Neuroscience最新文献_第9页

Effects of the direction of sound stimuli on body sway in young healthy individuals 声音刺激方向对年轻健康个体身体摇摆的影响。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-19 DOI: 10.1016/j.neuroscience.2025.05.029

Shintaro Otsuka, Tadashi Nishimura, Tadao Okayasu, Osamu Saito, Tadashi Kitahara

{"title":"Effects of the direction of sound stimuli on body sway in young healthy individuals","authors":"Shintaro Otsuka, Tadashi Nishimura, Tadao Okayasu, Osamu Saito, Tadashi Kitahara","doi":"10.1016/j.neuroscience.2025.05.029","DOIUrl":"10.1016/j.neuroscience.2025.05.029","url":null,"abstract":"<div><div>Sound has been suggested to improve human balance control; however, the optimal direction of sound presentation is unclear. This study aimed to evaluate the effect of sound presentation direction on postural stability. Thirty-one healthy young volunteers (mean age 24.1 ± 2.6 years) participated. Posturography was performed in five acoustic conditions (white noise at 60 dBA delivered from thefront, back, left, and right and a silence condition), two visual conditions (eyes open/eyes closed), and two standing conditions (foam surface/firm surface). The total sway area, mean sway velocity, and root mean square (RMS) sway were measured. A three-way repeated-measures analysis of variance with a within-group factor was conducted, followed by post hoc pairwise comparisons using Bonferroni adjustments. When standing on foam with the eyes closed, total sway area and RMS sway were significantly smaller with sound from behind than in silence, and mean sway velocity was significantly smaller with sound from the front than from the left. Sound presented from behind or the front reduced posturography parameter values, suggesting that the direction of sound presentation helps stabilize postural sway.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 322-331"},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Neurosteroids as emerging therapeutics for treatment-resistant depression: Mechanisms and clinical potential 神经类固醇作为治疗难治性抑郁症的新疗法：机制和临床潜力。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-19 DOI: 10.1016/j.neuroscience.2025.05.022

Krutika Nagpurkar , Pratik Ghive , Mayur Kale , Neha Nistane , Brijesh Taksande , Milind Umekar , Rashmi Trivedi

{"title":"Neurosteroids as emerging therapeutics for treatment-resistant depression: Mechanisms and clinical potential","authors":"Krutika Nagpurkar , Pratik Ghive , Mayur Kale , Neha Nistane , Brijesh Taksande , Milind Umekar , Rashmi Trivedi","doi":"10.1016/j.neuroscience.2025.05.022","DOIUrl":"10.1016/j.neuroscience.2025.05.022","url":null,"abstract":"<div><div>Treatment-resistant depression (TRD) is a severe and persistent subset of major depressive disorder (MDD) that remains unresponsive to at least two different classes of antidepressants. Given the limitations of conventional treatments, neurosteroids have emerged as promising alternatives due to their rapid and multi-faceted mechanisms of action. Neurosteroids such as allopregnanolone, pregnenolone, and dehydroepiandrosterone (DHEA) modulate key neurotransmitter systems, including gamma-aminobutyric acid (GABA_A) and N-methyl-D-aspartate (NMDA) receptors, enhancing inhibitory transmission and promoting synaptic plasticity. They regulate the hypothalamic–pituitary–adrenal (HPA) axis, mitigating stress-related neurotoxicity and restoring neurochemical balance. Preclinical studies have demonstrated the efficacy of neurosteroids in reversing depressive-like behaviors in rodent models of chronic stress, while clinical trials highlight their potential for rapid and sustained antidepressant effects. Notably, the FDA approval of brexanolone for postpartum depression underscores the translational potential of neurosteroid-based therapies. However, challenges such as limited bioavailability, long-term safety concerns, and regulatory hurdles must be addressed to optimize their clinical application. This review explores the therapeutic potential of neurosteroids in TRD, discussing their mechanisms, clinical evidence, and future directions. The findings support the integration of neurosteroid-based treatments into TRD management, offering new hope for patients unresponsive to conventional antidepressants. This review uniquely highlights the paradigm shift offered by neurosteroids, moving beyond the traditional monoamine hypothesis, and positions them as novel, multi-target therapeutics capable of addressing the complex neurobiology of TRD.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 300-314"},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CISD2 ameliorates heatstroke-associated early cognitive deficits by inhibiting ferroptosis and maintaining dendritic spine density in hippocampal neurons in mice CISD2通过抑制铁下垂和维持小鼠海马神经元的树突棘密度来改善中暑相关的早期认知缺陷。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-19 DOI: 10.1016/j.neuroscience.2025.05.024

Liang Zeng , Jinhan Sun , Kai Ji , Lianxiang Zhang , Jiandong Niu , Kang Ma , Yan Yan , Zhiping Hei , Yuning Sun

{"title":"CISD2 ameliorates heatstroke-associated early cognitive deficits by inhibiting ferroptosis and maintaining dendritic spine density in hippocampal neurons in mice","authors":"Liang Zeng , Jinhan Sun , Kai Ji , Lianxiang Zhang , Jiandong Niu , Kang Ma , Yan Yan , Zhiping Hei , Yuning Sun","doi":"10.1016/j.neuroscience.2025.05.024","DOIUrl":"10.1016/j.neuroscience.2025.05.024","url":null,"abstract":"<div><div>Heatstroke encephalopathy is a universal primary manifestation of heatstroke. Early brain injury caused by heatstroke may lead to long-term cognitive impairment in survivors, yet it frequently evades detection by standard diagnostic techniques. Thus, the discovery of reliable biomarkers for early brain injury detection is necessary. In this study, CISD2 downregulation in HT-22 cells was observed following hyperthermia treatment by using transcriptomics analysis. Subsequent mechanistic investigations revealed that CISD2 downregulation triggeres ferroptosis via AMPK-dependent BECN1 phosphorylation at Ser93, while CISD2 overexpression confers ferroptosis resistance in HT-22 cells at 41 °C. Furthermore, the downregulation of CISD2 expression and ferroptotic alterations were firmly observed in hippocampal tissues of mice during the early stage of heatstroke, and the overexpression of CISD2 by injecting lentivirus overexpressing CISD2 into the hippocampus of mice significantly alleviated heatstroke-induced neuronal loss, and meanwhile, the density of dendritic spines in the CA1 pyramidal neurons of the mice was effectively preserved. Moreover, knockdown of the CISD2 in the hippocampus exacerbated the loss of hippocampal neurons and the reduction of dendritic spine density. In summary, our results illustrated that CISD2 plays a pivotal role in preserving normal hippocampal function by regulating lipid peroxidation and iron homeostasis of heatstroke conditions. These finds provide novel insights into the mechanisms underlying heatstroke-induced cognitive deficits and offer potential strategies for improving risk prediction of heatstroke encephalopathy.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 282-299"},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antagonism of GABA-A receptor inhibits the effects of progesterone on nociceptive behaviors and electrophysiological alterations in a rat model of neuropathic pain GABA-A受体拮抗抑制黄体酮对神经性疼痛大鼠伤害性行为和电生理改变的影响。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-17 DOI: 10.1016/j.neuroscience.2025.05.027

Morteza Jarrahi , Hossein Ali Safakhah , Payman Raise-Abdullahi , Ali Rashidy-Pour

{"title":"Antagonism of GABA-A receptor inhibits the effects of progesterone on nociceptive behaviors and electrophysiological alterations in a rat model of neuropathic pain","authors":"Morteza Jarrahi , Hossein Ali Safakhah , Payman Raise-Abdullahi , Ali Rashidy-Pour","doi":"10.1016/j.neuroscience.2025.05.027","DOIUrl":"10.1016/j.neuroscience.2025.05.027","url":null,"abstract":"<div><div>Growing evidence highlights the neuroprotective potential of progesterone in mitigating various forms of nervous system injury. In previous research, we demonstrated that progesterone ameliorates both electrophysiological and behavioral deficits associated with chronic constriction injury (CCI) of the sciatic nerve in rats. However, the precise mechanisms underlying these effects remain poorly understood. This study aimed to elucidate the involvement of GABA-A receptors in mediating the therapeutic effects of progesterone on nociceptive behaviors, specifically thermal hyperalgesia and mechanical allodynia, as well as electrophysiological alterations in a rat model of CCI-induced neuropathic pain. Male rats received daily intraperitoneal injections of progesterone (6 mg/kg) starting on day 12 post-CCI and continuing through day 26. To evaluate the role of GABA-A receptors, the antagonist bicuculline (0.5 or 2 mg/kg, i.p.) was administered 30 min prior to progesterone in designated groups. Behavioral assessments were conducted on days 0, 12, 26, 28, and 35 post-CCI, followed by electrophysiological evaluations of the tibial and sural nerves. The results revealed that progesterone significantly attenuated both thermal hyperalgesia and mechanical allodynia and reversed CCI-induced electrophysiological impairments. Nevertheless, pretreatment with bicuculline blocked these beneficial effects at both behavioral and electrophysiological levels, suggesting that progesterone’s neuroprotective and analgesic properties are, at least in part, mediated through GABA-A receptor signaling pathways.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 154-160"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perineuronal net degradation causes a delayed change in resting and sound evoked responses in the mouse auditory cortex 神经网络退化导致小鼠听觉皮层静息和声音诱发反应的延迟变化。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-17 DOI: 10.1016/j.neuroscience.2025.05.026

A. Hussain , K.A. Razak

{"title":"Perineuronal net degradation causes a delayed change in resting and sound evoked responses in the mouse auditory cortex","authors":"A. Hussain , K.A. Razak","doi":"10.1016/j.neuroscience.2025.05.026","DOIUrl":"10.1016/j.neuroscience.2025.05.026","url":null,"abstract":"<div><div>Perineuronal nets (PNNs) are extracellular matrix assemblies that preferentially cover parvalbumin-expressing (PV+) interneurons in the neocortex. PV+ cells and PNNs are impaired in a variety of neurodevelopmental disorders including Fragile X Syndrome and schizophrenia. In both of these disorders, electroencephalograph (EEG) recordings show similar phenotypes, including elevated resting gamma band power and reduced temporal fidelity in the 40 Hz auditory steady state response (ASSR). Whether there is a causal link between PNN integrity and EEG abnormalities remains unclear. We tested this link by recording EEG responses in the auditory cortex (AC) in wildtype mice in which PNNs were enzymatically degraded (Chondroitinase ABC or ChABC). EEGs were recorded at two different time points (4- or 14-days post injection, cross-sectional design). In comparison to saline control, ChABC injected mice showed a ∼50 % reduction in PNN density after 4-days. However, there was no difference in resting EEG power spectral density, auditory event-related potential amplitudes or ASSR temporal fidelity between saline and ChABC mice. At the 14-day time point, there was a recovery of PNN density in the AC. Interestingly, EEG responses were abnormal at this time point, with elevated gamma band activity and reduced ASSR temporal fidelity. Thus, the electrophysiological consequences of PNN loss are not seen acutely, but over a delayed time course, suggesting abnormal plasticity after a circuit perturbation. Taken together, these data indicate acute shaping of auditory cortical responses is less dependent on PNNs, but long-term stability of responses following a circuit perturbation depends on the integrity of PNNs.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 252-263"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effects of a synthetic cannabinoid, 5F-MDMB-PICA, on metabolites and glutamatergic transporters in U87 cell line 合成大麻素5F-MDMB-PICA对U87细胞株代谢物和谷氨酸转运蛋白的影响

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-17 DOI: 10.1016/j.neuroscience.2025.05.016

Ibrahim N. Alsulaihim , Mohammed Mufadhe Alanazi , Khaled A. Alhosaini , Syed Rizwan Ahamad , Mohammad R. Khan , Fahad S. Almezied , Abdullah A. Aldossari , Thamer H. Abekairi , Mohammed A. Assiri , Fawaz Alasmari

{"title":"Effects of a synthetic cannabinoid, 5F-MDMB-PICA, on metabolites and glutamatergic transporters in U87 cell line","authors":"Ibrahim N. Alsulaihim , Mohammed Mufadhe Alanazi , Khaled A. Alhosaini , Syed Rizwan Ahamad , Mohammad R. Khan , Fahad S. Almezied , Abdullah A. Aldossari , Thamer H. Abekairi , Mohammed A. Assiri , Fawaz Alasmari","doi":"10.1016/j.neuroscience.2025.05.016","DOIUrl":"10.1016/j.neuroscience.2025.05.016","url":null,"abstract":"<div><div>Brian metabolic pathways have been impaired in animals exposed to drugs of abuse. The misuse of cannabinoids is associated with neuronal death and synaptic plasticity. Astrocytic glutamate transporters are therapeutic targets in several preclinical models of substance use disorders. Abused drugs could impair metabolic pathways in animal models, particularly those involving astrocytes, where glutamate transporters are critical regulators of neurotransmission. We here aimed to evaluate the metabolomic profile of a human glioblastoma cell line following exposure a synthetic cannabinoid, 5F-MDMB-PICA (5F-M-P), using an <em>in vitro</em> cell model (U87, glioblastoma astrocytic origin cell line). Additionally, we evaluated the effects of 5F-M-P on the expression of astrocytic glutamate transporters. After treatments, the cells were collected for metabolomic study using gas chromatography-mass spectrometry, and protein expression study using western blotting assay. 5F-M-P, especially at a concentration of 100 μM, altered the abundance of numerous metabolites. Enrichment analysis identified that specific signaling pathways were involved in the effects of 5F-M-P on metabolites, including the glutamate neurotransmission pathway. Additionally, 5F-M-P at 200 μM reduced the expression of glutamate transporter-1 and glutamate-aspartate co-transporter. Therefore, 5F-M-P exposure altered key metabolic pathways in astrocytes including glutamatergic pathways, an effect associated with reduced astrocytic glutamate transporter expression.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 190-199"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Schaftoside restrains neuroinflammation and ameliorates cerebral ischemic injury associated with LncGm36 mediated COP1 upregulation 与lnncgm36介导的COP1上调相关的神经炎症和脑缺血损伤的改善。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-16 DOI: 10.1016/j.neuroscience.2025.05.023

Ermei Lu , Jie Chen , Qiaoyun Wu , Jiayu Wu , Kecheng Zhou

{"title":"Schaftoside restrains neuroinflammation and ameliorates cerebral ischemic injury associated with LncGm36 mediated COP1 upregulation","authors":"Ermei Lu , Jie Chen , Qiaoyun Wu , Jiayu Wu , Kecheng Zhou","doi":"10.1016/j.neuroscience.2025.05.023","DOIUrl":"10.1016/j.neuroscience.2025.05.023","url":null,"abstract":"<div><div>Schaftoside(SS), a bioactive compound derived fromHerba Desmodii Styracifolii, has demonstrated anti-inflammatory properties in microglial cells; However, its role in ischemic brain injury in mice remains unclear. This study aimed to investigate the neuroprotective effects of schaftoside in a mouse model of middle cerebral artery occlusion (MCAO) and elucidate the underlying molecular mechanism. RNA sequencing revealed that schaftoside significantly upregulated the long noncoding RNA Gm32496 (LncGm36), which was prominently downregulated in the ischemic penumbra of MCAO mice. Administration of schaftoside reduced the infarct size, alleviated brain edema, and improved neurological outcomes in MCAO mice through LncGm36 upregulation. Mechanistically, schaftoside-induced LncGm36 expression was accompanied by elevated levels of COP1, a key regulator involved in neuroinflammation. RNA pull-down assays confirmed a direct interaction between LncGm36 and COP1. Silencing of either LncGm36 or COP1 attenuated schaftoside-mediated anti-inflammatory microglial polarization and neuroprotection. Collectively, these results indicate that schaftoside confers neuroprotection against ischemic brain injury by promoting an anti-inflammatory phenotypic shift of microglia through the LncGm36/COP1 pathway, suggesting its potential as a therapeutic agent for ischemic stroke.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 93-104"},"PeriodicalIF":2.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The genetic risk factors, molecular pathways, microRNAs, and the gut microbiome in Alzheimer’s disease 阿尔茨海默病的遗传风险因素、分子途径、microrna和肠道微生物组。

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-13 DOI: 10.1016/j.neuroscience.2025.05.021

Aathira N.S , Amanpreet Kaur , Arun Kumar , Ghulam Mehdi Dar , Nimisha , Abhay Kumar Sharma , Pinki Bera , Bhawna Mahajan , Atri Chatterjee , Sundeep Singh Saluja

{"title":"The genetic risk factors, molecular pathways, microRNAs, and the gut microbiome in Alzheimer’s disease","authors":"Aathira N.S , Amanpreet Kaur , Arun Kumar , Ghulam Mehdi Dar , Nimisha , Abhay Kumar Sharma , Pinki Bera , Bhawna Mahajan , Atri Chatterjee , Sundeep Singh Saluja","doi":"10.1016/j.neuroscience.2025.05.021","DOIUrl":"10.1016/j.neuroscience.2025.05.021","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most prevalent form of dementia worldwide. It is a multifaceted condition resulting from interplay of genetic mutations (e.g., <em>APP, PSEN1, PSEN2</em>) that account for less than 5% of cases, several genetic risk variants such as <em>APOE4, TREM2, CD33, CLU, SORL1,</em> and <em>CR1</em> contribute to disease susceptibility and epigenetic factors, which may mediate the influence of environmental and lifestyle factors over time. Other critical contributors such as aging, protein misfolding and aggregation (amyloid-β and tau), molecular and transcriptomic dysregulation affecting neuronal function, and modifiable lifestyle factors like diet, physical activity, and environmental exposures presents challenges in accurate diagnosis and management. Research has predominantly focused on the diverse molecular pathways in the pathogenesis of AD, with particular attention given to the amyloidogenic pathways, tau pathology, calcium signalling, endolysosomal pathways, and others, whether they are directly or indirectly involved. Apart from these known molecular pathways, miRNAs are gaining attention as important regulators, which have been implicated in moderating the expression of mRNA targets involved in various processes associated with the clearance of pathogenic β-amyloid proteins. A mounting body of research suggests the possible role of gut microbiota in AD which regulates inflammation, neurotransmitters, and the blood–brain barrier. Gut dysbiosis can trigger neuroinflammation and amyloid-beta aggregation, making microbiome composition a potential early AD biomarker. This review aims to explore briefly the diverse risk encompassing genetic polymorphisms, altered molecular pathways implicated in AD pathogenesis, miRNA regulatory mechanisms, and the potential impact of gut microbiota on AD risk.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 217-227"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A novel predictive model constructed based on the combination of SIX3OS1, miR-511-3p and RBP4 for stroke-prost cognitive impairment 基于SIX3OS1、miR-511-3p和RBP4联合构建脑卒中前期认知障碍预测模型

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-12 DOI: 10.1016/j.neuroscience.2025.05.020

Te Wang , Rui Wang , Junsheng Zeng , Wei Zhao , Yan Liu , Hui Xiao

{"title":"A novel predictive model constructed based on the combination of SIX3OS1, miR-511-3p and RBP4 for stroke-prost cognitive impairment","authors":"Te Wang , Rui Wang , Junsheng Zeng , Wei Zhao , Yan Liu , Hui Xiao","doi":"10.1016/j.neuroscience.2025.05.020","DOIUrl":"10.1016/j.neuroscience.2025.05.020","url":null,"abstract":"<div><h3>Background</h3><div>The incidence of stroke is increasing year by year. Post-stroke cognitive impairment (PSCI) is one of the most serious complications of stroke, which lacks effective early prediction tools.</div></div><div><h3>Methods</h3><div>A total of 147 S patients and 80 healthy individuals were enrolled, with corresponding clinical data and serum samples collected. The expression of SIX3OS1, miR-511-3p and retinol binding protein 4 (RBP4) were detected by reverse transcription-quantitative PCR (RT-qPCR). These data were then used to build a logistic regression model, and receiver operating characteristic (ROC) curves were drawn to evaluate the clinical value of SIX3OS1, miR-511-3p and RBP4.</div></div><div><h3>Results</h3><div>Our study found that SIX3OS1, miR-511-3p and RBP4 abnormally expressed in stroke and the area under the curve (AUC) of the combined detection of these was 0.965. Additionally, ROC curve showed that the AUC of SIX3OS1, miR-511-3p and RBP4 combined was 0.955 for the prediction of PSCI. Based on SIX3OS1 (X1), miR-511-3p (X2) and RBP4 (X3), we developed multivariate logistic regression predictive model, <em>p</em> = 1/ [1 + e (7.190–5.400X1 + 11.109X2–3.585X3)].</div></div><div><h3>Conclusion</h3><div>Serum SIX3OS1, miR-511-3p and RBP4 are candidate diagnostic biomarker in stroke and PSCI patients, which achieve good diagnostic performance when used in combination with other factors, and may have the potential to be novel therapeutic targets for PSCI.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 47-53"},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Evidence of a hormetic-like cytoprotective effect by erythropoietin in the SH-SY5Y cell model of oxygen-glucose deprivation 促红细胞生成素在氧-葡萄糖剥夺SH-SY5Y细胞模型中具有刺激样细胞保护作用的证据

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-12 DOI: 10.1016/j.neuroscience.2025.05.018

Alejandra Guadalupe Marín-López, Rafael de Jesús Macias-Velez, José Jaime Jarero-Basulto, Martha Catalina Rivera-Cervantes

{"title":"Evidence of a hormetic-like cytoprotective effect by erythropoietin in the SH-SY5Y cell model of oxygen-glucose deprivation","authors":"Alejandra Guadalupe Marín-López, Rafael de Jesús Macias-Velez, José Jaime Jarero-Basulto, Martha Catalina Rivera-Cervantes","doi":"10.1016/j.neuroscience.2025.05.018","DOIUrl":"10.1016/j.neuroscience.2025.05.018","url":null,"abstract":"<div><div>Erythropoietin is recognized as a neuroprotective agent for the brain and it has been suggested that may have a biphasic hormetic-like response, with low to intermediate doses providing greater cytoprotective benefits, whereas high doses have been associated with undesirable side effects related to its systemic application; however, it is unknown whether this occurs in brain and what mechanisms could be implicated. This study investigated the potential hormetic effects of recombinant human erythropoietin (rhEPO) on SH-SY5Y cells subjected to oxygen and glucose deprivation (OGD) and reoxygenation (reox) injury. We developed an <em>in vitro</em> protocol to investigate the rhEPO's hormetic effect under conditions similar to ischemic stroke. Cell vitality assays were conducted, and the gene and protein expression of EPO, erythropoietin receptor (EPOR), β-common receptor (βcR), and Bcl-xL were analyzed. We found that all evaluated doses of rhEPO exhibited a cytoprotective effect on cells treated during the 24 h reox period. Notably, the intermediate 50 IU/mL dose showed significantly higher cell vitality than the high 100 IU/mL dose (p < 0.05), suggesting a potential hormetic-like effect. Interestingly, both EPO and EPOR mRNA levels increased after OGD, followed by an increase in EPOR protein levels after the reox period. However, no changes were observed in EPOR or Bcl-xL mRNA expression after 4 and 8 h of rhEPO treatment during reox. Finally, βcR mRNA expression was not detected in any group. While further research is needed, these results suggest that rhEPO treatment may exert a hormetic-like effect and offer cytoprotection against ischemic stroke-like injury.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 114-122"},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144068248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0