Brain Research Bulletin最新文献

{"title":"The uptake of β-amyloid by various brain cells exhibits heterogeneity and correlates with the CD14 expression","authors":"Jingming Shi ,&nbsp;Yandong Ma ,&nbsp;Lei Gao ,&nbsp;Yuting Dai ,&nbsp;Qian Chen ,&nbsp;Xudong Li ,&nbsp;Hang Liu ,&nbsp;Ruotong Li ,&nbsp;Jie Zhang ,&nbsp;Chaoren Yan","doi":"10.1016/j.brainresbull.2025.111699","DOIUrl":"10.1016/j.brainresbull.2025.111699","url":null,"abstract":"<div><div>The involvement of β-amyloid (Aβ) in the pathogenesis of Alzheimer's disease (AD) remains a contentious topic within the scientific community. For a long time, many studies have been highly interested in the topic of brain cells internalizing Aβ. Nonetheless, the precise processes and mechanisms underlying Aβ internalization by neurons, astrocytes, and microglia under AD settings have yet to be clarified. This study investigated primary neurons and glial cells cultured in vitro, as well as APP/PS1 mouse models. Laser confocal microscopy, frozen brain sections, and intraventricular injection in mice and other methods were employed to evaluate the uptake of Aβ42 monomers and oligomers (ADDL) by neurons, microglia, astrocytes. The results revealed that both microglia and neurons internalized Aβ oligomers. In the experiment, the Aβ that adhered to the cells, as visible using the laser confocal microscope, likely comprised two components: the portion that attached to the cells and the portion that was internalized by them. Contrary to prior observations, astrocytes exhibited limited in ability to internalize Aβ oligomers. The disparities in internalization across the three cell types were probably associated with CD14. This work elucidated the intricacies of several different types of cells internalization of Aβ processes and support a crucial role for CD14 in regulating Aβ internalization.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111699"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145910515","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":"Bile acid profile and white matter microstructural changes in early Alzheimer’s disease","authors":"Ye Mo ,&nbsp;Yifeng Peng ,&nbsp;Alzheimer's disease Neuroimaging Initiative (ADNI)","doi":"10.1016/j.brainresbull.2025.111642","DOIUrl":"10.1016/j.brainresbull.2025.111642","url":null,"abstract":"<div><h3>Background</h3><div>Although recent disease-modifying treatments such as Lecanemab have shown promise in reducing amyloid burden and modestly slowing cognitive decline in early Alzheimer’s disease (AD), effective long-term interventions remain limited. Emerging evidence links dysregulated gut-liver bile-acid (BA) metabolism to AD pathology. We examined whether peripheral BA signatures correspond to early white-matter microstructure changes in prodromal AD.</div></div><div><h3>Methods</h3><div>Baseline data were drawn from the Alzheimer’s Disease Neuroimaging Initiative. One-hundred-twenty-seven participants (46 cognitively normal controls, 81 amnestic mild cognitive impairment [MCI]; 55–90 y) contributed serum concentrations of 33 BAs plus three predefined BA ratios, cerebrospinal-fluid biomarkers, and diffusion-tensor MRI. Fractional anisotropy (FA), mean (MD), radial (RD) and axial (AxD) diffusivities were derived using tract-based spatial statistics and atlas-based regions of interest.</div></div><div><h3>Results</h3><div>Higher FA was associated with greater taurochenodeoxycholic acid, <span>L</span>-aspartate and <span>L</span>-asparagine, and with lower apocholic and 12-ketolithocholic acids. Elevated AxD, MD and RD tracked with reduced dehydrolithocholic acid and the glycolithocholic acid to chenodeoxycholic acid (GLCA/CDCA) ratio, and with higher palmitic acid. Participants with high cholic acid to chenodeoxycholic acid (CA/CDCA) ratio exhibited greater AxD in the left hippocampal cingulum; high GLCA/CDCA related to diffusivity increases in the right hippocampal cingulum and uncinate fasciculus. The glycodeoxycholic acid to taurodeoxycholic acid (GDCA/TDCA) ratio showed the strongest pattern, producing widespread AxD, MD and RD elevations in the uncinate fasciculus and cerebral peduncles and reduced FA in the fornix (p ≤ 0.0068).</div></div><div><h3>Conclusion</h3><div>Specific peripheral BA profiles—especially the gut-derived GDCA/TDCA ratio—mirror limbic and motor white-matter degeneration in amnestic MCI, independent of demographic and genetic risk. These findings implicate disrupted hepatic–microbial BA metabolism as a modifiable contributor to prodromal AD and highlight BA-targeted gut interventions as potential disease-modifying strategies.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111642"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534314","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":"Cerebellar deep brain stimulation rescues Purkinje cell mitochondrial density in a genetic mouse model of cerebellar ataxia","authors":"Lauren N. Miterko-Myers ,&nbsp;Lauren E. Peacoe ,&nbsp;Lita Duraine ,&nbsp;Zhongyuan Zuo ,&nbsp;Roy V. Sillitoe","doi":"10.1016/j.brainresbull.2025.111704","DOIUrl":"10.1016/j.brainresbull.2025.111704","url":null,"abstract":"<div><div>Deep brain stimulation (DBS) improves motor function in a growing list of movement diseases including Parkinson’s disease, dystonia, and tremor. There is evidence that DBS may also be effective in ataxia. It is not known why DBS is effective, but modulating cell activity and conferring neuroprotection are hypothesized to underlie its benefits. Understanding the effects of DBS on neurons is paramount to extending its clinical use in the treatment of various motor and non-motor diseases. Here, we stimulated the cerebellum of <em>Car8 waddles</em> (<em>Car8</em>^<em>wdl</em>) mice, given the cerebellum’s important role in ataxia pathophysiology. Using transmission electron microscopy, we tested the effects of therapeutic neuromodulation on Purkinje cell subcellular structures, including the mitochondria and their proximity to the endoplasmic reticulum (ER). In the absence of stimulation, we found increased putative mitochondria-ER contacts in <em>Car8</em>^<em>wdl</em> Purkinje cells as well as mitochondrial size and density alterations. Low-frequency cerebellar DBS rescued mitochondrial density, but not size or putative contacts in <em>Car8</em>^<em>wdl</em> Purkinje cells. Although increased mitochondrial density and sustained ER contact are specific to DBS treatment, they do not determine efficaciousness. These data uncover a mode of intracellular plasticity in Purkinje cells after stimulation, enhancing our mechanistic understanding of DBS for cerebellar disorders.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111704"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145843219","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":"Investigation of dipyridamole-elicited signaling in the brain of Niemann Pick type C mice: A multi-omic study","authors":"Sabrina Tait ,&nbsp;Federica Fratini ,&nbsp;Zaira Boussadia ,&nbsp;Lucia Gaddini ,&nbsp;Manuela Marra ,&nbsp;Loredana Le Pera ,&nbsp;Gloria Venturini ,&nbsp;Antonella Ferrante","doi":"10.1016/j.brainresbull.2025.111708","DOIUrl":"10.1016/j.brainresbull.2025.111708","url":null,"abstract":"<div><div>Niemann Pick type C1 (NPC1) is a rare, fatal disorder characterized by endo-lysosomal (EL) lipid accumulation that leads to damage of both peripheral organs and central nervous system, with cerebellum and hippocampus being particularly affected. Currently very few therapeutic options exist in Europe for NPC. In fact, miglustat is the only approved drug and <span>L</span>-acetylleucine was recently granted for marketing authorization by European Medicine Agency. Thus, the identification of new treatments is mandatory. We have previously demonstrated that dipyridamole (DIP), an approved medicine that is clinically employed as an antiplatelet agent, could rescue recognition memory and increase hippocampal expression of calbindin. On the contrary, the drug was unable to improve cerebellar-dependent motor function. In order to elucidate the mechanism of these region-specific changes induced by DIP, in this work we performed a multi-omic analysis of genes and proteins modulated by the treatment in the hippocampus and cerebellum of a mouse model of NPC1 (Npc1^-/-). Our results revealed that DIP significantly affected various pathways in the hippocampus at protein level, but it had no significant impact on pathways in the cerebellum (either at gene or protein level). Interestingly, the most affected pathways in the hippocampus of Npc1^-/- mice administered with DIP were those related to cGMP-PKG activation and to mitochondrial function. Our results paved the way to test DIP in experimental models of other neurodegenerative disorders, such as Alzheimer’s disease that is similarly marked by hippocampal and mitochondrial dysfunctions.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111708"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848839","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":"A multimodal fusion framework reveals the heterogeneity of basal ganglia atrophy and its molecular mechanisms in temporal lobe epilepsy","authors":"Guiming Weng ,&nbsp;Xiaochuan Fu ,&nbsp;Cuimi Luo ,&nbsp;Qin Zhou ,&nbsp;Huoyou Hu ,&nbsp;Bailing Qin ,&nbsp;Binghua Lv ,&nbsp;Zirong Chen ,&nbsp;Jinou Zheng","doi":"10.1016/j.brainresbull.2025.111682","DOIUrl":"10.1016/j.brainresbull.2025.111682","url":null,"abstract":"<div><div>The heterogeneity of basal ganglia (BG) atrophy in temporal lobe epilepsy (TLE) has not been fully elucidated. This study employed a multimodal fusion framework to examine the potential heterogeneity of BG atrophy among TLE patients. 89 patients diagnosed with TLE were recruited. Structural magnetic resonance imaging (sMRI), resting - state functional magnetic resonance imaging (fMRI), consensus clustering (CC), and neuroimaging - transcriptomic approaches were integrated to explore the structural and functional alterations in the BG and their molecular mechanisms. Canonical correlation analysis (CCA) was employed to investigate the associations between MRI features and clinical characteristics. An individualized prediction model was constructed to facilitate clinical decision-making. CC identified a significant subgroups of BG atrophy in TLE: widespread BG atrophy (TLE-Cluster1, TLE-C1). In TLE-C1, the functional connectivity between the BG and cortical regions associated with sensation, emotion, and memory was notably enhanced. These patients additionally exhibited more severe cognitive impairment as well as higher degrees of anxiety and depression. Transcriptomic analysis established a connection between the heterogeneity of BG atrophy and specific gene expression patterns that were enriched in biological processes such as synaptic function, neurostructural development, and learning and memory. Further analyses uncovered a positive correlation between the gray matter volume of BG and cognitive performance. A classifier based on a Neural Network (NNET) predicted cognitive function with an area under curve (AUC) of 0.983. This study characterizes BG atrophy heterogeneity in TLE, its molecular mechanisms, and clinical relevance, offering insights for personalized diagnosis and management.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111682"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145734693","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":"VPS25 alleviates depression-like behavior in rats by inhibiting apoptosis in the hippocampus","authors":"Lili Yuan ,&nbsp;Xiaofang Huang ,&nbsp;Qi Wang ,&nbsp;Beibei Hou ,&nbsp;Sifan Xu ,&nbsp;Zhiming Zhou ,&nbsp;Yigao Wu ,&nbsp;Jiucui Tong","doi":"10.1016/j.brainresbull.2025.111705","DOIUrl":"10.1016/j.brainresbull.2025.111705","url":null,"abstract":"<div><h3>Background</h3><div>Depression is a psychiatric disorder manifested by significant and persistent depressive symptoms. In recent years, autophagy has been identified with a key role in neuronal survival, synaptic plasticity, and depression. We previously observed that vacuolar protein sorting 25 (VPS25) was up-regulated in the hippocampus of depressive rats, but the mechanisms were unclear.</div></div><div><h3>Methods</h3><div>In chronic unpredictable mild stress (CUMS)-stimulated rats, lateral ventricles were injected with adeno-associated virus (AAV) to silence <em>VPS25</em>. Depression status in rats was evaluated using behavioral tests. In the corticosterone (CORT)-induced PC12 cell apoptosis model, Cell Counting Kit-8 (CCK-8) assays were used to determine cell viability. We next investigated the effects of CORT and VPS25 on PC12 apoptosis and proliferation using flow cytometry and cell proliferation assays. <em>VPS25</em> mRNA expression was determined using qRT-PCR, while VPS25, Bax, Bcl-2, cleaved-caspase3, P62, Beclin-1, LC3, JAK1, p-JAK1, STAT1, and p-STAT1 levels of expression were assessed using western blotting.</div></div><div><h3>Results</h3><div>Our data demonstrate that in CORT-induced PC12 cells or a CUMS-induced rat depression model, <em>VPS25</em> silencing not only alleviated CUMS-induced neuronal apoptosis in rats but also reduced CORT-induced apoptosis in PC12 cells. Notably, <em>VPS25</em> silencing alleviated CUMS-provoked depression-like behaviors, reduced neuronal apoptosis (as evidenced by TUNEL staining), and promoted autophagy flux by increasing the LC3-II/LC3-I ratio. These effects were associated with the blockade of JAK/STAT signaling.</div></div><div><h3>Conclusion</h3><div>These results indicate that silencing <em>VPS25</em> alleviates depression symptoms by promoting autophagy and inhibiting neuronal apoptosis, partly through the JAK/STAT signaling pathway.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111705"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833324","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":"CAF-derived exosomes promote the proliferation and invasion of pituitary adenoma cells via miR-184 transfer","authors":"Qiu Du ,&nbsp;Zhiyong Chen ,&nbsp;Weiyu Zhang ,&nbsp;Mengchao Zhu ,&nbsp;Zhichao Yang ,&nbsp;Yaru Li ,&nbsp;Lei Xu ,&nbsp;Jianmin Zhang ,&nbsp;Aijun Peng ,&nbsp;Qingling Feng","doi":"10.1016/j.brainresbull.2025.111678","DOIUrl":"10.1016/j.brainresbull.2025.111678","url":null,"abstract":"<div><div>Pituitary adenomas (PAs) are common intracranial tumors whose mass effects and endocrine dysfunction pose serious threats to patient health. However, the mechanisms underlying their progression, particularly the role of the tumor microenvironment (TME), remain insufficiently studied. Within this context, cancer-associated fibroblasts (CAFs) have been shown to drive tumor development via extracellular matrix remodeling and extracellular vesicle release, but their specific contributions to PA progression remain unclear. In this study, we observed a correlation between PA invasiveness and fibroblast density in the TME. Functionally, both CAFs and CAF-derived exosomes significantly enhanced the proliferation and invasion of PA cells compared to normal fibroblasts. Small RNA sequencing identified 16 upregulated and 8 downregulated miRNAs in CAF-derived exosomes, with KEGG analysis indicating enrichment in MAPK signaling, regulation of actin cytoskeleton, and lysosome-related pathways. Among these, miR-184 was notably upregulated in both CAF-derived exosomes and PA specimens. We further demonstrated that exosomal miR-184 from CAFs could be transferred into PA cells, promoting their proliferation and invasion, while miR-184 knockdown attenuated the tumor-promoting effects of CAF-derived exosomes. Mechanistically, TLE1 was validated as a direct functional target of miR-184. In summary, our study reveals exosomal miR-184 as a key mediator of CAF-driven PA progression, highlighting its potential as a therapeutic target for PAs.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111678"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145695852","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":"Comparison of epilepsy mouse models induced by kainic acid through different administration routes","authors":"Li-Wei Xing ,&nbsp;Chen Yang ,&nbsp;Wenxuan Tang ,&nbsp;Yongjie Deng ,&nbsp;Wen-Xu Wang ,&nbsp;Jia-Hui Guo ,&nbsp;Xin-Yi Wang ,&nbsp;Run-Chen Fang ,&nbsp;Jian Guan ,&nbsp;Jing Cang ,&nbsp;Shi-Bin Li","doi":"10.1016/j.brainresbull.2025.111684","DOIUrl":"10.1016/j.brainresbull.2025.111684","url":null,"abstract":"<div><div>Sleep disruption associated with epilepsy is frequently observed in clinical practice. Various epilepsy animal models including the widely-used chemoconvulsant kainic acid (KA) have been developed to unveil the mechanisms underlying this life-threatening central disorder and improve sleep management. However, a systematic comparison of epilepsy models induced through different KA administration routes (intrahippocampal, IH, vs. intraperitoneal, IP) remains lacking. In this study, we monitored the dynamic changes of sleep/wake architecture, the development of epilepsy, and performed histological mapping of brain regions potentially implicated in epileptogenesis. We observed a more severe disruption of sleep architecture associated with seizures perpetuating for a longer time in the IHKA group. IHKA induced a more robust epilepsy pattern with significant increases of wakefulness and reductions of sleep during the acute phase. A chronic epilepsy model was developed in the IHKA group, but not in the IPKA group. Both IHKA and IPKA groups developed NREM sleep fragmentation during the chronic phase. Isolated spikes induced by IHKA appeared more frequently than those induced by IPKA at all time points, and gradually declined before stabilization around day 14 post-administration. Both IPKA and IHKA induced elevated c-Fos expression within 3 h after the drug administration as compared to their controls. Pearson correlation analyses of c-Fos expression across brain regions revealed that the IHKA group exhibited more correlations among multiple brain regions, reflecting a broader network of activated regions compared with the IPKA group after local KA exposure. Therefore, IHKA creates a more robust epilepsy mouse model characterized by a more fragmented sleep pattern, more seizures, and more isolated spikes.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111684"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755139","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":"Examining clinical symptoms in schizophrenia based on visual-spatial working memory and resting-state EEG","authors":"Yajing Si ,&nbsp;Yunmeng Bai ,&nbsp;Bingke Liu ,&nbsp;Jiaxin Wang ,&nbsp;Simin Cai ,&nbsp;Wenjing Zhong ,&nbsp;Haiqi Zheng ,&nbsp;Nan Zhao ,&nbsp;Jicheng Liu ,&nbsp;Hongxing Zhang","doi":"10.1016/j.brainresbull.2025.111696","DOIUrl":"10.1016/j.brainresbull.2025.111696","url":null,"abstract":"<div><div>Schizophrenia (SZ) is a serious and disabling mental illness characterized by compromised brain network interactions. The current study investigated the potential associations between the resting-state electroencephalogram (EEG) and individual cognitive traits/clinical recordings in SZ patients. Furthermore, the positive and negative syndrome scale (PANSS) scores based on the connectivity revealed in the resting-state EEG and working memory (WM) when SZ patients participated in the visual-spatial WM task were predicted. The results demonstrated that stronger frontal-parietal linkages for the SZ group were associated with lower response accuracy compared to the HC group in the alpha and beta frequency bands during the resting-state process. There were significant relationships between PANSS scores and the resting-state network properties; increased PANSS scores were accompanied by a larger clustering coefficient, as well as global and local efficiency, and shorter characteristic path length. Moreover, based on the built multivariable linear regression model, the PANSS scores were predicted accurately, as indicated by a rather large correlation coefficient between predicted and actual PANSS scores in the SZ group. Current findings may deepen our knowledge of SZ and accelerate progress in early diagnosis and intervention approaches.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111696"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145787838","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":"The pulvinar nucleus and its role in cognitive functions","authors":"Nelson Cortes,&nbsp;Capucine Mandel,&nbsp;Lamyae Ikan,&nbsp;Christian Casanova","doi":"10.1016/j.brainresbull.2025.111672","DOIUrl":"10.1016/j.brainresbull.2025.111672","url":null,"abstract":"<div><div>The pulvinar is a higher-order thalamic hub with widespread cortico-cortical and cortico-limbic connectivity. Here we synthesize evidence that pulvinar circuits shape perception and cognition via three computations: (i) precision-weighted gain for routing information across visual hierarchies, (ii) priority mapping that supports selection of behaviorally relevant stimuli, and (iii) temporal alignment that facilitates feature binding and multisensory integration. We summarize lesion, inactivation and imaging studies linking these operations to attention, sensory gain, and socio-emotional processing. We then review pulvinar-related alterations across neuropsychiatric conditions (e.g., schizophrenia, autism spectrum disorder, major depressive disorder, anxiety), focusing on convergent patterns of thalamo-cortical reconfiguration rather than disorder-general clinical descriptions. Finally, we integrate these findings with contemporary frameworks (predictive coding; distributed global workspace; constructionist theory of emotions), outlining testable predictions about frequency-specific coupling and state-dependent routing between occipito-temporal, fronto-parietal and limbic networks. This concise account situates the pulvinar as a modulatory hub that can influence both sensory and affective dimensions of cognition, and highlights priorities for causal human and animal work.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"234 ","pages":"Article 111672"},"PeriodicalIF":3.7,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145683996","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}