IBRO Neuroscience Reports最新文献

{"title":"Toxoplasma TgCtwh3 Δrop16Ⅰ/Ⅲ accelerates neuronal apoptosis and APP production in mouse with acute infection","authors":"Di Yang ,&nbsp;Cong Wang ,&nbsp;Qing Tao ,&nbsp;Lei Liu ,&nbsp;Mengmeng Jin ,&nbsp;Haiping Cai ,&nbsp;Meijuan Zheng ,&nbsp;Mengtao Gong ,&nbsp;Li Yu ,&nbsp;Jian Du ,&nbsp;Qingli Luo ,&nbsp;Jilong Shen ,&nbsp;Kunpeng Qin ,&nbsp;Deyong Chu","doi":"10.1016/j.ibneur.2025.05.009","DOIUrl":"10.1016/j.ibneur.2025.05.009","url":null,"abstract":"<div><h3>Objective</h3><div>To explore the mechanism by which <em>rop16</em>_{<em>Ⅰ/Ⅲ</em>}-deficient/<em>gra15</em>_<em>Ⅱ</em>-dominant <em>toxoplasma gondii</em> Chinese 1 genotype Wh3 (TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>}) strain induced neuron apoptosis, APP and BACE1 production <em>in vivo</em> and <em>vitro</em>.</div></div><div><h3>Method</h3><div>BALB/c mice were infected by intraperitoneal injection with TgCtwh3 wild type (TgCtwh3 WT) and TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites, respectively. One week after infection, the morphology and number of hippocampal neurons were examined by hematoxylin-eosin (H&amp;E) and Nissl staining. Expression levels of apoptosis-related proteins, APP, BACE1 as well as inflammatory factors proteins and genes in the hippocampus were evaluated using western blotting and qRT-PCR. The hippocampal neuron cell line HT22 was infected with TgCtwh3 WT and TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoite, respectively, and the expression of target proteins was analyzed through immunofluorescence staining and western blotting. Furthermore, HT22 apoptosis was assessed using flow cytometry.</div></div><div><h3>Result</h3><div>BALB/c mice injected with TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites presented abnormal appearance and posture changes as well as declined vitality. The hippocampus assay demonstrated that TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} <em>toxoplasma</em> caused neuron loss, neuron alignment disorder, neuronal nucleus abnormal deep-stained and neuron apoptosis. Furthermore, TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites caused obvious production of APP, BACE1and expression increase of pro-inflammatory factors in hippocampal tissue compared to these in mice infected with TgCtwh3 WT tachyzoites. Contrarily, the expression of transforming growth factor beta 1 (TGF-β1), a pivotal anti-inflammatory cytokine was significantly decreased in TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} infected mice. Further study showed that TgCtwh3 Δ<em>rop16</em>_{<em>Ⅰ/Ⅲ</em>} tachyzoites induced HT22 apoptosis through triggering ERS, meanwhile promoted HT22 to produce APP, BACE1 by activating NF-κB signaling pathway.</div></div><div><h3>Conclusion</h3><div>Our results indicated that the GRA15_Ⅱ effector may play a crucial part in neuron apoptosis, pro-inflammatory factors secretion, and APP, BACE1 production. Inversely, ROP16_Ⅰ/Ⅲ effector may play a potentially protective role in this process.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 830-843"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144178004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin D and brain volumetric changes: An updated systematic review and meta-analysis","authors":"Rozhina Tamannaeifar ,&nbsp;Salar Yousefzadeh ,&nbsp;Sana Rahmani ,&nbsp;Maedeh Bayani ,&nbsp;Mahdiyeh Nozad Varjovi ,&nbsp;Nima Eftekhari ,&nbsp;Mona Ranjkesh ,&nbsp;Mahsa Kohansal Vajargah ,&nbsp;Sajjad Hajihosseini ,&nbsp;Faezeh Ahanj ,&nbsp;Hadis Sarlak ,&nbsp;Komeil Aghazadeh-Habashi ,&nbsp;Melika Arab Bafrani ,&nbsp;Alaleh Alizadeh ,&nbsp;Yaser Khakpour ,&nbsp;Niloofar Deravi","doi":"10.1016/j.ibneur.2025.04.011","DOIUrl":"10.1016/j.ibneur.2025.04.011","url":null,"abstract":"<div><h3>Background</h3><div>In this systematic review and meta-analysis, we aimed to investigate the relationship between vitamin D levels and brain volumetric changes in human studies.</div></div><div><h3>Method</h3><div>We conducted a comprehensive search in PubMed, Scopus, and Google Scholar databases up to December 2024. A total of 450 studies were identified. Following title, abstract, and full-text screening, we included three studies for analysis. Data were extracted from these studies and analyzed using appropriate statistical methods.</div></div><div><h3>Result</h3><div>Our analysis revealed that the included case-control and cohort studies were conducted in the United States, Norway, and the Netherlands. The studies exhibited a range of characteristics, including sample size (number of patients: 183–240), demographic variables, and methods of assessing both vitamin D levels and brain volume. Brain volume assessments included gray matter, white matter, and total brain volume. The total follow-up duration across studies was 11 years. The age of participants ranged from 30 to 64 years in one study, while in another, they were aged 65 years or older. The meta-analysis indicated no significant association between vitamin D levels and brain volumetric changes across the included studies (effect size: 0.07, 95 % CI= [-0.01, 0.15], P = 0.07, I²=54.44 %).</div></div><div><h3>Conclusion</h3><div>This meta-analysis did not establish a significant association between vitamin D levels and brain volumetric changes. These findings highlighted the need for further large-scale studies to clarify the potential role of vitamin D in brain volume and to better understand the underlying mechanisms involved.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 844-852"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144185229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the knowledge of epilepsy and Potassium Channels: A scientometric analysis in CiteSpace and VOSviewer","authors":"Zheng Li","doi":"10.1016/j.ibneur.2025.05.004","DOIUrl":"10.1016/j.ibneur.2025.05.004","url":null,"abstract":"<div><div>Epilepsy is one of the most common neurological diseases. Studies have suggested that epileptic seizures are directly related to ion channel abnormalities in the central nervous system. Activation of potassium ion channels may lead to increased cell excitability and abnormal neuronal excitation. Over the past decade, significant progress has been achieved in understanding the potassium ion channel abnormalities related to epilepsy. To facilitate further research, in this paper, we adopted the bibliometrics method (based on Web of Science database) and used CiteSpace and VOSviewer to visualize literature in the field (Potassium Channels-related epilepsy) from 2010 to 2023. A total of 2415 original research and summary papers were included, and the basic situation, subject theme, and knowledge structure evolution were analyzed and discussed step by step from macro to micro perspectives.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 1-16"},"PeriodicalIF":2.0,"publicationDate":"2025-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144195622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CHPG's role in regulating apoptosis in heat-stressed microglia through endoplasmic reticulum stress: A new perspective☆","authors":"Yan-xuan He ,&nbsp;Zhi-qiang Zhang ,&nbsp;Xin-xin Zheng ,&nbsp;Fan Huang ,&nbsp;Guoxin He ,&nbsp;Xi-chong Yu ,&nbsp;An-cong Xu","doi":"10.1016/j.ibneur.2025.05.011","DOIUrl":"10.1016/j.ibneur.2025.05.011","url":null,"abstract":"<div><h3>Objective</h3><div>This study aims to explore the influence of microglia-mediated endoplasmic reticulum (ER) stress on cell apoptosis during heat stroke. Understanding this is important as it may help develop new therapies for heat-induced cellular damage and protect glial cells and brain health.</div></div><div><h3>Methods</h3><div>BV-2 cells were used as a cell model for this study. The negative control group was kept at 37°C throughout the experiment. Cells in the experimental group were pretreated with 1 mM CHPG (a selective mGluR5 agonist) for 0.5 hours, followed by heat shock (HS) for 0.5 hours at 40°C and then further cultivation at 37°C for 12 hours. The positive control cells underwent same condition except for drug pretreatment. Several assays were used including CCK8 assay for cell viability, flow cytometry for cell apoptosis index, immunofluorescence for the expression of GRP78, CHOP, and Caspase-12, as well as Western blotting for detecting the protein expression level of GRP78, CHOP, and Caspase-12.</div></div><div><h3>Results</h3><div>Heat shock induced a significant release of endoplasmic reticulum-related proteins and increased the expression levels of GRP78, CHOP, and Caspase-12 in BV-2 cells. CHPG was found to inhibit endoplasmic reticulum stress and cell apoptosis.</div></div><div><h3>Conclusion</h3><div>CHPG may primarily participate in heat shock by mediating endoplasmic reticulum stress and affecting microglia apoptosis.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 823-829"},"PeriodicalIF":2.0,"publicationDate":"2025-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of neuroinflammation on the progression of Alzheimer’s disease and its significant ramifications for novel anti-inflammatory treatments","authors":"Pritam Kamila ,&nbsp;Koyel Kar ,&nbsp;Sailee Chowdhury ,&nbsp;Priyanka Chakraborty ,&nbsp;Ria Dutta ,&nbsp;Sowmiya S ,&nbsp;Ankul Singh S ,&nbsp;Bhupendra Gopalbhai Prajapati","doi":"10.1016/j.ibneur.2025.05.005","DOIUrl":"10.1016/j.ibneur.2025.05.005","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is increasingly recognized as a disorder not solely of amyloid and tau accumulation but also of chronic immune dysregulation. Emerging evidence highlights the critical role of neuroinflammation, characterized by sustained activation of microglia and astrocytes, cytokine release, and inflammasome activation in accelerating AD progression. Genome-wide studies have further identified key inflammatory genes and immune pathways associated with increased disease risk. This review critically evaluates the mechanistic underpinnings of neuroinflammation in AD, focusing on glial cell behavior, immune signaling, and their contribution to neuronal dysfunction. Importantly, the review highlights recent advances in anti-inflammatory therapeutic approaches, including modulators of IL-1β, TNF-α, TREM2, and CB2 pathways. By integrating mechanistic and therapeutic insights, this work underscores the potential of immunomodulatory strategies as viable interventions in AD and provides a novel framework for future research in targeted anti-neuroinflammatory treatments.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 771-782"},"PeriodicalIF":2.0,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions","authors":"Chenghu Xie ,&nbsp;Cunxin Zhang ,&nbsp;Kefeng Zhang ,&nbsp;Shanshan Zhang","doi":"10.1016/j.ibneur.2025.05.007","DOIUrl":"10.1016/j.ibneur.2025.05.007","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease is a progressive neurodegenerative disorder. Current therapeutic agents primarily focus on symptom alleviation and fail to effectively halt disease progression. Therefore, there is a need to develop novel therapeutic strategies, particularly those involving natural active compounds with multi-target actions.</div></div><div><h3>Objective</h3><div>To investigate the intervention effects and multi-target regulatory mechanisms of Ginsenoside C-K (GCK) on β-amyloid (Aβ) oligomer-induced Alzheimer's disease (AD) pathological progression.</div></div><div><h3>Methods</h3><div>BV2 microglia and HT22 neurons were used as in vitro models. Cell viability was measured via CCK-8 assay, cell migration ability assessed by scratch assay, and apoptosis rate analyzed using Annexin V/PI dual staining. A conditioned medium (CM) strategy was employed to validate microglia-neuron interactions. Western blot was performed to detect key NF-κB signaling pathway proteins (p-IκBα, p-p65) and inflammatory cytokines (TNF-α, IL-1β).</div></div><div><h3>Results</h3><div>GCK pretreatment significantly ameliorated Aβ₁₋₄₂ oligomer-induced BV2 cell dysfunction (viability recovery rate &gt;80 %, p &lt; 0.01), suppressed pro-inflammatory cytokine secretion (TNF-α reduced by 62.3 %, IL-1β by 57.8 %), and inhibited NF-κB pathway activation (p-IκBα/p-p65 expression downregulated &gt;50 %). In HT22 neurons, GCK directly counteracted Aβ toxicity (apoptosis rate decreased from 38.7 % to 15.2 %) and exerted indirect neuroprotection by modulating microglia-derived conditioned medium (CM2 group showed a 2.1-fold increase in neuronal viability compared to CM1).</div></div><div><h3>Conclusion</h3><div>GCK mitigates AD pathology through dual mechanisms-direct inhibition of Aβ neurotoxicity and indirect regulation of microglial homeostasis-with NF-κB signaling suppression as a core mechanism. This study provides new experimental evidence for natural product-based multi-target AD therapies, though further animal studies are required to validate its in vivo efficacy and safety.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 783-793"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A study on structural imaging changes and serum neurofilament light chain (NfL) levels in individuals with white matter hyperintensities, combining imaging techniques with biomarker analysis","authors":"Meini Wu ,&nbsp;Zihao Li ,&nbsp;Yuhang Ren ,&nbsp;Siou Li ,&nbsp;Weina Zhao ,&nbsp;Jian Xing ,&nbsp;Jiangnan Yi ,&nbsp;Fengze Zhao ,&nbsp;Changhao Yin","doi":"10.1016/j.ibneur.2025.05.008","DOIUrl":"10.1016/j.ibneur.2025.05.008","url":null,"abstract":"<div><h3>Objective</h3><div>To elucidate the association between serum neurofilament light chain (NfL) levels and structural brain alterations in individuals exhibiting white matter hyperintensities (WMHs), as well as to investigate the potential utility of serum NfL as a predictive biomarker for the progression of WMH.</div></div><div><h3>Methods</h3><div>A total of 151 subjects were included in the study, among whom 117 demonstrated the presence of white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI). We assessed the relationship between changes in serum neurofilament light chain (NfL) levels and alterations in brain volume across three distinct groups. Additionally, we analyzed trends in brain structural changes and serum NfL level variations within the population exhibiting varying severities of WMHs, exploring the correlation between these two variables.</div></div><div><h3>Results</h3><div>Serum NfL levels were significantly elevated in individuals with WMHs compared to those with none-low WMHs (p &lt; 0.001). Furthermore, higher serum NfL levels were observed in individuals with severe-moderate WMHs compared to those with mild WMHs (p &lt; 0.01). Within the mild WMHs group, serum NfL levels exhibited a negative correlation with gray matter volume. In contrast, within the severe to moderate WMHs group, serum NfL levels were negatively correlated with both gray matter volume (GMV) and white matter volume (WMV). Voxel-based morphometry (VBM) analysis indicated the presence of gray matter atrophy in several brain regions when comparing the none-low WMHs group with the severe to moderate WMHs group, as well as when comparing the mild WMHs group with the severe-moderate WMHs group. However, no significant differences were observed in the comparison between the none to low WMHs group and the mild WMHs group.</div></div><div><h3>Conclusion</h3><div>Serum NfL levels have been observed to rise in conjunction with the increasing severity of WMH and show a correlation with gray matter atrophy in individuals exhibiting WMHs. These levels are anticipated to serve as a biological marker for predicting the progression of WMH.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 794-802"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Governor Vessel combined with local acupoints electroacupuncture improves the therapeutic effect of nerve conduit transplantation bridging long segment defects of the median nerve","authors":"Yu Cheng ,&nbsp;Fanqi Meng ,&nbsp;Zhanmou Liang ,&nbsp;Xin Zhou ,&nbsp;Wenya Pei ,&nbsp;Jingwen Ruan ,&nbsp;Xiaozhou Lu ,&nbsp;Ying Ding ,&nbsp;Guanheng He","doi":"10.1016/j.ibneur.2025.05.003","DOIUrl":"10.1016/j.ibneur.2025.05.003","url":null,"abstract":"<div><div>Nerve defect is a relatively serious injury in peripheral nerve injury, which often leads to the neuron apoptosis of the corresponding spinal cord segment and the difficulty of long-distance regeneration of the damaged nerve fibers, collectively resulting in poor recovery of nerve function after surgery. All experimental rats were randomly assigned to the following groups: Control, Conduit, Local acupoints electroacupuncture (EA) (Local-EA), and governor vessel (GV) combined with local acupoints electroacupuncture (GV+Local-EA) groups. A 10-mm defect model was established in the left median nerve, and a chitosan nerve conduit was used to bridge the defect. After 4 weeks, nerve regeneration and functional recovery were evaluated using immunofluorescence histochemistry, behavioral assays, and electrophysiological measurements. Results showed that the GV+Local-EA group exhibited significantly elevated the number of ChAT-positive motor neurons and enhanced the GDNF expression within the C8 spinal cord anterior horn compared with other experimental groups (<em>P</em> &lt; 0.01). Furthermore, the density of NF-positive nerve fibers and S100β-positive Schwann cells in the middle and distal parts of the transplanted conduits was significantly higher in the GV+Local-EA group than in other groups (<em>P</em> &lt; 0.05). The behavioral improvements and the median nerve conduction complex action potential were significantly better in the GV+Local-EA group (<em>P</em> &lt; 0.05). These results suggest that GV combined with local acupoints electroacupuncture can prevent the loss of spinal motor neurons and upregulating the GDNF expression, and then facilitates the regeneration of damaged median nerve fibers along the Schwann cell-formed Bungner band toward the distal end, thereby accelerating functional recovery of the affected forelimb and demonstrating superior therapeutic efficacy compared with conventional local acupoint protocols.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 814-822"},"PeriodicalIF":2.0,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168750","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An approach to screen susceptible rats and efficacy of an antidepressive treatment after chronic stress","authors":"Kenji B. Valencia-Flores ,&nbsp;Yahel Vidal-de-laO ,&nbsp;Diana Paz-Trejo ,&nbsp;Hugo Sánchez-Castillo","doi":"10.1016/j.ibneur.2025.05.001","DOIUrl":"10.1016/j.ibneur.2025.05.001","url":null,"abstract":"<div><div>Chronic stress during life has been considered a risk factor for the development of psychiatric illness in humans. Chronic unpredictable stress battery (CUSB) is an animal model to study depression through stress exposition in rodents. CUSB induces depression and anxiety behavioral markers that could be modulated with fluoxetine an antidepressant treatment. However, it is well known that not all subjects develop depression-like behaviors or do not respond to antidepressant treatments. The way to screen these individual differences in susceptibility to stress or the efficacy of antidepressant therapy in depression models is not well studied. Here we show that saccharine consumption, immobility and time spent in the center of the area could be useful as behavioral markers for screening susceptibility to stress and depression, also we show that fluoxetine treatment had different efficacy depending on the age when the stress occurred. First, we found that after CUSB (during adolescence, adulthood, or both) rodents show depression and anxiety profiles. Second, we found that fluoxetine (10 mg/kg) could recover depression but no anxiety profile in all the groups exposed to stress. Finally, we use the machine learning clustering method (k-means), to classify the subjects in all groups based on the individual effects modulated by stress exposure and antidepressant treatment to find the ratio of stress effects and pharmacological efficacy. Using altered behaviors as classifiers, we found three possible clusters, (1) Without alterations, (2) Moderated anxiety and depression profile (3) Serious anxiety and depression profile, suggesting two groups of susceptible animals with different intensities of altered behavior. Also, fluoxetine could change the ratio of rats previously classified in groups 2 or 3, showing the beneficial effects of antidepressant treatment. Our results demonstrate that CUSB has different consequences even in subjects that experienced the same stress protocol. Also, fluoxetine has different efficacy in recovering behavior associated with the age of exposure to stress. Finally, we suggest k-means as an easy and useful method to apply in susceptible rodent studies of depression and to study the individual efficacy of antidepressant treatment.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 803-813"},"PeriodicalIF":2.0,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Environmental restraint: A hidden risk factor for stress-induced depression in rats","authors":"Hiroko Mochizuki-Kawai ,&nbsp;Seita Nakazawa ,&nbsp;Hideaki Oike ,&nbsp;Hiromi Kimoto ,&nbsp;Satoru Tomita ,&nbsp;Michimasa Toyoshima ,&nbsp;Tingbi Xiong ,&nbsp;Kazuo Yamada","doi":"10.1016/j.ibneur.2025.05.002","DOIUrl":"10.1016/j.ibneur.2025.05.002","url":null,"abstract":"<div><div>Little is known about the impact of environmental restraint, characterized by limited space and a lack of stimulating elements, on adult mental and physical health. We examined the influence of environmental restraint on depression-like behaviors and physical status in rats, and the potential mitigating effects of <em>Lactococcus cremoris</em> H61 as a beneficial bacterium. Rats subjected to environmental restraint exhibited prolonged maladaptive immobility in the forced swim test without showing changes in body weight, locomotion, or social motivation. Daily activities remained unaffected. These findings suggest that environmental restraint may be a covert risk factor for stress-induced depression, potentially alleviated by supplementation with strain H61.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 754-758"},"PeriodicalIF":2.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}