Brain Research最新文献

{"title":"Corrigendum to “Sensitivity and reliability of fNIRS to detect cochlear implant-induced auditory cortical activation in prelingually deaf children with inner ear malformation or cochlear nerve deficiency” [Brain Res. 1856 (2025) 149578]","authors":"Hiroshi Yamazaki , Saburo Moroto , Tomoko Yamazaki , Rinko Tamaya , Naoko Fujii , Keizo Fujiwara , Yasushi Naito","doi":"10.1016/j.brainres.2025.149615","DOIUrl":"10.1016/j.brainres.2025.149615","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149615"},"PeriodicalIF":2.7,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143799774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperglycemia as driver of glioblastoma progression: Insights from Mendelian randomization and single-cell transcriptomics","authors":"Jin Li ,&nbsp;Wenjing Wu ,&nbsp;Liguo Ye ,&nbsp;Bo Zheng","doi":"10.1016/j.brainres.2025.149636","DOIUrl":"10.1016/j.brainres.2025.149636","url":null,"abstract":"<div><h3>Background</h3><div>Hyperglycemia and diabetes may influence GBM progression by altering tumor metabolism and the tumor microenvironment. However, the causal relationship between blood glucose levels and GBM remains unclear.</div></div><div><h3>Methods</h3><div>Mendelian randomization (MR) analysis was performed using GWAS data from the UK Biobank and FinnGen databases, with fasting blood glucose, plasma glucose, cerebrospinal fluid (CSF) glucose, and diabetes as exposures. Single-cell RNA sequencing of GBM mouse models on high-glucose and control diets was conducted to explore the cellular landscape of the tumor microenvironment under hyperglycemic conditions. Additionally, gene set enrichment analysis (GSEA) was performed on transcriptomic data from brain tissues of diabetic patients to assess the activity of GBM-related pathways.</div></div><div><h3>Results</h3><div>MR analysis demonstrated a significant genetic relationship between elevated fasting blood glucose and GBM risk, with an odds ratio (OR) of 40.991 (95 % CI: 2.066–813.447, p = 0.015). Type 2 diabetes (T2D) also showed a potential causal link with GBM, with the Weighted Median and Inverse Variance Weighted methods yielding ORs of 2.740 (95 % CI: 1.033–7.273, p = 0.043) and 2.100 (95 % CI: 1.029–4.287, p = 0.042), respectively. Single-cell transcriptomic analysis of GBM mouse models revealed an increased proportion of GBM tumor stem cells and pro-tumorigenic M2 macrophages in the high-glucose diet (HGD) group. GSEA of diabetic patient brain tissue revealed heightened activity of GBM-related pathways, particularly in astrocytes, endothelial cells, and neurons.</div></div><div><h3>Conclusion</h3><div>These findings suggest that hyperglycemia may actively contribute to GBM progression by promoting cellular changes within the tumor microenvironment and activating GBM-related pathways in brain tissues.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149636"},"PeriodicalIF":2.7,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143814683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Collaborative multitasking framework for enhanced hippocampus segmentation and Alzheimer’s disease classification","authors":"Lingling Fang,&nbsp;Xin Fu,&nbsp;Yongcheng Yu,&nbsp;Deshan Liu","doi":"10.1016/j.brainres.2025.149610","DOIUrl":"10.1016/j.brainres.2025.149610","url":null,"abstract":"<div><div>The early diagnosis of Alzheimer’s disease has faced significant challenges, as the initial patients have hidden symptoms that are difficult to distinguish from conventional symptoms. In view of this, this article designs a collaborative multitasking algorithm framework that implements a positive feedback loop between classification tasks, significantly improving processing accuracy. Specifically, the algorithm consists of three sub networks: the initial segmentation sub network accurately identifies the hippocampus boundary and generates the initial segmentation mask; The classification subnetwork relies on initial segmentation information to effectively distinguish different stages of Alzheimer’s disease; Finally, the fine segmentation sub network finely adjusts the contour of the hippocampus based on the classification results. To verify the superiority of this method, this study used 269 MRI sample of Alzheimer’s disease patients, including clinical and public datasets. The experimental results demonstrate that the proposed method exhibits superior performance in both hippocampal classification and segmentation tasks. Specifically, in terms of segmentation, the method achieved an average Dice Similarity Coefficient (DSC) of 94.0% and a Jaccard Index (JA) of 80.6%. For classification tasks, the method demonstrated an accuracy (AC) of 98.8%, sensitivity (SEN) of 98.8%, specificity (SP) of 98.6%, and F1 score (F1) of 97.8%, collectively indicating excellent clinical performance.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1858 ","pages":"Article 149610"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143808503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An enriched environment restored hippocampal cell patterns and enhanced short-term memory in gestational and breastfeeding protein-restricted male offspring.","authors":"Gabriel Boer Grigoletti-Lima, Patrícia Aline Boer, José Antonio Rocha Gontijo","doi":"10.1016/j.brainres.2025.149598","DOIUrl":"https://doi.org/10.1016/j.brainres.2025.149598","url":null,"abstract":"<p><p>Maternal undernutrition impacts neuron proliferation and differentiation, non-neuron onset, and cell migration, leading to changes in long-term offspring's brain morphology and functionality. This study evaluated the effect of maternal protein intake restriction and enriched environment on the structural hippocampus and behavioral tests in 42-day-old male (low-protein) LP compared to NP (control) offspring. The study supports the selfish brain theory, which suggests that the brain maintains its mass despite significant changes in body weight. The hippocampus cellularity pattern was profoundly altered by reduced neuron numbers in the LP compared to the age-matched NP progeny, as revealed by the isotropic fractionation technique. Detailed data analysis revealed a discrepancy between behavioral tests and reduced hippocampal stem cells and neuron number, accompanied by increased non-neuronal cells, linked to a significant decrease in fear-reflecting behavior. However, the enriched environment (EE) was found to restore the altered neuronal hippocampi cellularity significantly and modify the discrimination ratio, enhancing the ability of both progenies to discriminate between novel and familiar objects in a short time, potentially associated with reversing abnormal hippocampus cell patterns. Immunohistochemistry further validated these findings, showing reduced progenitor cells, neurons and total cells in mitosis in the LP offspring. At the same time, the enriched environment significantly increased hippocampal cell proliferation, a promising result that could lead to the recovery of neuronal stem cell numbers. The present data underscore the detrimental impact of gestational protein restriction on brain development and highlight EE's potential to restore altered neuronal hippocampi cellularity, offering a hopeful outlook for future research and interventions.</p>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":" ","pages":"149598"},"PeriodicalIF":2.7,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations in NFAT5 and ATP6V1E1 expression as potential diagnostic biomarkers in blood and brain for Alzheimer’s disease: A study of gene overlap","authors":"Farnoosh Akbari ,&nbsp;Roksana Soheilian ,&nbsp;Samin Tavalaeian ,&nbsp;Atefeh Zamani ,&nbsp;Mohammad Mahdevar","doi":"10.1016/j.brainres.2025.149599","DOIUrl":"10.1016/j.brainres.2025.149599","url":null,"abstract":"<div><h3>Introduction</h3><div>Alzheimer’s disease (AD), a prevalent cause of dementia, is characterized by amyloid plaques and tau tangles. It requires early diagnosis through the use of blood markers. This study examined changes in gene expression in blood and brain samples from patients with AD as potential diagnostic biomarkers.</div></div><div><h3>Methods</h3><div>The study utilized gene expression data from publicly available studies, including GSE4757, GSE5281, GSE28146, GSE48350, and GSE63060, to investigate expression changes in AD. Data integration and differential expression analysis were performed, and pathways related to candidate genes were identified using the Enrichr and BioPlents databases. Blood samples from 50 AD and controls were collected, followed by RNA extraction, cDNA synthesis, and qRT-PCR analysis using specific <em>NFAT5</em> and <em>ATP6V1E1</em> gene primers.</div></div><div><h3>Results</h3><div>We found 394 genes with increased expression and 759 with decreased expression in brain tissue. Upregulated genes were linked to TGF-B, BDNF, apoptosis, Hippo, P53, and IL-2 and IL-4 pathways. In contrast, downregulated genes were associated with pathways related to oxidative phosphorylation, PGC1-A, GABA, Alzheimer’s, and calcium. Blood expression data showed 1147 probes with increased expression and 1413 with significant decreases. We found 31 genes that were upregulated and 87 genes that were downregulated, consistent across both blood and brain samples. Among the overlapping genes, RT-qPCR results indicated that the expression levels of <em>NFAT5</em> and <em>ATP6V1E1</em> may have diagnostic potential in the blood samples of Alzheimer’s patients.</div></div><div><h3>Conclusion</h3><div>The study identified changes in gene expression related to Alzheimer’s in blood and brain samples. These changes affect pathways such as IL-2 and oxidative phosphorylation. Both in silico and ex vivo results revealed that the expression levels of <em>NFAT5</em> and <em>ATP6V1E1</em> in blood samples can serve as potential diagnostic biomarkers for Alzheimer’s patients.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149599"},"PeriodicalIF":2.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From encoding to recognition: Exploring the shared neural signatures of visual memory","authors":"Berfin Ozdemir,&nbsp;Géza Gergely Ambrus","doi":"10.1016/j.brainres.2025.149616","DOIUrl":"10.1016/j.brainres.2025.149616","url":null,"abstract":"<div><div>This study investigated the shared neural dynamics underlying encoding and recognition processes across diverse visual object stimulus types in short term experimental familiarization, using EEG-based representational similarity analysis and multivariate cross-classification. Building upon previous research, we extended our exploration to the encoding phase. We show early visual stimulus category effects around 150 ms post-stimulus onset and old/new effects around 400 to 600 ms. Notably, a divergence in neural responses for encoding, old, and new stimuli emerged around 300 ms, with items encountered during the study phase showing the highest differentiation from old items during the test phase. Cross-category classification demonstrated discernible memory-related effects as early as 150 ms. Anterior regions of interest, particularly in the right hemisphere, did not exhibit differentiation between experimental phases or between study and new items, hinting at similar processing for items first encountered, irrespective of experiment phase. While short-term experimental familiarity did not consistently adhere to the old &gt;new pattern observed in long-term personal familiarity, statistically significant effects are observed specifically for experimentally familiarized faces, suggesting a potential unique phenomenon specific to facial stimuli. Further investigation is warranted to elucidate underlying mechanisms and determine the extent of face-specific effects. Lastly, our findings underscore the utility of multivariate cross-classification and cross-dataset classification as promising tools for probing abstraction and shared neural signatures of cognitive processing.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149616"},"PeriodicalIF":2.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Shared and unique genes and pathways between neuropathic and inflammatory pain assays","authors":"Shuxian Wang ,&nbsp;Lingji Zhou ,&nbsp;Weiyu Pu ,&nbsp;Jiajia Dai ,&nbsp;Song Cao","doi":"10.1016/j.brainres.2025.149614","DOIUrl":"10.1016/j.brainres.2025.149614","url":null,"abstract":"<div><h3>Background</h3><div>Current studies mostly concentrate on behavioral differences and have not yet systematically elucidated the molecular distinctions among various chronic pain models.</div></div><div><h3>Methods</h3><div>To identify the similarities and differences in gene expression among mice of three kinds of pain models, i.e., spared nerve injury (SNI) model, chronic constriction injury of the sciatic nerve (CCI) model, and the complete Freund’s adjuvant-induced chronic inflammatory pain (CFA) model. The lumbar enlargement segments (L5-L6) were collected. Total mRNA was extracted for RNA sequencing. The differentially expressed genes were analyzed by bioinformatics, including GO analysis, KEGG analysis, and PPI network to explore the functions.</div></div><div><h3>Results</h3><div>Commonalities and significant variations in gene expression were observed among the three pain models. Compared with Sham, there were 60 shared differential genes among the three models, which were mainly involved in oxidative phosphorylation-related biological process (e.g., mt-Nd1). Compared with CCI, SNI upregulated genes were associated with inflammation response (e.g., Ifi204, Ifi27), while downregulated genes were linked to microtubule-based movement (e.g., Dnah7b, Hcmn1); When compared with SNI, CFA upregulated genes were related to axon development (e. g., Oprm1, Gucy1a2, Syn3), whereas downregulated genes were associated with oxidative phosphorylation (e. g., Rpl41, Rpl21); In contrast to CCI, CFA upregulated genes pertained to axon development (e. g., Zbtb16), while downregulated genes were connected to oxidative phosphorylation (e. g., Cyp3a13).</div></div><div><h3>Conclusions</h3><div>The three widely employed chronic pain models exhibit both similarities and distinctions, and genes that vary across all three models may serve as potential targets for chronic pain research.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149614"},"PeriodicalIF":2.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Direct hybridization and bioinformatics analysis of circulating microRNAs in patients with Alzheimer’s disease under intravenous trehalose treatment","authors":"Shabnam Radbakhsh ,&nbsp;Diana Marisol Abrego-Guandique ,&nbsp;Tiziana Bacchetti ,&nbsp;Seyed Hamid Aghaee-Bakhtiari ,&nbsp;Ali Mahmoudi ,&nbsp;Ali Akhonpour Manteghi ,&nbsp;Mohammad Javad Bazyari ,&nbsp;Erika Cione ,&nbsp;Gianna Ferretti ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.brainres.2025.149607","DOIUrl":"10.1016/j.brainres.2025.149607","url":null,"abstract":"<div><div>Trehalose has been proposed as a possible therapeutic option for attenuating the neuropathological changes associated with neurodegeneration, including Alzheimer’s disease (AD). The administration of trehalose in human and murine models was linked to restoring antioxidant status, decreasing lipoperoxidation, and alleviating neuroinflammation. This latter biochemical mechanism was associated with the upregulation of specific brain-enriched microRNAs (miRNA). Herein, using a direct hybridization approach, we evaluate trehalose intravenous treatment in AD patients, conducting a phase two clinical trial (IRCT20130829014521N15) examining the alteration of microRNA profiles before and after the treatment. Twenty patients were recruited and randomly assigned to two groups: the intervention group received 15 g/week of intravenous trehalose. The control group received placebo in the form of normal saline. The period chosen was 12 weeks. Blood samples were obtained at the beginning and end of the study. Circulating microRNAs expression data between the placebo and treatment groups were assessed using microarray analysis. Subsequently, differentially expressed (DE) miRNAs specific to the trehalose-treated group were identified, and their gene targets were determined by bioinformatics-based approaches. The analysis of DE miRNAs pointed out modulation in unique miRNAs between treatment and placebo groups. Specifically, hsa-miR-1268a, −3605-3p, −555, and −6511a-3p were significantly downregulated, while hsa-miR-324-3p and −539-5p showed significant upregulation. Of the 147 overlapped validated genes identified in the bioinformatics analysis, several are related to autophagy, protein aggregation, oxidative stress, and inflammation. KEGG enrichment pathways reveal regulation of actin cytoskeleton, axon guidance, and neurotrophin signaling pathways. The results identify significant modulation in unique miRNAs in AD patients under trehalose. These findings suggest the potential utility of these microRNAs as biomarkers for trehalose pharmacological monitoring in AD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149607"},"PeriodicalIF":2.7,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protection of dauricine and daurisoline on PC12 cells damaged by glutamate or Aβ25-35","authors":"Xiao-Han Ma ,&nbsp;Hui Dai ,&nbsp;Song-Yao Liu ,&nbsp;Xiao-Na Liu ,&nbsp;Jing Zhang ,&nbsp;Xue-Lian Meng","doi":"10.1016/j.brainres.2025.149609","DOIUrl":"10.1016/j.brainres.2025.149609","url":null,"abstract":"<div><div>Glutamate (Glu) excitotoxicity and amyloid-β (Aβ) deposition are significant factors in the occurrence and development of Alzheimer’s disease (AD). Dauricine and daurisoline are two alkaloid components of <em>Menispermum dauricum</em> DC<em>.</em> that have a protective effect on the nervous system. The protection of dauricine and daurisoline on Glu-injured PC12 cells and the protection dauricine on Aβ_25-35-injured PC12 cells were investigated in this study. The results of the study demonstrated that on PC12 cells damaged by Glu (20 mM), dauricine and daurisoline (3 and 10 μM) increased the cell viability, reduced cell apoptosis, and enhanced mitochondrial membrane potential (MMP) levels. Dauricine and daurisoline can also reduce the levels of intracellular ROS and free Ca²⁺, and suppression the expression of CaM, p-CaMKII, and p-Tau in Glu-damaged PC12 cells. In addition, on PC12 cells damaged by Aβ_25-35 (30 μM), dauricine (3 and 10 μM) can also significantly increase the cell viability and MMP levels, inhibit cell apoptosis, reduce intracellular ROS and free Ca²⁺ levels, and down-regulate protein expression of CaM, p-CaMKII, and p-Tau. This study demonstrates for the first time that dauricine and daurisoline may inhibit the excessive phosphorylation of Tau protein and subsequent cell apoptosis by suppressing the Ca²⁺-CaM/CaMKII pathway, thereby protecting PC12 cells damaged Glu or Aβ_25-35 <em>in vitro</em>. Dauricine and daurisoline have the potential to treat AD effectively and have further research value.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149609"},"PeriodicalIF":2.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143776621","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Researching the causal relationship between immune cells and frontotemporal Dementia: A Mendelian Randomization analysis","authors":"Yueming Cheng ,&nbsp;Xia He ,&nbsp;Xialian Huang ,&nbsp;Fengle Mao ,&nbsp;Fuli Qin ,&nbsp;Yanqiu Wang","doi":"10.1016/j.brainres.2025.149608","DOIUrl":"10.1016/j.brainres.2025.149608","url":null,"abstract":"<div><h3>Background</h3><div>Frontotemporal dementia (FTD) is a prevalent dementia syndrome with poorly understood immunological underpinnings. Despite the widespread adoption of high-density genotyping technologies like SNPs and CNVs, and advances in genome-wide association studies (GWAS), the immunological mechanisms underlying FTD remain elusive. This study aims to elucidate the causal relationships between immune cell traits and FTD using Mendelian randomization (MR).</div></div><div><h3>Methods</h3><div>We utilized summary data for FTD (cases = 129, controls = 392,463) from the FinnGen dataset and summary statistics for 731 immune cell traits from the GWAS catalog. These traits included morphological parameters (MP = 32), median fluorescence intensity (MFI = 389), absolute cell counts (AC = 118), and relative cell counts (RC = 192). Our approach encompassed forward MR (immune cell traits as exposure) and reverse MR (FTD as exposure), accompanied by rigorous sensitivity analyses to assess the robustness and heterogeneity of the findings.</div></div><div><h3>Results</h3><div>FTD did not have a statistically significant impact on immune phenotypes. Notably, we identified 13 immune phenotypes as protective against FTD, including various T cell and B cell markers. Conversely, 8 phenotypes were associated with increased FTD risk, involving markers on myeloid cells and subsets of T and B cells;</div></div><div><h3>Conclusion</h3><div>This MR study identifies specific immune phenotypes associated with FTD, highlighting potential pathways for future clinical research and therapeutic intervention.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1857 ","pages":"Article 149608"},"PeriodicalIF":2.7,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}