Neuroscience最新文献_第2页

Miro1: A potential target for treating neurological disorders Miro1：治疗神经系统疾病的潜在靶点

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-20 DOI: 10.1016/j.neuroscience.2025.05.019

Linghua Zeng , Juan Yang , Conghui Zhang , Junjie Zhu , Saichun Zhong , Xing Liu , Haiyu Xie , Lifeng Wang , Li Chen , Maolin Zhong , Fuzhou Hua , Weidong Liang

{"title":"Miro1: A potential target for treating neurological disorders","authors":"Linghua Zeng , Juan Yang , Conghui Zhang , Junjie Zhu , Saichun Zhong , Xing Liu , Haiyu Xie , Lifeng Wang , Li Chen , Maolin Zhong , Fuzhou Hua , Weidong Liang","doi":"10.1016/j.neuroscience.2025.05.019","DOIUrl":"10.1016/j.neuroscience.2025.05.019","url":null,"abstract":"<div><div>The Miro1 protein is a member of the mitochondrial Rho GTPase (Miro) protein family and plays a crucial role in regulating the dynamic processes of mitochondria and participating in cellular movement and mitochondrial transport. In the nervous system, it ensures adequate energy supply for normal neuronal function and synaptic transmission. Additionally, Miro1 actively participates in the regulation of mitochondrial quality control and stress responses within neurons. Its primary function is to sense intracellular stress signals to regulate mitochondrial movement and metabolism, thereby adapting to environmental changes. Multiple studies have indicated that the Miro1 protein is associated with the pathogenesis of various neurological disorders, such as Alzheimer’s Disease(AD), Parkinson’s Disease(PD), and Amyotrophic Lateral Sclerosis(ALS). This article reviews the mechanistic role of Miro1 in these diseases and summarizes the latest research on its involvement in neurological disorders. These efforts aim to provide unified treatment strategies for certain neurological disorders and explore the potential for treating complex neurological diseases.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 228-239"},"PeriodicalIF":2.9,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115750","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

Differences in neurophysiological resting-state alpha spectral events in 4–12-year-old children with prenatal exposure to alcohol relative to typically developing controls 产前接触酒精的4-12岁儿童与正常发育对照组的神经生理静息状态α谱事件差异

IF 2.9 3区医学

Neuroscience Pub Date : 2025-05-19 DOI: 10.1016/j.neuroscience.2025.05.028

D. Roberts , F.T. Candelaria-Cook , D. Mun , O. Myers , M. Schendel , M. Alsameen , P. Sanjuan , C. Cerros , D. Hill , J. Stephen

{"title":"Differences in neurophysiological resting-state alpha spectral events in 4–12-year-old children with prenatal exposure to alcohol relative to typically developing controls","authors":"D. Roberts , F.T. Candelaria-Cook , D. Mun , O. Myers , M. Schendel , M. Alsameen , P. Sanjuan , C. Cerros , D. Hill , J. Stephen","doi":"10.1016/j.neuroscience.2025.05.028","DOIUrl":"10.1016/j.neuroscience.2025.05.028","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the effects of age and prenatal alcohol exposure (PAE) on the constituent parameters underlying mean alpha power.</div></div><div><h3>Methods</h3><div>Resting-state magnetoencephalography (MEG) alpha events were characterized by measuring event spectral power, number of events per epoch, duration of events, and frequency span within the alpha band (7–13 Hz) in 82 typically developing controls (TDCs) and 53 participants with PAE/FASD. We examined the relationship between these parameters and overall mean alpha power as well as how they differ with age and PAE/FASD.</div></div><div><h3>Results</h3><div>Age negatively correlated with mean event duration in both groups, (<em>r</em> = -0.29, <em>p</em> < 0.001) with duration reduced in older participants. Age negatively correlated with mean alpha power’s association with mean event duration in PAE/FASD (<em>r</em> = -0.38, <em>p</em> < 0.05) and positively correlated with mean alpha power’s association with mean event frequency span in both groups (r = 0.22, p < 0.05). The correlation between mean alpha power and mean event duration (p = 0.038) was stronger in TDCs. Despite the group difference, longer event durations led to more mean alpha power in both groups. Mean alpha power negatively correlated with mean event frequency span in both groups but the negative correlation was stronger in the TDC group (p = 0.036)</div></div><div><h3>Conclusion</h3><div>The differences found in alpha events with age and PAE may provide valuable insights into the physiological correlates of attention and highlight the potential of alpha oscillations as biomarkers for understanding attention-related deficits in children with prenatal alcohol exposure.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 332-342"},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144120297","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 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":"https://doi.org/10.1016/j.neuroscience.2025.05.023","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":" ","pages":""},"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