Neuroscience最新文献

{"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":"Monoacylglycerol lipase inhibition improves motor function and reduces oxidative stress in hemiparkinsonian mice","authors":"Delia Maciel Mendoza-Camacho ,&nbsp;Juan Manuel Viveros-Paredes ,&nbsp;Mario Eduardo Flores-Soto ,&nbsp;Alma Hortensia Martínez-Preciado ,&nbsp;Aldo Rafael Tejeda-Martínez","doi":"10.1016/j.neuroscience.2025.12.025","DOIUrl":"10.1016/j.neuroscience.2025.12.025","url":null,"abstract":"<div><div>Parkinson’s Disease (PD) is characterized by motor symptoms, loss of dopaminergic neurons, and oxidative stress in the Substantia Nigra pars compacta (SNpc) and striatum of patients, as well as in models of parkinsonism. Recent studies show that the endocannabinoid system present in the basal ganglia has a strong influence on the progression of PD, with the inhibition of the enzyme Monoacylglycerol Lipase (MAGL) being a promising therapeutic strategy. Therefore, the aim of this study was to evaluate the effect of MAGL inhibition on locomotion and oxidative stress in a murine model of hemiparkinsonism. For this study, male C57BL/6J mice were divided into four groups: 1) Control group, 2) 6-OHDA group, which received the hemiparkinsonism model, 3) JZL184 group, which received a dose of 8 mg/kg/day for 7 days of the JZL184 inhibitor, and 4) 6-OHDA + JZL184 group, which had the hemiparkinsonism model and, 14 days later, began administration with JZL184. It was found that the hemiparkinsonism mice showed significant improvements both in locomotor performance and in levels of lipoperoxidation, total antioxidant capacity, superoxide dismutase activity, and in quantity and activity of mitochondrial complex I, once the MAGL inhibitor was administered to this group. Treatment with the JZL184 inhibitor demonstrated improved locomotor ability and reduced oxidative stress levels in the SN<em>pc</em> and striatum of mice with hemiparkinsonism. This suggests that MAGL inhibition could be a therapeutic alternative for PD in the future.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"594 ","pages":"Pages 1-10"},"PeriodicalIF":2.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145760569","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":"Classification of EEG-fNIRS bimodal brain signals for motor imagery tasks based on wavelet transform and spatio-temporal domain processing","authors":"Lingyue Zhang,&nbsp;Baojiang Li,&nbsp;Manliang Cao,&nbsp;Cheng Peng,&nbsp;Haiyan Wang","doi":"10.1016/j.neuroscience.2025.12.036","DOIUrl":"10.1016/j.neuroscience.2025.12.036","url":null,"abstract":"<div><div>The fusion of Electroencephalography (EEG) and functional near-infrared spectroscopy (fNIRS) provides richer neural information for brain–computer interface decoding. However, due to their distinct physiological mechanisms and heterogeneous temporal and statistical properties, EEG and fNIRS are difficult to temporally align and to project into a shared latent representation. To address this challenge, we propose BiCAT, a lightweight bimodal decoding framework that integrates wavelet-based preprocessing, artifact-aware time-domain refinement, and early feature-level fusion with a compact Transformer encoder. Wavelet transform is first applied to separate signal and noise components across frequency bands, after which spatio-temporal domain processing suppresses motion and physiological artifacts while preserving task-relevant patterns. The cleaned EEG and fNIRS features are concatenated and fed into a single-encoder Transformer, where joint self-attention captures salient temporal cues within each segment.BiCAT is evaluated on two publicly available EEG–fNIRS datasets covering motor imagery (MI), mental arithmetic (MA), and word generation (WG) tasks. The model achieves 93.41 % accuracy on MI, outperforming the strongest unimodal baseline (fNIRS) by 4.39 percentage points. On MA and WG, BiCAT attains 96.47 % and 96.41 % accuracy, corresponding to gains of 10.39 and 3.86 points over the best unimodal fNIRS and HbR baselines, respectively. Despite having only 111 k parameters, BiCAT performs competitively with representative multimodal fusion methods on the same benchmarks. These results demonstrate that BiCAT provides effective bimodal feature integration and robust performance across multiple EEG–fNIRS tasks while maintaining low computational complexity.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"594 ","pages":"Pages 42-57"},"PeriodicalIF":2.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145781527","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":"Preferred tempo influence on learning transfer from perceptual to stepping timing in Parkinson’s disease","authors":"Itzamná Sánchez-Moncada ,&nbsp;Gabriel Neri-Nani ,&nbsp;Adrián Elías ,&nbsp;Hugo Merchant","doi":"10.1016/j.neuroscience.2025.12.039","DOIUrl":"10.1016/j.neuroscience.2025.12.039","url":null,"abstract":"<div><div>Parkinson’s disease (PD) patients show gait and motor timing impairments that can be improved with different behavioral therapies. This study involved an intervention with seventeen PD patients utilizing a pre-training–training–post-training protocol. The experimental paradigm included a march-in-place task (MPT) and an auditory synchronization-continuation stepping task (SCT). During these tasks, their foot movements were tracked with an infrared motion-capture system. In addition, patients undertook intensive in-house personalized training on an auditory interval discrimination task (IDT) for six consecutive days. The goal was to improve the precision of the stepping tasks as a result of the learning transfer from the IDT. We measured the spontaneous motor tempo of 17 patients (six females) during the pre-training MPT and found two segregated clusters, one with fast and another with slow preferred stepping intervals. Notably, patients with slow preferred stepping intervals, on average, showed a significant decrease in the variability of their interstep intervals during the MPT and the continuation epoch of the SCT due to the intense training in the IDT. These findings suggest that PD patients exhibiting slow spontaneous tempos are more suitable candidates for timing rehabilitation.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"594 ","pages":"Pages 85-94"},"PeriodicalIF":2.8,"publicationDate":"2026-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145794303","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}