each. The groups were: 1- Control, 2- Phosphate-buffered saline (PBS), 3- bLf, 4- Colchicine (COL) (for the TAU model), 5- Okadaic acid (OKA) (for the Aβ model), 6- COL + bLf, 7- OKA + bLf. Cognitive deficits were tested using the Morris Water Maze (MWM). Motor coordination and anxiety levels were assessed using the OFT. Following these assessments, cerebrospinal fluid (CSF), hippocampal tissue, serum, and whole blood samples were collected. Aβ, TAU, Ferritin, TAS, and TOS levels in these samples were measured using ELISA. For genetic modulation, the gene expression patterns of Fpn, Bax, Bcl-2, p38, FoxO, and GSK-3β were analyzed by quantitative Real-Time PCR (qRT-PCR).</p><p><strong>Results: </strong>bLf reduced oxidative stress. Decreases in Aβ and TAU levels were observed in the hippocampus and CSF. Ferritin levels were relatively lower in the hippocampus, CSF, and serum. Fpn and Bcl-2 were downregulated in the hippocampus of AD models but upregulated after bLf treatment. Expression levels of Bax, p38, FoxO, and GSK-3β were also downregulated following bLf administration.</p><p><strong>Conclusion: </strong>These findings were consistent across both models. Overall, bLf holds promise as a therapeutic candidate capable of simultaneously targeting two key pathological features of AD.</p>","PeriodicalId":8823,"journal":{"name":"Behavioural Brain Research","volume":" ","pages":"116453"},"PeriodicalIF":2.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"心理学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}