BMC Neuroscience最新文献

{"title":"Short- and long-term neurobehavioural impairments in mice offspring following chronic perinatal caffeine exposure and withdrawal.","authors":"Funmilayo Eniola Olopade, Oluwabusayo Racheal Folarin, Taidinda Tashara Gilbert, James Olukayode Olopade","doi":"10.1186/s12868-025-00981-5","DOIUrl":"10.1186/s12868-025-00981-5","url":null,"abstract":"<p><p>This study explored neurodevelopmental and adult neurobehavioural outcomes in mouse offspring following chronic perinatal caffeine exposure and subsequent withdrawal. Healthy adult female BALB/c mice were mated and, at gestational day (GD) 10, were randomly assigned to one of three groups (n = 4): control, low-dose caffeine, and high-dose caffeine. The caffeine-exposed groups received either a low (50 mg/kg) or high (100 mg/kg) dose of caffeine daily via oral gavage from GD 10 until the end of lactation at postnatal day (PND) 21, whereas the control group received sterile water. At PND 21, a subset of offspring from the caffeine-exposed and control groups underwent neurodevelopmental behavioural assessments, including negative geotaxis, cliff avoidance, and surface righting tests, to evaluate the effects of chronic perinatal caffeine exposure on sensorimotor reflex functions. The remaining offspring were allowed to grow into adulthood and, at three months of age, underwent neurobehavioural assessments to evaluate motor function, anxiety-like behaviour, and cognition via the pole test, open field test, and Morris water maze (MWM) test. Compared with those in the high-dose caffeine group, the mice in the low-dose caffeine group had accelerated attainment of neurological milestones, such as the righting reflex and cliff avoidance. Conversely, compared with the control and low-dose caffeine treated offspring, the high-dose caffeine-treated offspring presented delayed eye opening and impaired negative geotaxis. However, there were no significant differences between the caffeine-exposed and control groups in the adult neurobehavioural assessments following caffeine withdrawal. These findings suggest that perinatal caffeine exposure can influence early neurodevelopmental processes but does not seem to have persistent effects on motor function, cognition, or anxiety in adulthood. This study underscores the transient nature of caffeine’s impact on brain development and highlights the need for further research to explore the long-term consequences of prenatal caffeine exposure.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"63"},"PeriodicalIF":3.3,"publicationDate":"2025-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12606910/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145494538","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":"Effects of different transcranial magnetic stimulation coil types on phosphene thresholds and their association with motor cortex excitability.","authors":"Halit Fidancı, Halil Can Alaydın, Cemre Cöddü, İrem Yakıcı, Zülfikar Arlıer","doi":"10.1186/s12868-025-00977-1","DOIUrl":"10.1186/s12868-025-00977-1","url":null,"abstract":"<p><p>BACKGROUND: Phosphenes can be induced by applying transcranial magnetic stimulation (TMS) to the visual cortex. Since multiple factors influence phosphene perception, this study aimed to examine the effects of different TMS coil types on phosphene thresholds (PTs). Additionally, the relationship between PT and motor cortex excitability was explored. METHODS: In Session 1, TMS was applied to the left visual cortex of 22 healthy individuals using a round coil and a figure-eight coil, and PT was recorded. Resting motor threshold (RMT), active motor threshold (AMT), and short-interval intracortical inhibition (SICI) were assessed by stimulating the left motor cortex. After 5–7 days, the visual cortex was stimulated again in Session 2 with the same healthy individuals. RESULTS: In Session 1, the mean PTs obtained with the round and figure-eight coils were 39.71 ± 9.67% (n = 17) and 53.93 ± 14.26% (n = 15), respectively (p = 0.001). In Session 2, the mean PTs were 37.83 ± 11.34% and 51.53 ± 14.03% (p = 0.001) for the round and figure-eight coils, respectively. The intraclass correlation coefficients for PTs across studies were 0.832 for the round coil and 0.591 for the figure-eight coil. No significant correlation was found between PT and AMT, RMT, or SICI. CONCLUSION: PTs were lower with the round coil than with the figure-eight coil. The reliability of PTs can be considered good for round coil and moderate for figure-eight coil. Additionally, the findings suggested that motor cortex and visual cortex excitability are different entities.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"62"},"PeriodicalIF":3.3,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12532860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306852","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":"Dexmedetomidine pretreatment improves postsurgical delay in neurocognitive recovery in aged mice by inhibiting hippocampal microglial activation via activation of cholinergic anti-inflammatory pathways.","authors":"Qidi Zhang, Shiyu Hao, Guicheng Wang, Chengxiao Liu, Gongming Wang, Jie Zhang, Jinyang Zhao, Xiaowei Li, Jingjing Li, Jiangnan Wu, Xu Wang","doi":"10.1186/s12868-025-00969-1","DOIUrl":"10.1186/s12868-025-00969-1","url":null,"abstract":"<p><strong>Background: </strong>Perioperative use of dexmedetomidine (DEX) reduces the incidence of Delayed Neurocognitive Recovery (DNR) in elderly patients, though mechanisms remain unclear. This study investigated whether DEX improves DNR by inhibiting microglial activation and explored the cholinergic anti-inflammatory pathway's role.</p><p><strong>Methods: </strong>An exploratory laparotomy model was established in aged C57BL/6J mice, with preoperative treatment using DEX or DEX combined with α-bungarotoxin. Cognitive function was assessed through the novel object recognition (NOR) and Morris water maze (MWM) tests, while immunofluorescence was used to observe microglial morphology, and qPCR and ELISA were employed to detect inflammatory factor expression.</p><p><strong>Results: </strong>DEX pretreatment significantly reduced the escape latency of aged mice on postoperative days 3-5 (50.50 ± 3.73 vs. 55.01 ± 4.01, P = 0.04; 36.36 ± 4.31 vs. 43.42 ± 5.64, P = 0.01; 27.00 ± 3.94 vs. 34.50 ± 5.54, P = 0.006), increased number of times crossing the previous platform location (2.50 ± 1.31 vs. 1.08 ± 0.90, P = 0.02), and percentage of dwell time in the target quadrant (37.87 ± 9.66 vs. 25.00 ± 4.48, P < 0.001). DEX pretreatment also reduced the expression of pro-inflammatory cytokines in the hippocampus (TNF-α, 604.10 ± 165.40 vs. 915.30 ± 97.64, P = 0.002; IL-6, 145.30 ± 12.11 vs. 176.50 ± 16.15, P = 0.002; IL-1β, 59.68 ± 4.29 vs. 68.73 ± 3.11, P = 0.001) of aged mice postoperatively, as well as in the spleen and serum. Additionally, DEX pretreatment reduces microglia count (96.60 ± 11.84 vs. 136.20 ± 32.62, P = 0.05), fluorescence (0.96 ± 0.06 vs. 1.10 ± 0.02, P < 0.001), morphology (7.20 ± 2.17 vs.12.80 ± 2.28, P = 0.002) in aged mice post-surgery. Pre-administration of α-bungarotoxin before DEX pretreatment partially reversed these effects.</p><p><strong>Conclusions: </strong>DEX pretreatment ameliorated DNR in aged mice is related to inhibition of microglial activation, which was at least partially attributed to activation of the cholinergic anti-inflammatory pathway.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"61"},"PeriodicalIF":2.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12522617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298309","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":"Long-term neprilysin gene transfer is associated with reduced levels of intracellular Abeta and behavioral improvement in APP transgenic mice.","authors":"Brian Spencer, Robert A Marr, Edward Rockenstein, Leslie Crews, Anthony Adame, Rewati Potkar, Christina Patrick, Fred H Gage, Inder M Verma, Eliezer Masliah","doi":"10.1186/s12868-025-00980-6","DOIUrl":"10.1186/s12868-025-00980-6","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"60"},"PeriodicalIF":2.3,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12512934/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273677","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":"Characterisation of the expression of P2X7 receptor, cancer stem cell markers and immunological mediators in human high-grade gliomas.","authors":"Liyen K Kan, Matthew Drill, Andrea Muscat, Paul Sanfilippo, Richard P Sequeira, Padmakrishnan C Jayakrishnan, Anh Vo, Nicholas C Wong, Marian Todaro, Catriona McLean, Katherine J Drummond, Martin Hunn, David A Williams, Terence J O'Brien, Mastura Monif","doi":"10.1186/s12868-025-00973-5","DOIUrl":"10.1186/s12868-025-00973-5","url":null,"abstract":"<p><strong>Introduction: </strong>Glioblastoma is the most aggressive primary brain cancer. It is considered an 'immunologically cold' tumour where immune infiltrates are polarised to drive immunosuppression-and therefore tumour proliferation. An important driver of neuroinflammation in glioma is the purinergic P2X7 receptor (P2X7R). While much of the complex glioma microenvironment has been characterised, studies expounding the associations between various cytokines/chemokines, immune cell markers, P2X7R expression and glioma stemness are lacking. Here we aimed to characterise the mRNA expression profiles of various tumour markers, and common 'pro-' and 'anti-tumour' inflammatory mediators, and correlate this to P2X7R expression in human high-grade glioma samples compared to 'healthy' non-tumour post-mortem brain.</p><p><strong>Methods: </strong>High grade gliomas were collected from 34 patients undergoing routine tumour resection surgery and compared to 12 'healthy' post-mortem controls. High throughput qPCR was performed on extracted RNA converted to cDNA to examine a custom-made panel of 38 tumour and immune related genes.</p><p><strong>Results: </strong>Markers of innate immunity including CD68, S100A9, HLADR, NLPR3, interleukin (IL) 1β, IL-6, TNFα and NF-κB were significantly increased in human derived glioblastoma samples compared to healthy control brain. P2X7R was also upregulated in the glioma microenvironment and its expression was linked to the expression of VEGFB, MMP9, PCNA, IL-4 and IL-8. The level of expression of P2X7R was not associated with overall survival in high grade gliomas.</p><p><strong>Discussion: </strong>Collectively, this study confirms the significant overexpression of P2X7R in human high-grade gliomas as well as highlights the presence of a multidirectional neuroinflammatory milieu in which both tumour-promoting and tumour-suppressive genes are overexpressed.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"59"},"PeriodicalIF":2.3,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12486668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205102","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":"Publisher Correction: Mir-199a-3p aggravates neuroinflammation in an Alzheimer's disease transgenic mouse model by promoting M1-polarization microglia.","authors":"Chenyang Wang, Xiaolu Bu, Mengyao Cao, Yunyu Lian, Haocong Ling, Mo You, Junfei Yi, Xiaoya Gao, Duobin Wu, Yang Li","doi":"10.1186/s12868-025-00974-4","DOIUrl":"10.1186/s12868-025-00974-4","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"58"},"PeriodicalIF":2.3,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145069014","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":"Investigating topological alterations in procedural memory network across neuropsychiatric disorders using rs-fMRI and graph theory.","authors":"Mahdi Mohammadkhanloo, Hamid Sharini, Mitra Yousefpour, Mohammad Pooyan","doi":"10.1186/s12868-025-00979-z","DOIUrl":"10.1186/s12868-025-00979-z","url":null,"abstract":"<p><p>BACKGROUND: Cognitive network dysfunction represents a core pathophysiological feature across major neuropsychiatric disorders, including Attention Deficit Hyperactivity Disorder (ADHD), bipolar disorder (BD), and schizophrenia (SZ). The procedural memory network (PMN), involving cortico-striatal-cerebellar circuits, is vital for skill learning and automatic cognition. However, its topological changes and link to cognitive impairments have not been studied across major neuropsychiatric disorders. METHODS: This study analyzed resting-state functional MRI (rs-fMRI) data from 40 individuals with ADHD, 49 with BD, 50 with SZ, and 50 healthy controls (HCs). PMN was defined using 34 regions of interest (ROIs) from Harvard-Oxford Atlas, with graph theory measures calculated for all regions. Significant network disruptions emerged, showing altered local efficiency (LE), average path length (APL), and degree (P < 0.05) across groups. RESULTS: Key findings show that in ADHD, increased APL in left cerebellar lobule VII indicates disrupted information flow and emotional processing, while decreased connectivity in the right claustrum may impair integration and working memory. In BD, reduced LE in right cerebellar lobule II is linked to attention and motor control deficits; increased APL in lobules I and VIII suggests disrupted network communication and emotional processing; and decreased connectivity in the right subthalamic nucleus and lobule VIII may contribute to mood swings and attention problems. In SZ, decreased LE in right putamen and left cerebellar lobule VIII relates to working memory and emotional processing deficits; reduced APL in right caudate and cerebellar lobule II implies more effort for regional communication; and increased connectivity in the caudate and right cerebellar lobules I and II likely reflects compensatory or pathological hyperactivity. Comparisons indicate SZ shows increased connectivity in the claustrum and cerebellar lobule I, unlike ADHD which shows decreases in these areas; SZ has lower network efficiency but higher caudate connectivity than BD, which has more cerebellar and subthalamic disruptions; and BD shows decreased connectivity in the claustrum and subthalamic nucleus compared to ADHD, which has more cerebellar and attention network changes. CONCLUSION: These findings suggest that the PMN, particularly its segregation and integration properties, plays a key role in explaining cognitive deficits in ADHD, BD, and SZ. CLINICAL TRIAL NUMBER: Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"57"},"PeriodicalIF":3.3,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12403410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941883","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":"SRT1720 ameliorates LPS-induced depressive-like behaviors in mice and activates Parkin-mediated mitophagy.","authors":"Luna Sun, Chaoran Li, Jianli Shi, Wenfeng Zeng, Lingling Wu, Shunlun Wan, Yunxia Wang","doi":"10.1186/s12868-025-00968-2","DOIUrl":"10.1186/s12868-025-00968-2","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence suggests a connection between mitophagy-a key mitochondrial quality control mechanism-and depression. Furthermore, sirtuin 1 (SIRT1), a NAD⁺-dependent deacetylase, has been implicated in the pathophysiology of depression, though its precise role remains elusive. This study aimed to investigate how SIRT1 modulates depressive-like behaviors in mice and to determine whether mitophagy mediates this process.</p><p><strong>Methods: </strong>Male BALB/c mice were administered lipopolysaccharide (LPS) to mimic depressive-like behaviors. The treatment group received a pre-administration of SRT1720 (50 mg/kg, i.p.), a specific SIRT1 activator. Depressive-like behaviors were assessed by sucrose preference test (SPT) and forced swimming test (FST). Additionally, hippocampal neuronal and mitochondrial ultrastructure was detected via transmission electron microscopy (TEM), and mitophagy-related protein expression was examined by western blotting.</p><p><strong>Results: </strong>Results demonstrated that activation of SIRT1 significantly mitigated LPS-induced depressive-like behaviors in mice. Moreover, it was observed that SIRT1 activation protected against LPS-induced neuronal and mitochondrial damage in the hippocampus. TEM analysis revealed a marked increase in hippocampal autophagosomes following SIRT1 activation, accompanied by significantly elevated expression of LC3II and Parkin, suggesting enhanced mitophagy. In vitro experiment using HT-22 cells provided additional evidence that SIRT1 activation ameliorated LPS-induced mitochondrial dysfunction and promoted mitophagy via Parkin-mediated pathway.</p><p><strong>Conclusions: </strong>These findings suggested that activation of SIRT1 could alleviate depressive-like behaviors in mice following LPS challenge, potentially through a Parkin-dependent mitophagy mechanism.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"56"},"PeriodicalIF":2.3,"publicationDate":"2025-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12398113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941902","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":"Threat context impairs cognitive control of neutral words processing in social anxiety individuals: evidence from ERP and theta oscillations.","authors":"Haiyan Zhao, Feng Si, Hui Meng, Haibo Yang, Dawei Sun, Longyan Peng, Jianqin Cao","doi":"10.1186/s12868-025-00976-2","DOIUrl":"10.1186/s12868-025-00976-2","url":null,"abstract":"<p><strong>Background: </strong>Social anxiety (SA) is characterized by cognitive control impairments, particularly in the processing of threat, yet how threat-laden environments modulate cognitive control over neutral stimuli remains unclear. This study examined whether threat context impairs the processing of neutral words in individuals with high social anxiety (HSA) through electrophysiological and oscillatory dynamics.</p><p><strong>Methods: </strong>A total of 151 participants (HSA vs. low social anxiety, LSA) completed a Stroop task in two conditions: (1) threat context (neutral words intermixed with social threat words), and (2) neutral-only (neutral words only). Behavioral responses (RTs), ERP (N2, N450, SP), and frontal-midline theta oscillations were analyzed.</p><p><strong>Results: </strong>Threat context significantly prolonged RTs in HSA compared to LSA individuals. ERP data revealed that LSA individuals exhibited larger N450 and reduced SP under threat than under neutral-only conditions, indicating efficient conflict resolution. However, LSA individuals showed blunted N450 but amplified SP, suggesting prolonged attentional engagement with neutral stimuli in threat contexts. Time-frequency analyses further demonstrated that LSA participants increased frontal theta power in the threat context, whereas HSA individuals displayed suppressed theta activity, reflecting impaired top-down cognitive control. Threat contexts contaminate the processing of neutral stimuli in HSA individuals, marked by attenuated conflict detection (N450), increased attention engagement (SP), and deficient theta-mediated control.</p><p><strong>Conclusion: </strong>These findings indicate that threat context impairs cognitive control of neutral word processing in HSA individuals when threat is possible, bridging cognitive and clinical models of attentional dysregulation.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"54"},"PeriodicalIF":2.3,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12392606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941961","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":"Comparative study of ¹⁸F-labeled PET radiopharmaceuticals in an Alzheimer's disease mouse model.","authors":"Bok-Nam Park, Su-Min Kim, Young-Sil An","doi":"10.1186/s12868-025-00978-0","DOIUrl":"10.1186/s12868-025-00978-0","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia, characterized by memory loss, cognitive decline, and significant social and economic burdens. Despite extensive research into amyloid positron emission tomography (PET) radiopharmaceuticals, the effectiveness of various ¹⁸F-labeled tracers for imaging amyloid plaques in AD mouse models remains uncertain. This study aimed to evaluate the performance of three radiopharmaceuticals-¹⁸F-florbetaben (FBB), ¹⁸F-flutemetamol (FMM), and ¹⁸F-florapronol (FPN)-in differentiating amyloid deposition in AD and control mice.</p><p><strong>Results: </strong>¹⁸F-FMM and ¹⁸F-FBB demonstrated significantly higher standardized uptake value ratios (SUVRs) in AD mice than in controls. For ¹⁸F-FBB, the mean SUVR in AD mice was 1.06, significantly higher than the 0.81 in controls (p < 0.001). Similarly, ¹⁸F-FMM showed a mean SUVR of 0.97 in AD mice compared to 0.94 in controls (p = 0.024). In contrast, ¹⁸F-FPN did not show significant SUVR differences between AD and control groups (p = 0.071). Comparative analysis revealed that ¹⁸F-FBB exhibited a significantly greater SUVR difference between AD and control groups compared to ¹⁸F-FMM (p < 0.001).</p><p><strong>Conclusions: </strong>¹⁸F-FBB emerged as the most effective radiopharmaceutical for imaging amyloid deposition in AD mouse models, providing superior differentiation between AD and control groups. These findings support the optimization of amyloid PET tracers for preclinical studies, facilitating advancements in Alzheimer's research.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"55"},"PeriodicalIF":2.3,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12392510/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941899","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}