Neuroscience最新文献

{"title":"Longitudinal brain-wide recordings reveal early neurophysiological alterations in memory-impaired mice","authors":"Abdelrahman B.M. Eldaly ,&nbsp;Stephen K. Agadagba ,&nbsp;Antara Verma ,&nbsp;Kongyan Li ,&nbsp;Lee Wei Lim ,&nbsp;Leanne Lai-Hang Chan","doi":"10.1016/j.neuroscience.2025.12.035","DOIUrl":"10.1016/j.neuroscience.2025.12.035","url":null,"abstract":"<div><div>Scopolamine, a muscarinic receptor antagonist, is widely utilized to pharmacologically model Alzheimer’s disease (AD) due to its ability to mimic cholinergic deficits and induce memory impairments. Despite its common use in investigating behavioral and cognitive impairments in memory deficit animal models, the longitudinal brain-wide electrophysiological alterations associated with scopolamine administration remain largely unexplored. This study integrated electrophysiological and behavioral analyses to investigate scopolamine-induced cognitive deficits in mice. Using a 16-channel intracranial electroencephalography (iEEG) array, we tracked brain-wide oscillatory changes and functional connectivity over 6 weeks during memory task-related and task-free activities. The mouse’s pre-attentive sensory memory was assessed by auditory evoked potentials (AEPs) within the passive oddball mismatch negativity (MMN) paradigm, and the mouse’s spatial working memory was further evaluated using a Y-maze spontaneous alternation task. The auditory MMN responses indicated significant sensory discrimination impairments from Week 2 onward, and spontaneous theta oscillations demonstrated widespread disruptions by Week 3. Concurrently, scopolamine degraded the animal’s Y-maze successful alternation rates. The decline in alternation performance was correlated with the observed electrophysiological alterations, revealing the progressive impact of scopolamine on cognitive and neural functions. Furthermore, this study identified early electrophysiological biomarkers of brain functional network changes associated with memory impairments, in which functional connectivity abnormalities were observed from the first week of scopolamine administration, suggesting they have diagnostic potential in preclinical AD research. By bridging behavioral outcomes with brain-wide iEEG metrics, this work emphasizes the translational relevance of scopolamine models for understanding AD-like pathology and evaluating therapeutic interventions.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 93-111"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804835","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}

{"title":"D-galactose administration via semicircular canal induces accelerated cochlear aging: A novel model of oxidative stress-mediated presbycusis","authors":"Chunli Zhao ,&nbsp;Zijing Yang ,&nbsp;Zhongrui Chen ,&nbsp;Ke Liu ,&nbsp;Zhengde Du ,&nbsp;Shusheng Gong","doi":"10.1016/j.neuroscience.2025.12.052","DOIUrl":"10.1016/j.neuroscience.2025.12.052","url":null,"abstract":"<div><div>Age-related hearing loss (ARHL) is a progressive, bilateral sensorineural impairment with significant socio-psychological consequences. Current ARHL models (natural aging or systemic D-galactose (D-gal) injection) face limitations: prolonged timelines, high variability, and inconsistent D-gal protocols. To concentrate aging pathology within the peripheral auditory system, we developed a novel accelerated cochlear aging model by targeted delivery of D-gal via the posterior semicircular canal. This approach aimed to concentrate aging pathology within the peripheral auditory system. Auditory brainstem response testing was employed to assess murine hearing thresholds for determining optimal D-gal concentration and exposure duration. Results demonstrated that by post-administration day 14, the D-gal-H group exhibited pronounced auditory characteristics consistent with ARHL. Morphological staining further revealed significant outer hair cells loss and ribbon synapses degeneration. Concurrently, immunohistochemical analysis of 4-HNE and 8-OHdG showed elevated oxidative stress levels in the stria vascularis, spiral ganglion cells, and inner hair cells of D-gal-treated groups. Substantial alterations in aging-associated proteins were also observed. Mitochondrial membrane potential assessment indicated significant depolarization in treated cochleae. Accordingly, we established a rapid, targeted, and pathologically validated model of cochlear aging, which provides a valuable tool for investigating the mechanisms underlying peripheral auditory aging.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 187-195"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145804780","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}

{"title":"Bone-brain crosstalk: emerging roles of osteocalcin in central nervous system disorders","authors":"Hui Chen ,&nbsp;Zhaoxia Zhang ,&nbsp;Wenjin Yi ,&nbsp;Nan Wang ,&nbsp;Xuan Dong ,&nbsp;Ying Xing ,&nbsp;Qingquan Liu ,&nbsp;Yumei Wu ,&nbsp;Xue Ma","doi":"10.1016/j.neuroscience.2025.12.028","DOIUrl":"10.1016/j.neuroscience.2025.12.028","url":null,"abstract":"<div><div>Despite significant advancements in understanding the pathogenesis of various central nervous system (CNS) disorders, challenges remain in the early intervention and targeted therapies for common neurodegenerative and psychiatric conditions such as Parkinson’s disease (PD), Alzheimer’s disease (AD), anxiety, depression, and strokes. Recent studies have increasingly focused on the interaction between the peripheral and central nervous systems, emphasizing the regulatory influence of peripheral mechanisms on CNS disorders. This evolving perspective paves the way for innovative treatment strategies for CNS diseases, with the bone-brain axis emerging as a key regulatory pathway. This axis was first systematically proposed to highlight the role of bone-derived hormones in brain function. Importantly, bone tissue extends its functions beyond mere structural support and movement; it secretes molecules like osteocalcin (OCN) that influence neuronal and glial cell activities. This interaction is vital for regulating multiple CNS processes, including mood, cognition, inflammation, and the formation and differentiation of myelin. Upon release from bone tissue, OCN enters the bloodstream and affects peripheral organs via the Gprc6a receptor, while also crossing the blood–brain barrier to interact with receptors such as Gpr158 and Gpr37 in specific brain areas. This intra-brain interaction significantly impacts the progression and prognosis of various CNS disorders. This article undertakes a comprehensive analysis of OCN modulation in CNS disorders and its underlying mechanisms, laying the groundwork for further exploration of its clinical applications and suggesting new research avenues and therapeutic strategies for CNS diseases.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 1-8"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145757134","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}

{"title":"Characterization of the expression and function of schizophrenia risk gene Dtnbp1 in the suprachiasmatic nucleus","authors":"Genavieve Elizabeth Maloney ,&nbsp;Marie-Ève Cloutier ,&nbsp;Micah Joseph Provost ,&nbsp;Lalit K. Srivastava ,&nbsp;Nicolas Cermakian","doi":"10.1016/j.neuroscience.2025.12.029","DOIUrl":"10.1016/j.neuroscience.2025.12.029","url":null,"abstract":"<div><div>Schizophrenia (SZ) is a debilitating neurodevelopmental disorder with environmental and genetic origins. Circadian rhythm disruption is observed in a large proportion of patients with SZ. We previously found that Sandy (Sdy) mice, which carry a mutation in the SZ-associated gene <em>dystrobrevin binding protein 1</em> (<em>Dtnbp1,</em> also called <em>Dysbindin-1</em>), show altered rhythms of locomotor activity. To address the possible mechanisms underlying the circadian phenotype of these mice, we set out to address the expression and function of <em>Dtnbp1</em> in the suprachiasmatic nucleus (SCN), the location of the central circadian clock in mammals. Immunohistochemistry revealed that DTNBP1 protein was expressed throughout the SCN, with stronger expression in the dorsal part. DTNBP1 immunoreactive signal colocalized with neurons expressing either arginine vasopressin peptide (AVP) or vasoactive intestinal peptide (VIP). Fluorescent in situ hybridization showed a time-dependent variation of expression of <em>Dtnbp1</em> transcript, and confirmed its location in cell bodies of AVP- and VIP-expressing cells. Since DTNBP1 is known to be implicated in synaptic transmission, we studied the effect of <em>Dtnbp1</em> gene mutation on SCN neuropeptide expression and neuroanatomy in Sdy mice. There was no significant effect of the <em>Dtnbp1</em> mutation on AVP and VIP expression in the SCN. We then used transmission electron microscopy to study synaptic morphology and secretory vesicles. There was no effect of the <em>Dtnbp1</em> mutation on these neuroanatomical features. Our data show that <em>Dtnbp1</em> is expressed with a daily rhythm across the SCN, but that a loss-of-function mutation did not impair AVP or VIP neuropeptide expression nor general synaptic architecture.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 250-261"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145757170","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}

{"title":"Non-canonical role of DNA mismatch repair on sensory processing in mice","authors":"Sadia N. Rahman ,&nbsp;Demetrios Neophytou ,&nbsp;Siboney Oviedo-Gray ,&nbsp;Bao Q. Vuong ,&nbsp;Hysell V. Oviedo","doi":"10.1016/j.neuroscience.2025.12.066","DOIUrl":"10.1016/j.neuroscience.2025.12.066","url":null,"abstract":"<div><div>DNA repair mechanisms are essential for cellular development and function. In post-mitotic neurons, deficiencies in DNA damage response proteins can lead to severe neurodegenerative and neurodevelopmental disorders. One highly conserved factor involved in DNA repair is MutS Homolog 2 (<em>Msh2</em>), which is responsible for correcting base–base mismatches and insertion/deletion loops during cell proliferation. However, its role in mature neurons remains poorly understood. This study investigates the impact of <em>Msh2</em> loss on sensory processing in mice. Using electrophysiological and molecular assays, we identified<!--> <!-->significant deficits in cortical and thalamic sound processing in <em>Msh2^−/−</em> mice. These deficits were linked to dysfunction of the thalamic reticular nucleus (TRN), which critically regulates corticothalamic and thalamocortical activity. Our findings revealed increased oxidative damage, aberrant neuronal activity, and elevated parvalbumin (PV) expression in PV⁺ neurons in the TRN of <em>Msh2^−/−</em> mice. Additionally, we observed the presence of connexin plaques, indicating that disrupted gap junction formation may contribute to impaired TRN function. These results highlight <em>Msh2</em>′s crucial role in supporting PV⁺ neurons in the TRN, profoundly influencing sensory processing. This study provides new insight into how DNA repair mechanisms regulate neuronal development and function in a region-specific manner, potentially contributing to our understanding of their role in neurological disorders.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 59-72"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892917","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}

{"title":"Contextual & physiological markers for individual distress (CP-MIND). Brain health as a comprehensive framework for Mental-health equity","authors":"Juan Pablo Morales ,&nbsp;Fiorella Macchiavello ,&nbsp;Felipe Rojas-Thomas","doi":"10.1016/j.neuroscience.2025.12.034","DOIUrl":"10.1016/j.neuroscience.2025.12.034","url":null,"abstract":"<div><div>Socioeconomic disadvantage shapes brain–mind health by intensifying exposures, resource scarcity, nutritional insecurity, violence, and weak social support, which dysregulate stress and immune systems. These conditions promote allostatic overload, whereby adaptive stress responses become maladaptive, degrading neural circuits for cognitive control and emotion regulation. In parallel, the microbiota–gut–brain axis links contextual adversity and diet quality to inflammation, barrier dysfunction, and neuroendocrine perturbations that further compromise resilience. Converging evidence connects these biological disruptions to structural and functional brain differences and higher risks of depression, anxiety, stress-related syndromes, and later neurodegeneration. While some sociocultural adaptations may bolster cooperation and communal coping, chronic physiological strain undermines durable resilience. This integrative review advances a combined framework, contextual &amp; physiological markers for Individual distress, nested within a brain–mind health perspective, to organise how socioeconomic disadvantage-related exposures are embedded biologically via allostatic and microbiota–gut–brain axis pathways and manifest as social-cognitive difficulties and affective symptoms. We synthesise evidence across behaviour, neural systems, and systemic physiology to identify leverage points for intervention. Priorities include early multi-domain strategies that reduce chronic stressors; strengthen sleep, nutrition, and social cohesion; and test mechanistic interventions (e.g., allostatic regulation, psychobiotic or dietary modulation) within equity-focused, life-course designs. Understanding how contextual and physiological markers interact is essential for designing effective, scalable policies and clinical approaches that mitigate adversity’s neurobiological impact and reduce long-term disparities in brain–mind health.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 154-170"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800565","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}

{"title":"Functional analysis of glucocorticoid treatment associated astrocyte-proteins","authors":"Chuin Hau Teo ,&nbsp;Liau Ze Huai ,&nbsp;Ishwar S. Parhar ,&nbsp;Tomoko Soga","doi":"10.1016/j.neuroscience.2025.12.067","DOIUrl":"10.1016/j.neuroscience.2025.12.067","url":null,"abstract":"<div><div>Stress induces various neurobiological changes related to neurodegenerative diseases or mental disorders, including elevated neuronal dysfunction, neurotransmitter degradation and turnover. Astrocytes regulate synapses bidirectionally as neuroprotective glia. While glucocorticoids are generally well studied, specific cellular mechanisms require further investigation. Neuronal dysfunction characterized by changes in glucocorticoid signaling is associated with changes in astrocytes; however, very little is known about the impact of glucocorticoids on astrocyte-specific cellular reactions. We have analyzed protein expression patterns following dexamethasone treatment of normal human astrocyte cultures. Protein analysis of cortical astrocyte cultures treated with dexamethasone for 48 h using LCMS/MS identified 3 unique proteins with ≥ twofold change in expression in the cell lysate and cell culture medium. Clustering analysis associated with these protein expression changes is known to be impacted by glucocorticoids. The upregulation of phosphoglycerate kinase and downregulation of pyruvate kinase strongly suggest a disrupted glycolytic process, which may hinder the astrocyte-neuron lactate shuttle critical for neuronal energy supply and cognitive function. Furthermore, the downregulation of insulin in the astrocyte culture medium indicates reduced insulin export from the astrocytes. These findings suggest that dexamethasone exposure has a pronounced effect on astrocyte metabolism and deploys astrocyte-specific patterns of regulatory responses to glucocorticoids and controls neuronal activation.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 50-58"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145864281","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}

{"title":"Impact of cardiometabolic factors and AD plasma biomarkers on white matter hyperintensities volume in individuals with cognitive complaints from the global south","authors":"Patricio Riquelme-Contreras ,&nbsp;Fernando Henriquez ,&nbsp;Cecilia Gonzalez-Campo ,&nbsp;Florencia Altschuler ,&nbsp;Matías Fraile-Vazquez ,&nbsp;Pamela C.L. Ferreira ,&nbsp;Bruna Bellaver ,&nbsp;Thomas K. Karikari ,&nbsp;Tharick A. Pascoal ,&nbsp;Cecilia Okuma ,&nbsp;Christian Gonzalez-Billault ,&nbsp;Felipe A. Court ,&nbsp;Mauricio Cerda ,&nbsp;Patricia Lillo ,&nbsp;Claudia Durán-Aniotz ,&nbsp;Mizanur Khondoker ,&nbsp;Michael Hornberger ,&nbsp;Andrea Slachevsky","doi":"10.1016/j.neuroscience.2025.11.013","DOIUrl":"10.1016/j.neuroscience.2025.11.013","url":null,"abstract":"<div><div>White matter hyperintensities (WMH) are a magnetic resonance imaging (MRI) sign associated with cognitive complaints in the Alzheimer’s Disease (AD) continuum, including the pre-dementia steps. Cardiovascular and neurodegenerative pathophysiology have been postulated as relevant factors in the origin of WMH in AD. However, this evidence comes mainly from northern global populations, where the epidemiological profile differs from other geographical regions. This study explores the relationship between WMH, cardiometabolic and plasma neurodegeneration biomarkers in individuals with cognitive complaints from a developing country in the global south, where cardiometabolic risk factors are highly prevalent. We analyzed 112 individuals with cognitive complaints, assessing plasma pTau217, Aβ42/Aβ40 ratio, blood pressure, and glycemia levels while quantifying and segmenting WMH volumes. Multiple regression analyses revealed that diastolic blood pressure was significantly associated with WMH in specific white matter tracts, including the anterior thalamic radiation, cingulum, forceps minor, and subcortical regions. In contrast, no associations were found with glycemia, pTau217, Aβ42/40, or systolic blood pressure. These findings suggest that cardiovascular factors could be more critical in WMH development than neurodegeneration markers in this population. Our study, in addition to reflecting, in part, the associations between cardiovascular risk factors and WMH, highlights the need for further research on neurovascular contributions to dementia pathophysiology in these populations, emphasizing the role of neurovascular integrity, blood–brain barrier function, and cerebrospinal fluid circulation in underrepresented geographical contexts.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 270-279"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145743327","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}

{"title":"Apremilast-mediated protection against Aβ-induced cytotoxicity correlates with PI3K/Akt pathway activation","authors":"Hao Yang ,&nbsp;Jianping Jia","doi":"10.1016/j.neuroscience.2025.12.054","DOIUrl":"10.1016/j.neuroscience.2025.12.054","url":null,"abstract":"<div><h3>Background</h3><div>Apremilast, a novel inhibitor of phosphodiesterase-4 (PDE4), has demonstrated anti-inflammatory, immunomodulatory, neuroprotective, and senolytic properties. Given these characteristics, Apremilast, similar to other PDE4 inhibitors, holds potential as a therapeutic candidate for Alzheimer’s disease (AD).</div></div><div><h3>Objective</h3><div>This study aims to investigate whether Apremilast can mitigate neurotoxicity induced by amyloid β (Aβ) in BV2 microglial and HT-22 hippocampal mouse cell lines, while also exploring its neuroprotective effects and the underlying molecular mechanisms.</div></div><div><h3>Methods</h3><div>To begin, network pharmacology was employed to identify potential shared targets between Apremilast and AD. Molecular docking was subsequently used to assess the binding affinity of Apremilast to key targets. At the cellular level, the Cell Counting Kit-8 (CCK-8) assay was conducted to evaluate Apremilast’s protective effects against Aβ-induced cytotoxicity in BV2 and HT-22 cells. Finally, Western blot (WB) analysis was performed to examine the expression of proteins in the PI3K/Akt signaling pathway, offering insights into the molecular mechanisms underlying Apremilast’s neuroprotective role.</div></div><div><h3>Results</h3><div>Target enrichment analysis identified several potential pathways, among which the PI3K/Akt pathway was chosen for further examination. The results showed that Apremilast effectively counteracted Aβ-induced cytotoxicity in both BV2 and HT-22 cells, leading to a significant improvement in cell viability. Moreover, Western blot analysis demonstrated an upregulation of phosphorylated Akt (p-Akt/Akt) and PI3K protein levels.</div></div><div><h3>Conclusion</h3><div>In conclusion, this study provides evidence that Apremilast may exert protective effects against Aβ-induced cytotoxicity in BV2 and HT-22 cells by modulating the PI3K/Akt signaling pathway. However, further validation of its dosage and efficacy in vivo is required.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"595 ","pages":"Pages 20-27"},"PeriodicalIF":2.8,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145828185","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}

{"title":"Scientific publishing, science integrity, and PubPeer.","authors":"Thomas C Südhof","doi":"10.1016/j.neuroscience.2026.02.009","DOIUrl":"https://doi.org/10.1016/j.neuroscience.2026.02.009","url":null,"abstract":"<p><p>This Perspective is motivated by the mounting distrust of science by the public fueled by integrity issues in scientific papers (1) and by the intense questioning of our own laboratory's work by PubPeer, a popular website for finding mistakes in papers (2). Science is primarily communicated via scientific papers whose integrity is being increasingly doubted because of often contradictory conclusions and large number of retractions. In this Perspective, I aim to discuss some of the underlying causes for the current science integrity problems and to offer potential solutions. My main proposition is that to regain the trust of the public in science, we scientists as a community need to reform science communication and science publishing and we need to manage and rectify science integrity issues more directly.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146207349","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}