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Arbutin improves spatial learning and memory in a lipopolysaccharide-induced neuroinflammation model via attenuating of astrocytes activation and oxidative stress 熊果苷通过减弱星形胶质细胞激活和氧化应激,改善脂多糖诱导的神经炎症模型中的空间学习和记忆
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-11 DOI: 10.1016/j.neulet.2025.138356
Amirreza Pouramir , Nasrin Nosratiyan , Hamid Askari , Maryam Ghasemi-Kasman , Moein Shirzad , Mahdi Pouramir
{"title":"Arbutin improves spatial learning and memory in a lipopolysaccharide-induced neuroinflammation model via attenuating of astrocytes activation and oxidative stress","authors":"Amirreza Pouramir ,&nbsp;Nasrin Nosratiyan ,&nbsp;Hamid Askari ,&nbsp;Maryam Ghasemi-Kasman ,&nbsp;Moein Shirzad ,&nbsp;Mahdi Pouramir","doi":"10.1016/j.neulet.2025.138356","DOIUrl":"10.1016/j.neulet.2025.138356","url":null,"abstract":"<div><div>Neuroinflammation has a key role in neurodegenerative disorders and can be mimicked by systemic administration of lipopolysaccharide (LPS), which impairs cognitive function and hippocampal structure. This study examined the neuroprotective effects of arbutin, a natural hydroquinone glycoside, in LPS-induced mouse model of neuroinflammation. Twenty-eight NMRI mice were divided into four groups: control, LPS, arbutin 25 mg/kg + LPS, and arbutin 50 mg/kg + LPS. Morris water maze behavioral assessment revealed that LPS significantly increased escape latency (P = 0.005) and distance explored (P = 0.003). Arbutin treatment significantly changed these effects at both doses, with 50 mg/kg showing higher efficacy (P = 0.009 vs. 25 mg/kg, P = 0.02). Histopathological analyses showed a remarkable decrease in the number of damaged neurons in CA1 and CA3 regions in arbutin-treated groups (P &lt; 0.001), with increased NeuN-positive neurons (P &lt; 0.05). Astrocyte reactivity, evaluated by GFAP immunostaining, was significantly suppressed by arbutin in both regions, specifically at 50 mg/kg (CA1: P = 0.0006; CA3: P = 0.0188). Oxidative stress assays demonstrated that arbutin preserved total antioxidant capacity (P = 0.0091) and reduced lipid peroxidation (P &lt; 0.0001). Collectively, these findings indicate that arbutin mitigates LPS-induced cognitive impairment and neuroinflammation through antioxidant, anti-inflammatory, and neuroprotective mechanisms in a dose-dependent manner, supporting its potential as a supplementary therapeutic agent for neuroinflammatory manifestations.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138356"},"PeriodicalIF":2.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144830507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Manipulation of bladder contraction by cell-type selective optogenetics of the anterior cingulate cortex neurons in a mouse model with increased urinary frequency 在尿频增加的小鼠模型中,前扣带皮层神经元的细胞型选择性光遗传学对膀胱收缩的操纵
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-11 DOI: 10.1016/j.neulet.2025.138355
Hiroshi Shimura , Satoshi Manita , Takanori Mochizuki , Satoru Kira , Norifumi Sawada , Haruhiko Bito , Kenji Sakimura , Masayuki Takeda , Kazuo Kitamura , Takahiko Mitsui
{"title":"Manipulation of bladder contraction by cell-type selective optogenetics of the anterior cingulate cortex neurons in a mouse model with increased urinary frequency","authors":"Hiroshi Shimura ,&nbsp;Satoshi Manita ,&nbsp;Takanori Mochizuki ,&nbsp;Satoru Kira ,&nbsp;Norifumi Sawada ,&nbsp;Haruhiko Bito ,&nbsp;Kenji Sakimura ,&nbsp;Masayuki Takeda ,&nbsp;Kazuo Kitamura ,&nbsp;Takahiko Mitsui","doi":"10.1016/j.neulet.2025.138355","DOIUrl":"10.1016/j.neulet.2025.138355","url":null,"abstract":"<div><div>Optogenetics is a powerful technique for both investigating the mechanism underlying neurological disorders and modifying them using disease model animals. However, there is limited evidence demonstrating the potential of optogenetics in disease (lower urinary tract<!--> <!-->dysfunction; LUTD) model with targeting<!--> <!-->the cerebral cortex.<!--> <!-->Here, we evaluated the effect of optogenetic stimulation of GABAergic neurons in<!--> <!-->the<!--> <!-->anterior cingulate cortex (ACC) on urodynamics in a urinary frequency mouse model.</div><div>Channelrhodopsin-2 (ChR2) was selectively expressed in parvalbumin expressing neurons of the ACC in mice. For the induction of urinary frequency, 0.1% acetic acid was perfused into the bladder, while normal saline was used for control. Photostimulation was delivered to the ACC and intercontraction intervals (ICIs) were measured before, during and after photostimulation.</div><div>Photostimulation prolonged ICI only during stimulation and ICI was recovered after stimulation in control condition. We found in the urinary frequency model that photostimulation also significantly prolonged ICI, which was recovered after stimulation.</div><div>Cell-type selective photoactivation in the ACC can modulate urodynamics in disease model. The application of optogenetics for the treatment of LUTD have an advantage of temporal specificity, making it useful for controlling immediate urgency.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138355"},"PeriodicalIF":2.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
DOPAnization of α-synuclein exacerbates dopaminergic neurodegeneration in the substantia nigra α-突触核蛋白的多巴化加剧了黑质多巴胺能神经变性。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-11 DOI: 10.1016/j.neulet.2025.138354
Keisuke Togawa , Sakiko Matsumoto , Lulu Deng , Mingyue Jin , Yoshiaki Itoh , Shinji Hirotsune
{"title":"DOPAnization of α-synuclein exacerbates dopaminergic neurodegeneration in the substantia nigra","authors":"Keisuke Togawa ,&nbsp;Sakiko Matsumoto ,&nbsp;Lulu Deng ,&nbsp;Mingyue Jin ,&nbsp;Yoshiaki Itoh ,&nbsp;Shinji Hirotsune","doi":"10.1016/j.neulet.2025.138354","DOIUrl":"10.1016/j.neulet.2025.138354","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is characterized by the selective and progressive loss of dopaminergic (DAergic) neurons in the substantia nigra (SN). Although abnormal forms and aggregates of the α-synuclein (αSyn) protein are considered to cause PD, the underlying mechanisms of the preferential death of dopaminergic neurons are largely unknown. We recently reported that a tyrosine hydroxylase post-translationally converted a tyrosine residue of αSyn to dihydroxyphenylalanine (DOPA), termed DOPAnization, in the DAergic neurons of PD patients, which facilitated the formation of αSyn oligomers and increased neuronal toxicity <em>in vitro</em>. However, whether DOPAnized αSyn promotes the progressive death of DAergic neurons <em>in vivo</em> has not been determined. Here, we report that intranigral administration of <em>in vitro</em>-prepared DOPAnized αSyn oligomers induced more severe and progressive neurodegeneration in DAergic neurons than did the administration of unmodified αSyn aggregates. We also found that DOPAnized αSyn oligomers enhanced microglial activation, preceding the severe loss of SN neurons and their nigrostriatal projections. These findings suggest that DOPAnized αSyn in DAergic neurons plays a key role in the pathogenesis of PD.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138354"},"PeriodicalIF":2.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144847974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Mini Review: How circular RNAs participate in neuro-degeneration 迷你回顾:环状rna如何参与神经变性。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-09 DOI: 10.1016/j.neulet.2025.138353
Sima Biswas , Angshuman Bagchi
{"title":"Mini Review: How circular RNAs participate in neuro-degeneration","authors":"Sima Biswas ,&nbsp;Angshuman Bagchi","doi":"10.1016/j.neulet.2025.138353","DOIUrl":"10.1016/j.neulet.2025.138353","url":null,"abstract":"<div><div>Circular RNAs have important implications in the onsets of various neurodegenerative diseases. Their broad functionalities involve miRNA sponging and binding to RBPs. Some circular RNAs have protein-coding potentials through specialized mechanisms. These products have varied functional implications in neurodegenerative diseases. However, the exact mechanisms of their involvement are not yet fully understood. This review gives an overview of the roles of the circular RNAs and their derived protein products in the onsets of neurodegenerative diseases.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138353"},"PeriodicalIF":2.0,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Takens’ theorem to assess EEG traces: Regional variations in brain dynamics 评估脑电图痕迹的Takens定理:脑动力学的区域差异。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-09 DOI: 10.1016/j.neulet.2025.138352
Arturo Tozzi , Ksenija Jaušovec
{"title":"Takens’ theorem to assess EEG traces: Regional variations in brain dynamics","authors":"Arturo Tozzi ,&nbsp;Ksenija Jaušovec","doi":"10.1016/j.neulet.2025.138352","DOIUrl":"10.1016/j.neulet.2025.138352","url":null,"abstract":"<div><div>Takens’ theorem (TT) proves that the behaviour of a dynamical system can be effectively reconstructed within a multidimensional phase space. This offers a comprehensive framework for examining temporal dependencies, dimensional complexity and predictability of time series data. We applied TT to investigate the physiological regional differences in EEG brain dynamics of healthy subjects, focusing on three key channels: FP1 (frontal region), C3 (sensorimotor region), and O1 (occipital region). We provided a detailed reconstruction of phase spaces for each EEG channel using time-delay embedding. The reconstructed trajectories were quantified through measures of trajectory spread and average distance, offering insights into the temporal structure of brain activity that traditional linear methods struggle to capture. Variability and complexity were found to differ across the three regions, revealing notable regional variations. FP1 trajectories exhibited broader spreads, reflecting the dynamic complexity of frontal brain activity associated with higher cognitive functions. C3, involved in sensorimotor integration, displayed moderate variability, reflecting its functional role in coordinating sensory inputs and motor outputs. O1, responsible for visual processing, showed constrained and stable trajectories, consistent with repetitive and structured visual dynamics. These findings align with the functional specialization of different cortical areas, suggesting that the frontal, sensorimotor and occipital regions operate with autonomous temporal structures and nonlinear properties. This distinction may have significant implications for advancing our understanding of normal brain function and enhancing the development of brain-computer interfaces. In sum, we demonstrated the utility of TT in revealing regional variations in EEG traces, underscoring the value of nonlinear dynamics.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138352"},"PeriodicalIF":2.0,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822140","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Inhibition of calcium-sensing receptor by its antagonist protects dopaminergic neurons from MPTP/MPP+-induced neurotoxicity via regulating mitochondrial function, autophagy, and apoptosis in vivo and in vitro 钙敏感受体拮抗剂通过调节线粒体功能、自噬和细胞凋亡,在体内和体外保护多巴胺能神经元免受MPTP/MPP+诱导的神经毒性。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-09 DOI: 10.1016/j.neulet.2025.138351
Huiping Qi , Dongfang Shen , Huan Wang , Wenxu Sang , Chenggong Jiang
{"title":"Inhibition of calcium-sensing receptor by its antagonist protects dopaminergic neurons from MPTP/MPP+-induced neurotoxicity via regulating mitochondrial function, autophagy, and apoptosis in vivo and in vitro","authors":"Huiping Qi ,&nbsp;Dongfang Shen ,&nbsp;Huan Wang ,&nbsp;Wenxu Sang ,&nbsp;Chenggong Jiang","doi":"10.1016/j.neulet.2025.138351","DOIUrl":"10.1016/j.neulet.2025.138351","url":null,"abstract":"<div><div>Parkinson’s disease (PD)‌ is characterized by progressive degeneration of dopaminergic neurons. The role of calcium-sensing receptor (CaSR) in the pathogenesis of PD remains poorly understood. We employed the CaSR antagonist NPS-2143 in both<!--> <!-->in vivo<!--> <!-->and<!--> <!-->in vitro<!--> <!-->experiments to investigate the therapeutic potential of CaSR modulation. Our findings revealed that MPTP/MPP<sup>+</sup> exposure significantly upregulated CaSR expression. Functionally, CaSR overexpression exacerbated intracellular Ca<sup>2+</sup> dyshomeostasis under MPTP/MPP<sup>+</sup> toxicity. Inhibition of CaSR with NPS-2143 demonstrated marked neuroprotection, evidenced by improved motor function and preservation of dopaminergic neurons in MPTP-treated mice, alongside reduced cellular apoptosis in MPP<sup>+</sup>-injured MN9D cells. Mechanistically, NPS-2143 enhanced autophagy in MPP<sup>+</sup>-exposed cells while reversing 3-MA-induced autophagy suppression. Furthermore, NPS-2143 mitigated mitochondrial dysfunction, as shown by reduced reactive oxygen species accumulation, restored mitochondrial membrane potential, and normalized ATP production in MPP<sup>+</sup>-treated cells. These results collectively demonstrate that CaSR antagonism protects dopaminergic neurons through coordinated regulation of mitochondrial homeostasis, autophagic flux, and apoptotic pathways. Our study highlights CaSR as a promising therapeutic target for PD prevention and identifies NPS-2143 as a potential neuroprotective agent targeting CaSR.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138351"},"PeriodicalIF":2.0,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144822138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Aβ-damaged neural stem cells migration and differentiation through Wnt3a/β-catenin pathway: Protective effects of 17β-E2 通过Wnt3a/β-catenin通路的a β损伤神经干细胞迁移和分化:17β-E2的保护作用
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-08 DOI: 10.1016/j.neulet.2025.138350
Ying Yang , Lingdi Zhang , Yixin Zhao , Zhihong Chen , Pei Wang , Zhenjun Yang
{"title":"Aβ-damaged neural stem cells migration and differentiation through Wnt3a/β-catenin pathway: Protective effects of 17β-E2","authors":"Ying Yang ,&nbsp;Lingdi Zhang ,&nbsp;Yixin Zhao ,&nbsp;Zhihong Chen ,&nbsp;Pei Wang ,&nbsp;Zhenjun Yang","doi":"10.1016/j.neulet.2025.138350","DOIUrl":"10.1016/j.neulet.2025.138350","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is a widespread central nervous system degenerative disease in the elderly population. This study aims to uniquely targets this sex-specific vulnerability by investigating the effects of 17β-E2 on the differentiation and migration capabilities of Aβ-damaged NSCs and its potential mechanisms—a critical gap for female-focused AD therapies. Primary NSCs isolated from neonatal SD rats were treated with Aβ25-35 (60 μM) to mimic AD pathology, followed by 17β-E2 (100 nM) with or without BX795 (a Wnt3a/β-catenin inhibitor). Results showed that Aβ significantly suppressed Wnt3a, LRP6, and β-catenin mRNA/protein levels while increasing GSK-3β expression. 17β-E2 treatment reversed these effects, enhancing phosphorylated GSK-3β (Ser9) and β-catenin, which were abolished by BX795. Transwell assays demonstrated that 17β-E2 rescued Aβ-damaged migration deficits, accompanied by elevated p-MLC and Cdc42 protein levels. Furthermore, 17β-E2 promoted neuronal differentiation, increasing MAP2 + and βIII-tubulin + cells with enhanced dendritic complexity, whereas BX795 counteracted these benefits. These findings indicate that 17β-E2 mitigates Aβ-damaged NSCs dysfunction by activating the Wnt3a/β-catenin pathway via GSK-3β phosphorylation, highlighting its therapeutic potential for AD by enhancing neurogenesis and NSC mobility.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138350"},"PeriodicalIF":2.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Differential cholinergic modulation of parafascicular thalamic neurons 丘脑束旁神经元的差异胆碱能调节。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-08 DOI: 10.1016/j.neulet.2025.138348
Héctor A. Vázquez-Vázquez, Aidán Ortega, Yohana Parrado, Antonio Laville, Dagoberto Tapia, Elvira Galarraga
{"title":"Differential cholinergic modulation of parafascicular thalamic neurons","authors":"Héctor A. Vázquez-Vázquez,&nbsp;Aidán Ortega,&nbsp;Yohana Parrado,&nbsp;Antonio Laville,&nbsp;Dagoberto Tapia,&nbsp;Elvira Galarraga","doi":"10.1016/j.neulet.2025.138348","DOIUrl":"10.1016/j.neulet.2025.138348","url":null,"abstract":"<div><div>The parafascicular (PF) thalamic nucleus participates in functions such as arousal, consciousness, learning, and behavioral flexibility, which are linked to its projections to the striatum and receives strong cholinergic input from the pedunculopontine nucleus. Using electrophysiological recordings, we identified two neuronal populations based on their afterhyperpolarization potential (AHP) characteristics: Brief AHP neurons and Prolonged AHP neurons. Only Prolonged AHP neurons were modulated by cholinergic receptor activation, which reduced AHP amplitude and duration, and increased their firing frequency. These effects were associated with SK-type calcium-activated potassium channels and specifically activated by M1 type muscarinic receptors. Together, these findings indicate clear differential cholinergic modulation in the PF thalamic nucleus, which may be related to its functional roles.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138348"},"PeriodicalIF":2.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817245","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer’s disease model blarcamesine预防阿尔茨海默病模型中的记忆障碍和海马损伤。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-08 DOI: 10.1016/j.neulet.2025.138349
Tangui Maurice
{"title":"Prevention of memory impairment and hippocampal injury with blarcamesine in an Alzheimer’s disease model","authors":"Tangui Maurice","doi":"10.1016/j.neulet.2025.138349","DOIUrl":"10.1016/j.neulet.2025.138349","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most common dementia, with rising global prevalence, still incomplete pathogenetic understanding and very limited effective therapies. Recent advances in biomarker identification of Aβ peptides and phospho-tau protein, and in anti-Aβ immunotherapy are suggesting that more early intervention will be more effective. Alternative therapeutic strategies to anti-Aß immunotherapy have received comparably less attention, yet one specific approach toward upstream neuroprotection by improvement of intracellular calcium homeostasis, activation of endogenous neuroprotection and restoration of autophagy through sigma-1 receptor activation recently demonstrated positive clinical data with oral blarcamesine in a phase IIb/III trial in 508 patients with early AD. AD-preventive approaches beyond lifestyle interventions become attractive candidates when meeting criteria of: (i) record of effective early intervention in mild disease, (ii) record of human safety, (iii) ease of administration, (iv) scalability to population level, (v) relative cost-effectiveness considering longer-term preventive use at population level. Here, we assessed blarcamesine’s efficacy at preventing memory impairment and brain oxidative injury in the mouse preclinical model induced by intracerebroventricular injection of aggregated Aβ<sub>25-35</sub> peptide, that permitted a clean preventive approach before administration of the pathology-inducing amyloidogenic Aβ fragment. We observed significant preventions of Aβ<sub>25-35</sub>-induced memory impairments, for both spatial working and contextual long-term memories, and of Aβ<sub>25-35</sub>-induced increase in lipid peroxidation in the mouse hippocampi. These new insights, together with blarcamesine’s clinical record in early AD render blarcamesine an attractive candidate for AD pharmacological prevention.</div></div>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":"865 ","pages":"Article 138349"},"PeriodicalIF":2.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 dysregulation of high glucose-induced iPSC-neural stem cells differentiation by caspase-1. caspase-1对高糖诱导的ipsc -神经干细胞分化的失调。
IF 2 4区 医学
Neuroscience Letters Pub Date : 2025-08-08 DOI: 10.1016/j.neulet.2025.138347
Hsien-Hui Chung
{"title":"The dysregulation of high glucose-induced iPSC-neural stem cells differentiation by caspase-1.","authors":"Hsien-Hui Chung","doi":"10.1016/j.neulet.2025.138347","DOIUrl":"10.1016/j.neulet.2025.138347","url":null,"abstract":"<p><p>Maternal diabetes (MD) increases the risk for neurodevelopmental disorders and leads to neural tube defects (NTDs) which are severe anomalies of the nervous system. In order to elucidate the etiology and pathological mechanisms causing NTDs in MD and try to search for new therapeutic strategies as well, the exposure of induced pluripotency stem cell (iPSC)-neural stem cells (NSCs) to high glucose (HG) may be associated with fetal progressive deterioration of neuronal functions in utero ultimately leading to MD-related NTDs. In the present study, although HG (25 mM) had no effect on the viability of undifferentiated iPSC-NSCs compared with the positive control mannitol (25 mM), HG attenuated iPSC-NSCs cell proliferation and induced the presence of decreased βIII-tubulin and neurite network length during 7-day neuronal differentiation, resulting in the inability of nerve-to-nerve connections to communicate effectively. Compared with mannitol, HG actually reduced gene and protein expressions of iPSC-NSCs differentiation marker βIII-tubulin on day 7. Moreover, HG increased protein expressions of caspase-1 during 7-day neuronal differentiation compared with mannitol, indicating the critical role of caspase-1 in HG-mediated neuronal inflammation. Thus, the present study indicated that HG-induced impairment in iPSC-NSCs differentiation was mediated by decreased βIII-tubulin, shorter neurite network length and increased caspase-1 expressions, which provided a direction for the clarification of MD-induced NTDs.</p>","PeriodicalId":19290,"journal":{"name":"Neuroscience Letters","volume":" ","pages":"138347"},"PeriodicalIF":2.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144817247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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