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Hippocampal functional imaging-derived radiomics features for diagnosing cognitively impaired patients with Parkinson's disease.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-28 DOI: 10.1186/s12868-025-00938-8
Wei Zeng, Xiao Liang, Jiali Guo, Weiling Cheng, Zhibiao Yin, Daojun Hong, Fangjun Li, Fuqing Zhou, Xin Fang
{"title":"Hippocampal functional imaging-derived radiomics features for diagnosing cognitively impaired patients with Parkinson's disease.","authors":"Wei Zeng, Xiao Liang, Jiali Guo, Weiling Cheng, Zhibiao Yin, Daojun Hong, Fangjun Li, Fuqing Zhou, Xin Fang","doi":"10.1186/s12868-025-00938-8","DOIUrl":"https://doi.org/10.1186/s12868-025-00938-8","url":null,"abstract":"<p><strong>Purpose: </strong>The aim of this retrospective study was to investigate whether radiomics features derived from hippocampal functional imaging can effectively differentiate cognitively impaired patients from cognitively preserved patients with Parkinson's disease (PD).</p><p><strong>Methods: </strong>The study included a total of 89 clinically definite PD patients, comprising 55 who werecognitively impaired and 34 who were cognitively preserved. All participants underwent functional magnetic resonance imaging and clinical assessments. Preprocessed functional data were utilized to derive the amplitude of the low-frequency fluctuations (ALFF), regional homogeneity (ReHo), voxel-mirrored homotopic connectivity (VMHC), and degree centrality (DC). A standardized set of radiomics features was subsequently extracted from the bilateral hippocampi, resulting in a total of 819 features. Following feature selection, the radiomics score (rad-score) and logistic regression (LR) models were trained. Additionally, the Shapley additive explanations (SHAP) algorithm was employed to elucidate and interpret the predictions made by the LR models. Finally, the relationships between the radiomics features derived from hippocampal functional imaging and the scores of the clinical measures were explored to assess their clinical significance.</p><p><strong>Results: </strong>The rad-score and LR algorithm models constructed using a combination of wavelet features extracted from ReHo and VMHC data exhibited superior classification efficiency. These models demonstrated exceptional accuracy, sensitivity, and specificity in distinguishing cognitively impaired PD patients (CI-PD) from cognitively preserved PD (CP-PD) patients, with values of 0.889, 0.900, and 0.882, respectively. Furthermore, SHAP values indicated that wavelet features derived from ReHo and VMHC were critical for classifying CI-PD patients. Importantly, our findings revealed significant associations between radiomics wavelet features and scores on the Hamilton Anxiety Scale, Non-Motor Symptom Scale, and Montreal Cognitive Assessment in CI-PD patients (P < 0.05, with Bonferroni correction).</p><p><strong>Conclusions: </strong>Our novel rad-score model and LR model, which utilize radiomics features derived from hippocampal functional imaging, have demonstrated their value in diagnosing CI-PDpatients. These models can enhance the accuracy and efficiency of functional MRI diagnosis, suggesting potential clinical applications.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"27"},"PeriodicalIF":2.4,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742234","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}
引用次数: 0
Experimental orthodontic pain drives anxiety state through the induction of alterations to the neuronal architecture in hippocampus. 实验性正畸疼痛通过诱导海马体神经元结构的改变而导致焦虑状态。
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-20 DOI: 10.1186/s12868-025-00945-9
Hongrui Que, Yuxuan Wang, Yi Feng, Shaoqin Tu, Jiaming Wei, Chiyuen Cheung, Nan Wei, Zheng Chen, Hong Ai
{"title":"Experimental orthodontic pain drives anxiety state through the induction of alterations to the neuronal architecture in hippocampus.","authors":"Hongrui Que, Yuxuan Wang, Yi Feng, Shaoqin Tu, Jiaming Wei, Chiyuen Cheung, Nan Wei, Zheng Chen, Hong Ai","doi":"10.1186/s12868-025-00945-9","DOIUrl":"10.1186/s12868-025-00945-9","url":null,"abstract":"<p><strong>Background: </strong>To explore the effect and mechanism of hippocampus on experimental orthodontic pain-induced anxiety.</p><p><strong>Methods: </strong>Herein, we document a novel modeling method whereby the nickel-titanium (Ni-Ti) orthodontic wire was fixed stably in the oral cavity of mice with a ligation technique to induce stable distal movement of maxillary incisors to mimic orthodontic tooth movement. At the experimental endpoint, serum corticosterone assay, Golgi staining and Micro-CT were performed in each group after oral-facial mechanical pain sensitivity assessment and open field test.</p><p><strong>Results: </strong>The mechanical pain sensitivity of experimental tooth movement pain (ETMP) mice had an apparent increased elicited following tooth movement. And anxiety-like behavior was developed: reduced the time proportion of center zone and the total moving distance in the open field test and the elevated serum corticosterone levels in ETMP mice relative to control group mice. The Golgi staining in ventral hippocampal CA1 revealed that neural spine density, dendritic length and number of dendrites are reduced markedly in ETMP mice compared with the control group.</p><p><strong>Conclusion: </strong>Experimental orthodontic pain drives emotional anxiety through the plasticity changes in decreased neuronal complexity and reduced spine density in ventral hippocampal CA1 in mice.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"26"},"PeriodicalIF":2.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668922","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}
引用次数: 0
Risk taking behaviour predicts consistent and heritable coping styles in zebrafish. 风险承担行为可预测斑马鱼一贯的、可遗传的应对方式。
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-20 DOI: 10.1186/s12868-025-00944-w
Lianne Koets, Tim van der Kwaak, Marcel Schaaf, Christian Tudorache
{"title":"Risk taking behaviour predicts consistent and heritable coping styles in zebrafish.","authors":"Lianne Koets, Tim van der Kwaak, Marcel Schaaf, Christian Tudorache","doi":"10.1186/s12868-025-00944-w","DOIUrl":"10.1186/s12868-025-00944-w","url":null,"abstract":"<p><strong>Background: </strong>Coping styles are individually coherent sets of behavioural and physiological responses to stress. Coping styles are thought to remain consistent across context and time, and display a certain level of heritability. Here, we examined whether risk taking is a predictor for consistency and heritability of stress coping styles in both larval and adult zebrafish (Danio rerio).</p><p><strong>Results: </strong>A group emergence test where fish emerge from a familiar housing compartment into a potentially dangerous novel environment, established the level of risk taking of F0 generation adult zebrafish. The degree of risk taking appeared to be consistent over time and context. Then, the F0 risk taking degree was further correlated with various behavioural parameters related to stress coping of the F1 and F2 generations. In larval fish, these parameters were measured during a light dark challenge which elicits an anxiety like response. In adults, they were measured during a single emergence test and a combined open field and mirror biting test, estimating the degree of risk taking and the level of explorativeness and aggressiveness. The results show that (i) parental risk taking behaviour is a good predictor for a large number of larval and adult behavioural parameters, within and between generations; (ii) a number of these parameters are consistent over ontogenetic (larval and adult) stages within the same generation, and (iii) four of these parameters representing risk taking, aggressiveness, and swimming behaviour, were correlated over multiple generations, establishing heritability of coping styles.</p><p><strong>Conclusion: </strong>We conclude that risk taking behaviour is a strong predictor of coping style within and between generations and behavioural parameters associated with risk taking are consistent over time and heritable over generations.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"25"},"PeriodicalIF":2.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924662/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668927","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}
引用次数: 0
Effects of repetitive transcranial magnetic stimulation on learning and memory cognitive function in rats with vascular cognitive impairment and its neural induction mechanism.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-18 DOI: 10.1186/s12868-025-00933-z
Jiati Wang, Huan Gao
{"title":"Effects of repetitive transcranial magnetic stimulation on learning and memory cognitive function in rats with vascular cognitive impairment and its neural induction mechanism.","authors":"Jiati Wang, Huan Gao","doi":"10.1186/s12868-025-00933-z","DOIUrl":"10.1186/s12868-025-00933-z","url":null,"abstract":"<p><strong>Background: </strong>The treatment of vascular cognitive impairment (VCI) is challenging, and its neurological mechanisms are not yet fully understood. Repetitive transcranial magnetic stimulation (rTMS) offers a new non-invasive treatment approach.</p><p><strong>Methods: </strong>One hundred male SD rats were grouped: intervention group (IG), model group (MG), sham group (SG), and control group (CG), to prepare the rat model of VCI. The Morris water maze (MWM) test was conducted, and oxidative stress (OS) markers, neurotrophic factors, apoptosis factors, and the amplitude of postsynaptic potential (PSP) in the hippocampus of rats were measured.</p><p><strong>Results: </strong>Post-intervention, IG's escape latency was lower than MG but higher than SG and CG. IG's hippocampal malondialdehyde (MDA) content, Bax, and Caspase-3 (Cas-3) were lower than MG but higher than SG and CG, while the tendency was opposite for Bcl-2 expression and the content of glutathione (GSH) and superoxide dismutase (SOD). IG's brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), and N-methyl-D-aspartate receptor 1 (NMDAR1) in the hippocampus were higher than MG but lower than SG and CG; The changes in the amplitude of PSP in the hippocampal region of IG at 10, 30, and 60 min were all higher than those in MG but lower than those in SG and CG (P < 0.05).</p><p><strong>Conclusion: </strong>Low-frequency rTMS visibly improved the learning and memory abilities of VCI rats and reduced OS levels.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"24"},"PeriodicalIF":2.4,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11916909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143656079","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}
引用次数: 0
Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-10 DOI: 10.1186/s12868-025-00943-x
Charles Etang Onukak, Omowumi Moromoke Femi-Akinlosotu, Adedunsola Adewunmi Obasa, Oluwabusayo Racheal Folarin, Temitayo Olabisi Ajibade, Olumayowa Olawumi Igado, Oluwaseun Olarenwaju Esan, Taiwo Olaide Oyagbemi, Adewunmi Victoria Adeogun, Ademola Adetokunbo Oyagbemi, Olufunke Eunice Ola-Davies, Temidayo Olutayo Omobowale, James Olukayode Olopade, Oluwafemi Omoniyi Oguntibeju, Momoh Audu Yakubu
{"title":"Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways.","authors":"Charles Etang Onukak, Omowumi Moromoke Femi-Akinlosotu, Adedunsola Adewunmi Obasa, Oluwabusayo Racheal Folarin, Temitayo Olabisi Ajibade, Olumayowa Olawumi Igado, Oluwaseun Olarenwaju Esan, Taiwo Olaide Oyagbemi, Adewunmi Victoria Adeogun, Ademola Adetokunbo Oyagbemi, Olufunke Eunice Ola-Davies, Temidayo Olutayo Omobowale, James Olukayode Olopade, Oluwafemi Omoniyi Oguntibeju, Momoh Audu Yakubu","doi":"10.1186/s12868-025-00943-x","DOIUrl":"10.1186/s12868-025-00943-x","url":null,"abstract":"<p><p>Diazinon is a commonly used organophosphate (OP) insecticide especially in developing countries for the control of insect pests, however, exposure to its toxic impact especially in humans and other non-target species remains an important public health concern. The study aimed to investigate the effect of epigallocatechin -3- gallate (EGCG), abundant in green tea plants on neurobehavioural, biochemical, and pathological changes in the brain of male Wistar rats following exposure to diazinon toxicity. Sixty adult male Wistar rats were acclimatized for seven days and subsequently randomly assigned into six treatment groups as follows: Group I: Control group (0.2 mL distilled water); Group II: Diazinon at 3 mg/kg (1% LD50); Group III: Diazinon (3 mg/kg) + EGCG (50 mg/kg, ~ 2% of LD50); Group IV: Diazinon (3 mg/kg) + EGCG (100 mg/kg, ~ 5% of LD50); Group V: EGCG (50 mg/kg) and Group VI: EGCG (100 mg/kg). All treatments were administered orally once daily for 14 days. Neurobehavioural studies, biomarkers of oxidative stress, histology, immunohistochemistry, and quantitative polymerase chain reaction (RT qPCR) were performed. Diazinon alone impaired recognition memory, increased oxidative stress markers and altered antioxidant defense in the brain. It upregulated TNF-α and IL-6 genes and repressed GPx 4 gene expressions. It was also associated with increased GFAP, Tau, and α-SN immunoreactivity. Microscopic examination revealed loss of Purkinje and hippocampal cells in brain. Co-treatment with EGCG however improved cognition, lowered oxidative stress markers, improved antioxidant status and suppressed TNF-α and IL-6. In conclusion, findings from this study demonstrated that EGCG offered protection against diazinon-induced neurotoxicity. Hence, natural sources of epigallocatechin -3- gallate such as fruits and vegetables could offer immense benefits by protecting against oxidative stress and inflammation in neurodegenerative disease conditions.Clinical trial number Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"22"},"PeriodicalIF":2.4,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595752","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}
引用次数: 0
Retraction Note: Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick's disease and fronto-temporal tauopathies.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-10 DOI: 10.1186/s12868-025-00942-y
Edward Rockenstein, Kiren Ubhi, Michael Mante, Jazmin Florio, Anthony Adame, Stefan Winter, Hemma Brandstaetter, Dieter Meier, Eliezer Masliah
{"title":"Retraction Note: Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick's disease and fronto-temporal tauopathies.","authors":"Edward Rockenstein, Kiren Ubhi, Michael Mante, Jazmin Florio, Anthony Adame, Stefan Winter, Hemma Brandstaetter, Dieter Meier, Eliezer Masliah","doi":"10.1186/s12868-025-00942-y","DOIUrl":"10.1186/s12868-025-00942-y","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"23"},"PeriodicalIF":2.4,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11892294/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595754","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}
引用次数: 0
Esketamine attenuates traumatic brain injury by modulating STAT3-mediated Glycolysis and immune responses.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-07 DOI: 10.1186/s12868-025-00941-z
Yufang Liu, Zheng Gong, Longfei Zhang, Xian Yang, Jie Zhu, Xin Zhou, Xingzhi Liao
{"title":"Esketamine attenuates traumatic brain injury by modulating STAT3-mediated Glycolysis and immune responses.","authors":"Yufang Liu, Zheng Gong, Longfei Zhang, Xian Yang, Jie Zhu, Xin Zhou, Xingzhi Liao","doi":"10.1186/s12868-025-00941-z","DOIUrl":"10.1186/s12868-025-00941-z","url":null,"abstract":"<p><strong>Background: </strong>Secondary injury following traumatic brain injury (TBI) involves neuroinflammation, immune cell infiltration, and metabolic dysregulation, leading to progressive neurological damage. This study evaluates the potential of esketamine, an NMDA receptor antagonist, to modulate immune responses, inhibit glycolysis, and mitigate secondary brain injury in a TBI mouse model.</p><p><strong>Methods: </strong>Male C57BL/6J mice were subjected to controlled cortical impact to induce TBI. Mice were treated with esketamine, either alone or combined with the STAT3 activator colivelin, or the glycolysis inhibitor 2-deoxyglucose (2-DG). Neurological function, BBB permeability, immune cell infiltration, macrophage polarization, and glycolytic activity were assessed using immunohistochemistry, flow cytometry, quantitative PCR, and enzyme-linked immunosorbent assay (ELISA).</p><p><strong>Results: </strong>Esketamine treatment significantly reduced structural brain tissue damage, including contusions, tissue loss, and edema, while also improving neurological outcomes in TBI mice. Mechanistically, esketamine inhibited CD4 + T cell activation and suppressed Th17 differentiation both in vivo and in vitro. It also promoted a shift in macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. Further analysis revealed that esketamine blocked STAT3 activation, which in turn reduced the expression of glycolytic genes (e.g., Hk2, Pgk1, Aldoa) essential for Th17 cell proliferation and M1 polarization. Co-treatment with colivelin reversed esketamine's effects on STAT3-mediated glycolysis, while 2-DG enhanced its anti-inflammatory actions.</p><p><strong>Conclusion: </strong>Esketamine attenuates TBI-induced neuroinflammation and tissue damage by inhibiting STAT3-mediated glycolysis, thus reducing Th17 and M1 macrophage activity and promoting regulatory and reparative immune responses. These findings highlight esketamine's potential as a therapeutic option for TBI, targeting both immune modulation and metabolic pathways to alleviate secondary injury.</p><p><strong>Clinical trial number: </strong>not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"21"},"PeriodicalIF":2.4,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889827/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584576","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}
引用次数: 0
The changes of digestive system inflammatory, oxidative stress, and histopathology factors following oral mesenchymal stem cells administration in rats with traumatic brain injury.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-06 DOI: 10.1186/s12868-025-00936-w
Masoud Eslami, Alireza Raji-Amirhasani, Mohammad Khaksari, Zakieh Keshavarzi, Farzaneh Rostamzadeh, Nazanin Sabet, Elham Jafari, Zahra Soltani, Saeed Karamouzian
{"title":"The changes of digestive system inflammatory, oxidative stress, and histopathology factors following oral mesenchymal stem cells administration in rats with traumatic brain injury.","authors":"Masoud Eslami, Alireza Raji-Amirhasani, Mohammad Khaksari, Zakieh Keshavarzi, Farzaneh Rostamzadeh, Nazanin Sabet, Elham Jafari, Zahra Soltani, Saeed Karamouzian","doi":"10.1186/s12868-025-00936-w","DOIUrl":"10.1186/s12868-025-00936-w","url":null,"abstract":"<p><strong>Background and aims: </strong>Mucous mesenchymal stem cells can migrate to damaged areas, and their use is proposed as a new approach to treating diseases. The present study aimed to investigate the effect of oral mesenchymal stem cells (OMSCs) on inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, intestine, and colon after traumatic brain injury (TBI).</p><p><strong>Methods and materials: </strong>Adult male rats were randomly divided into four groups: Sham, TBI, Vehicle (Veh), and Stem cell (SC). Intravenous injection of OMSCs was performed at 1 and 24 h after injury. The inflammatory, oxidative stress, and histopathological indices of the tissues of the stomach, small intestine, and colon were evaluated 48 h after injury.</p><p><strong>Results: </strong>After TBI, IL-1β and IL-6 levels increased and IL-10 levels decreased in the tissues of the stomach, small intestine, and colon, but the administration of OMSCS prevented these changes to a large extent. Oxidative stress indices (MDA, PC, TAC, SOD, and CAT) showed an increase in oxidative stress after TBI, but oxidative stress was less severe in the OMSC group. The administration of OMSCs after TBI improved the histopathological outcome in the tissues of the stomach, small intestine, and colon.</p><p><strong>Conclusion: </strong>Administration of OMSCs in rats suffering from TBI can improve inflammatory, oxidative stress, and histopathological indices in the tissues of the stomach, small intestine, and colon, which shows the beneficial effect of using OMSCs in TBI.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"20"},"PeriodicalIF":2.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571978","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}
引用次数: 0
Short-term lipopolysaccharide treatment leads to astrocyte activation in LRRK2 G2019S knock-in mice without loss of dopaminergic neurons.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-04 DOI: 10.1186/s12868-025-00939-7
Hoang Kieu Chi Ngo, Akriti Srivastava, Hoang Le, Samuel J Ayer, Grace F Crotty, Michael A Schwarzschild, Rachit Bakshi
{"title":"Short-term lipopolysaccharide treatment leads to astrocyte activation in LRRK2 G2019S knock-in mice without loss of dopaminergic neurons.","authors":"Hoang Kieu Chi Ngo, Akriti Srivastava, Hoang Le, Samuel J Ayer, Grace F Crotty, Michael A Schwarzschild, Rachit Bakshi","doi":"10.1186/s12868-025-00939-7","DOIUrl":"10.1186/s12868-025-00939-7","url":null,"abstract":"<p><strong>Background: </strong>The G2019S mutation of LRRK2, which enhances kinase activity of the protein, confers a substantial risk of developing Parkinson's disease (PD). However, the mutation demonstrates incomplete penetrance, suggesting the involvement of other genetic or environmental modulating factors. Here, we investigated whether LRRK2 G2019S knock-in (KI) mice treated with the inflammogen lipopolysaccharide (LPS) could model LRRK2 PD.</p><p><strong>Results: </strong>We found that short-term (2 weeks) treatment with LPS did not result in the loss of dopaminergic neurons in either LRRK2 G2019S KI or wild-type (WT) mice. Compared with WT mice, LRRK2 G2019S-KI mice showed incomplete recovery from LPS-induced weight loss. In LRRK2 G2019S KI mice, LPS treatment led to upregulated phosphorylation of LRRK2 at the autophosphorylation site Serine 1292, which is known as a direct readout of LRRK2 kinase activity. LPS treatment caused a greater increase in the activated astrocyte marker glial fibrillary acidic protein (GFAP) in the striatum and substantia nigra of LRRK2 G2019S mice than in those of WT mice. The administration of caffeine, which was recently identified as a biomarker of resistance to developing PD in individuals with LRRK2 mutations, attenuated LPS-induced astrocyte activation specifically in LRRK2 G2019S KI mice.</p><p><strong>Conclusions: </strong>Our findings suggest that 2 weeks of exposure to LPS is not sufficient to cause dopaminergic neuronal loss in LRRK2 G2019S KI mice but rather results in increased astrocyte activation, which can be ameliorated by caffeine.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"26 1","pages":"19"},"PeriodicalIF":2.4,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877714/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555749","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}
引用次数: 0
Visualization of perivascular spaces in the human brain with 5-T magnetic resonance imaging.
IF 2.4 4区 医学
BMC Neuroscience Pub Date : 2025-03-03 DOI: 10.1186/s12868-025-00925-z
Sirui Liu, Jianbo Li, Rui Hua, Yaowen Xing, Jiaojiao Wu, Jiang Lin, Jian Wang, Yan Shan, Lei Xu, Feng Shi, Mengsu Zeng
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