IBRO Neuroscience Reports最新文献

{"title":"Effect of microwave radiation on adult neurogenesis and behavior of prenatally exposed rats","authors":"Alexandra Popovičová ,&nbsp;Enikő Račeková ,&nbsp;Marcela Martončíková ,&nbsp;Kamila Fabianová ,&nbsp;Adam Raček ,&nbsp;Monika Žideková","doi":"10.1016/j.ibneur.2024.08.007","DOIUrl":"10.1016/j.ibneur.2024.08.007","url":null,"abstract":"<div><p>Postnatal neurogenesis appears to be highly sensitive to environmental factors, including microwave electromagnetic radiation (MWR). Here, we investigated the impact of MWR during intrauterine development on juvenile and adult neurogenesis in the rostral migratory stream (RMS) and the dentate gyrus of the hippocampus in the rat brain, as well as its effect on animal behavior. Female rats were exposed to MWR at a frequency of 2.45 GHz for 2 hours daily throughout pregnancy. The offspring of irradiated mothers survived to either juvenile age or adulthood. The brains of the rats were subjected to morphological analysis, assessing cell proliferation and death in both neurogenic regions. In the RMS, the differentiation of nitrergic neurons was also investigated. The effect of MWR on behavior was evaluated in rats surviving to adulthood. Prenatal MWR exposure caused significant changes in the number of proliferating and dying cells, depending on the age of the animals and the observed neurogenic region. In addition, MWR attenuated the maturation of nitrergic neurons in the RMS in both juvenile and adult rats. Morphological alterations in neurogenesis were accompanied by changes in animals’ behavior. Affected neurogenesis and changes in animal behavior suggest a high sensitivity of the developing brain to MWR.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 235-244"},"PeriodicalIF":2.0,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000782/pdfft?md5=1f16384ea2b024f7a34ebfb9afd9ced8&pid=1-s2.0-S2667242124000782-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142136894","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of CB1 cannabinoid receptor alters the electrophysiological properties of cerebellar Purkinje cells in harmaline-induced essential tremor","authors":"Hassan Abbassian ,&nbsp;Mehran Ilaghi ,&nbsp;Reza Saboori Amleshi ,&nbsp;Benjamin Jason Whalley ,&nbsp;Mohammad Shabani","doi":"10.1016/j.ibneur.2024.08.005","DOIUrl":"10.1016/j.ibneur.2024.08.005","url":null,"abstract":"<div><p>Essential tremor (ET) is one of the most common motor disorders with debilitating effects on the affected individuals. The endocannabinoid system is widely involved in cerebellar signaling. Therefore, modulation of cannabinoid-1 receptors (CB1Rs) has emerged as a novel target for motor disorders. In this study, we aimed to assess whether modulation of cannabinoid receptors (CBRs) could alter the electrophysiological properties of Purkinje cells (PCs) in the harmaline-induced ET model. Male Wistar rats were assigned to control, harmaline (30 mg/kg), CBR agonist WIN 55,212–2 (WIN; 1 mg/kg), CB1R antagonists AM251 (1 mg/kg) and rimonabant (10 mg/kg). Spontaneous activity and positive and negative evoked potentials of PCs were evaluated using whole-cell patch clamp recording. Findings demonstrated that harmaline exposure induced alterations in the spontaneous and evoked firing behavior of PCs, as evidenced by a significant decrease in the mean number of spikes and half-width of action potential in spontaneous activity. WIN administration exacerbated the electrophysiological function of PCs, particularly in the spontaneous activity of PCs. However, CB1R antagonists provided protective effects against harmaline-induced electrophysiological changes in the spontaneous activity of PCs. Our findings reinforce the pivotal role of the endocannabinoid system in the underlying electrophysiological mechanisms of cerebellar disorders and suggest that antagonism of CB1R might provide therapeutic utility.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 196-206"},"PeriodicalIF":2.0,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000757/pdfft?md5=3abe388053f012b412fd994055d69840&pid=1-s2.0-S2667242124000757-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142044365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Celastrol alleviates secondary brain injury following intracerebral haemorrhage by inhibiting neuronal ferroptosis and blocking blood-brain barrier disruption","authors":"Min Wei ,&nbsp;Yi Liu ,&nbsp;Dongsheng Li ,&nbsp;Xingdong Wang ,&nbsp;Xiaodong Wang ,&nbsp;Yuping Li ,&nbsp;Zhengcun Yan ,&nbsp;Hengzhu Zhang","doi":"10.1016/j.ibneur.2024.08.003","DOIUrl":"10.1016/j.ibneur.2024.08.003","url":null,"abstract":"<div><h3>Background</h3><p>Following recent research advancements, an increasing level of evidence had been published to indicate that celastrol exerted a therapeutic effect on a range of nervous system diseases. This study therefore aimed to investigate the potential involvement of celastrol on ferroptosis and the blood-brain barrier disruption in intracerebral haemorrhage.</p></div><div><h3>Methods</h3><p>We established a rat intracerebral haemorrhage and adrenal pheochromocytoma cell (PC12) OxyHb models using an ACSL4 overexpression vector. Ferroptosis-related indices were assessed using corresponding assay kits, and immunofluorescence and flow cytometry were used to measure reactive oxygen species (ROS) levels. Additionally, quantitative PCR (qPCR) and western blot analyses were conducted to evaluate the expression of key proteins and elucidate the role of celastrol in intracerebral haemorrhage (ICH).</p></div><div><h3>Results</h3><p>Celastrol significantly improved neurological function scores, blood-brain barrier integrity, and brain water content in rats with ICH. Moreover, subsequent analysis of ferroptosis-related markers, such as Fe2+, ROS, MDA, and SOD, suggested that celastrol exerted a protective effect against the oxidative damage induced by ferroptosis in ICH rats and cells. Furthermore, Western blotting indicated that celastrol attenuated ferroptosis by modulating the expression levels of key proteins, including acyl-CoA synthetase long-chain family member 4 (ACSL4), glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), and anti-transferrin receptor 1 (TFR1) both in vitro and in vivo. ACSL4 overexpression attenuated the neuroprotective effects of celastrol on ICH in vitro. Molecular docking analysis revealed that celastrol interacted with ACSL4 via the GLU107, GLN109, ASN111, and LYS357 binding sites.</p></div><div><h3>Conclusions</h3><p>Celastrol exerted antioxidant properties and aids in neurological recovery after stroke by suppressing ACSL4 expression during ferroptosis. As such, this drug represented a promising pharmaceutical candidate for the treatment of ICH.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 161-176"},"PeriodicalIF":2.0,"publicationDate":"2024-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000733/pdfft?md5=b58b04cfa9e8270a4cdf5448f845e38f&pid=1-s2.0-S2667242124000733-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mapping the effect of the antisecretory factor on GABAA receptor α1 and α6 subunits in cerebellar granule cells in vitro","authors":"Virginia Bazzurro ,&nbsp;Elena Gatta ,&nbsp;Elena Angeli ,&nbsp;Aroldo Cupello ,&nbsp;Stefan Lange ,&nbsp;Eva Jennische ,&nbsp;Mauro Robello ,&nbsp;Alberto Diaspro","doi":"10.1016/j.ibneur.2024.08.001","DOIUrl":"10.1016/j.ibneur.2024.08.001","url":null,"abstract":"<div><p>The Antisecretory Factor (AF) is a protein that can reduce intestinal hypersecretion and various inflammation disorders <em>in vivo</em>. Discovered in many mammalian tissues and plasma, its mechanism of action remains unknown. Interestingly, its induction has been found to counteract vertigo in patients with Méniere's disease. This suggests an inherent ability to control body balance and posture, an activity that may play a role in cerebellar function. Therefore, it may be worthwhile to investigate whether this activity can inhibit neuronal cells involved in cerebellar circuitries and its potential action on enteric nervous system ganglia, which could explain its antisecretory effect in the intestine.</p><p>Previously, we studied the role of AF on GABA_A receptors in cerebellar granule cells, taking advantage of electrophysiology and evaluating the effects of the administration of AF-16, an AF peptide. Treatment with AF-16 increased GABA_A receptor responses, especially those containing the α₆ subunit. Here, we performed immunofluorescence experiments by staining α₁ and α₆ subunits before and after incubation with AF-16, analyzed super-resolved images comparing pre- and post-treatment maps and critically examined these experimental results with our previous electrophysiological data to shed light on the mechanisms of action of AF protein on GABA_A receptor subpopulations, specifically the \"fast\" receptors of α_n β_2/3 γ₂ composition that contain either the α₁ or the α₆ subunit.</p><p>The results indicate that the α₆ subunit is redistributed, with a decrease in neurites and an increase in soma. Conversely, the α₁ subunit shows opposite results, with an increase in neurites and a decrease in soma.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 188-195"},"PeriodicalIF":2.0,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000721/pdfft?md5=731aa284e890c83420f997f2645bbcd6&pid=1-s2.0-S2667242124000721-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141979140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemokines play a role in nerve damage and neuroprotection in vascular dementia","authors":"Jinming Ma ,&nbsp;Manqing Zhang ,&nbsp;Peijie Fu ,&nbsp;Xiaoping Yin ,&nbsp;Zhiying Chen","doi":"10.1016/j.ibneur.2024.08.002","DOIUrl":"10.1016/j.ibneur.2024.08.002","url":null,"abstract":"<div><p>Various Chemotactic Factors (FCs) play different roles in neuronal injury in vascular dementia. CXCL5 and CCL11 exacerbate neurological injury by promoting inflammatory responses. CXCL12/SDF-1 and CX3CL1 play neuroprotective roles.CXCL13, XCL-1 and CCL2/ MCP-1 exacerbate neurological injury in the early stage, while exerting neuronal regeneration and neuroprotective effects in the chronic progressive phase. Chemokines often play an important role in the course of vascular dementia by regulating inflammatory responses, oxidative stress, and autophagy. Activation of microglia plays an important role in the regression of vascular dementia. Activated microglia M1 causes neuronal damage through the release of chemokines. And microglia M2 has anti-inflammatory effects and is involved in the repair of brain damage. Therefore, dynamic monitoring of various related FCs and understanding the relationship between FCs and microglia can help to understand and regulate the disease course progression of vascular dementia.At present, many scholars have confirmed in basic research that different subgroups of chemokines are closely related to vascular dementia. In clinical research, new immunotherapy methods that upregulate XCL-1 and drugs that regulate the activity of CCL2/CCR2 signaling pathways are being studied and promoted.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212400071X/pdfft?md5=2621e83bf9c81622baca20a8e1305936&pid=1-s2.0-S266724212400071X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-33 relieves nerve injury by mediating microglial polarization in neuromyelitis optica spectrum disorders via the IL-33/ST2 pathway","authors":"Lu Huang ,&nbsp;Congcong Fu ,&nbsp;Sha Liao ,&nbsp;Youming Long","doi":"10.1016/j.ibneur.2024.07.008","DOIUrl":"10.1016/j.ibneur.2024.07.008","url":null,"abstract":"<div><p>Interleukin-33 (IL-33) is a member of the interleukin-1 cytokine family. Its function in regulating microglial M1/M2 polarization in neuromyelitis optica spectrum disorder (NMOSD) is still unelucidated. To evaluate the role of IL-33 in NMOSD, we constructed NMOSD mice model by injecting purified serum IgG from AQP4-IgG seropositive NMOSD patients into experimental autoimmune encephalomyelitis (EAE) mice, and IL-33 was intraperitoneally injected into NMOSD mice 3 d before the model induction. We found that pretreatment of the NMOSD mice with IL-33 relieved brain neuron loss, and demyelination and improved the structure of axons, astrocytes, and mitochondria. In the neuronal and microglial coculture system, pretreatment with IL-33 in microglia alleviated NMOSD serum-induced inflammation and damaged morphology in cultured neurons. IL-33 transformed microglia to the M2 phenotype, and NMOSD serum promoted microglia to the M1 phenotype in cultured BV2 cells. Moreover, IL-33 influenced microglial polarity via the IL-33/ST2 pathway. IL-33 may be a novel insight useful for further developing NMOSD-targeted therapy and drug development.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 177-187"},"PeriodicalIF":2.0,"publicationDate":"2024-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000708/pdfft?md5=f227b6420c787bafa3e0955d021cd661&pid=1-s2.0-S2667242124000708-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bipolar disorder: Construction and analysis of a joint diagnostic model using random forest and feedforward neural networks","authors":"Ping Sun ,&nbsp;Xiangwen Wang ,&nbsp;Shenghai Wang ,&nbsp;Xueyu Jia ,&nbsp;Shunkang Feng ,&nbsp;Jun Chen ,&nbsp;Yiru Fang","doi":"10.1016/j.ibneur.2024.07.007","DOIUrl":"10.1016/j.ibneur.2024.07.007","url":null,"abstract":"<div><h3>Background</h3><p>To construct a diagnostic model for Bipolar Disorder (BD) depressive phase using peripheral tissue RNA data from patients and combining Random Forest with Feedforward Neural Network methods.</p></div><div><h3>Methods</h3><p>Datasets GSE23848, GSE39653, and GSE69486 were selected, and differential gene expression analysis was conducted using the limma package in R. Key genes from the differentially expressed genes were identified using the Random Forest method. These key genes' expression levels in each sample were used to train a Feedforward Neural Network model. Techniques like L1 regularization, early stopping, and dropout layers were employed to prevent model overfitting. Model performance was then validated, followed by GO, KEGG, and protein-protein interaction network analyses.</p></div><div><h3>Results</h3><p>The final model was a Feedforward Neural Network with two hidden layers and two dropout layers, comprising 2345 trainable parameters. Model performance on the validation set, assessed through 1000 bootstrap resampling iterations, demonstrated a specificity of 0.769 (95 % CI 0.571–1.000), sensitivity of 0.818 (95 % CI 0.533–1.000), AUC value of 0.832 (95 % CI 0.642–0.979), and accuracy of 0.792 (95 % CI 0.625–0.958). Enrichment analysis of key genes indicated no significant enrichment in any known pathways.</p></div><div><h3>Conclusion</h3><p>Key genes with biological significance were identified based on the decrease in Gini coefficient within the Random Forest model. The combined use of Random Forest and Feedforward Neural Network to establish a diagnostic model showed good classification performance in Bipolar Disorder.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 145-153"},"PeriodicalIF":2.0,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000691/pdfft?md5=bd0cf64abca37364e4ff55dbbc41772c&pid=1-s2.0-S2667242124000691-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141952844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reduced ischemia‐reperfusion oxidative stress injury by melatonin and N‐acetylcysteine in the male rat brain","authors":"Fatemeh Sabbaghziarani ,&nbsp;Pouria Soleimani ,&nbsp;Farideh Rajabian Eynshikh ,&nbsp;Fariba Zafari ,&nbsp;Ehsan Aali","doi":"10.1016/j.ibneur.2024.07.004","DOIUrl":"10.1016/j.ibneur.2024.07.004","url":null,"abstract":"<div><p>Middle cerebral artery occlusion (MCAO) is a model for inducing ischemic stroke in rodents, leading to devastating brain damage. Oxidative stress (OS) plays a crucial role in the pathogenesis of ischemia. In this study, the effect of melatonin and N-acetylcysteine on ischemia-reperfusion-induced oxidative stress injury in the cerebral cortex of male rats was investigated. 30 male Wistar rats were divided into sham, ischemic, NAC, melatonin and NAC + melatonin groups. All groups, except the sham group, underwent MCAO on the left side, and the treatment groups received intraperitoneal injections of either 50 mg/kg N-acetylcysteine (NAC) or 5 mg/kg melatonin or a combination of both 24 and 48 hours later. At 24 and 72 hours after surgery, the animals were examined for sensory and motor activity. The cerebral cortex was dissected after sacrificing the rats, infarct volume estimated and the concentrations of glutathione peroxidase (GPx), superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) and nuclear factor erythroid-2 related factor 2 (Nrf2) were analyzed by enzyme-linked immunosorbent assay (ELISA). The results indicate that the NAC + melatonin group exhibited elevated sensory-motor activity and a reduced infarct volume rate in comparison to the ischemic group (p≤ 0.05). Compared to the ischemic group, the NAC + melatonin group showed a significant increase in SOD concentration and a significant decrease in MDA (p≤ 0.05). It can therefore be concluded that the simultaneous administration of NAC and melatonin can reduce the cerebral infarction volume, and improve neurological functions by modulating SOD and MDA.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 131-137"},"PeriodicalIF":2.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000678/pdfft?md5=bd34eaf36ac6e60170151f6e01ae58d1&pid=1-s2.0-S2667242124000678-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141841929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of preladenant in improving motor symptoms in Parkinson's disease: A systematic review and meta-analysis","authors":"Mohammad Amin Karimi ,&nbsp;Alireza Ghajari ,&nbsp;Reza Khademi ,&nbsp;Mohammad Hossein Etemadi ,&nbsp;Narges Safar Firouz ,&nbsp;Behnaz Mohammadvand ,&nbsp;Kimia Janeshin ,&nbsp;Afra Darvishi ,&nbsp;Shafagh Asgarzadeh ,&nbsp;Sayedeh-Fatemeh Sadat-Madani ,&nbsp;Mohammad Abbasalizadeh ,&nbsp;Zahra Jafari Shendi ,&nbsp;Ata Akhtari Kohnehshahri ,&nbsp;Niloofar Deravi ,&nbsp;Seyed Amirhossein Mazhari ,&nbsp;Mahsa Aziz ,&nbsp;Matin Bidares ,&nbsp;Mohaddeseh Belbasi ,&nbsp;Mahdyieh Naziri ,&nbsp;Hossein Ashkpour Motlagh","doi":"10.1016/j.ibneur.2024.07.005","DOIUrl":"10.1016/j.ibneur.2024.07.005","url":null,"abstract":"<div><h3>Background</h3><p>Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by dopamine depletion and severe motor impairments. Preladenant, an adenosine A2 receptor antagonist, is an investigational treatment for PD. This systematic review and meta-analysis aimed to critically evaluate the efficacy of Preladenant in improving motor symptoms in patients with PD.</p></div><div><h3>Methods</h3><p>A comprehensive literature search was conducted in PubMed, Embase, and Cochrane Central Register of Controlled Trials from inception to March 2023, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Randomized controlled trials (RCTs) comparing Preladenant with placebo in PD patients were included. The primary outcome was the change in daily ON time without troublesome dyskinesia. Secondary outcomes included the change in daily OFF time and adverse events. The risk of bias was assessed using the Cochrane Risk of Bias tool.</p></div><div><h3>Results</h3><p>Four RCTs with a total of 2097 PD patients were included. Pooled analysis showed that Preladenant could generally increase daily ON time (pooled effect 0.15 and 95 % CI: −0.19–0.48) and reduce daily OFF time (pooled effect −0.04 and 95 % CI: −0.43–0.36) compared to placebo, however it was not significant. The included studies had moderate to high heterogeneity. No significant differences in adverse events were observed between Preladenant and placebo.</p></div><div><h3>Conclusion</h3><p>This meta-analysis suggests that Preladenant may improve motor fluctuations in PD patients by increasing ON time and reducing OFF time. However, the high heterogeneity among studies warrants further large-scale, high-quality RCTs to confirm these findings and establish the long-term safety and efficacy of Preladenant in PD management.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 207-219"},"PeriodicalIF":2.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667242124000666/pdfft?md5=f6421485ea34acd34a386ea855637c58&pid=1-s2.0-S2667242124000666-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141852178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two hub genes of bipolar disorder, a bioinformatics study based on the GEO database","authors":"Ping Sun ,&nbsp;Shunkang Feng ,&nbsp;Hui Yu ,&nbsp;Xiaoxiao Wang ,&nbsp;Yiru Fang","doi":"10.1016/j.ibneur.2024.07.006","DOIUrl":"10.1016/j.ibneur.2024.07.006","url":null,"abstract":"<div><p>Bipolar disorder is a mood illness that affects many people. It has a high recurrence frequency and will cause significant damage to the patient's social function. At present, the pathogenesis of BD is not clear. The National Center for Biotechnology Information (NCBI) established and maintained the Gene Expression Omnibus (GEO) database, a gene expression database. For bioinformatics analysis, researchers can obtain expression data from the internet. At present, the samples of the dataset used in the research of BD are mostly from brain tissue, and the data containing blood samples are rarely used. GEO databases (GSE46416, GSE5388, and GSE5389) were used to retrieve public data, and utilizing the online tool GEO2R, differentially expressed genes (DEGs) were retrieved. The common DEGs between the samples of patients with BD and the samples of the normal population were screened by Venn diagrams. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were used to perform functional annotation and pathway enrichment analysis of DEGs. A protein-protein interaction network (PPI) was built to investigate hub genes on this basis. There were 117 up-regulated DEGs and 38 down-regulated DEGs discovered, with two hub genes [SRC, CDKN1A] among the up-regulated DEGs. These two hub genes were also highly enriched in the oxytocin signaling pathway, proteoglycans in cancer and bladder cancer, according to KEGG analysis. The results of the receiver operating characteristic curve (ROC) of SRC and CDKN1A in the three datasets strongly suggested that SRC and CDKN1A were potential diagnostic markers of BD. The results strongly suggest that SRC and CDKN1A are related to the pathogenesis of BD.</p></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 122-130"},"PeriodicalIF":2.0,"publicationDate":"2024-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266724212400068X/pdfft?md5=57f8aa3e5c5bec03d7fd24fd92a248d1&pid=1-s2.0-S266724212400068X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141845905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}