IBRO Neuroscience Reports最新文献

Burden of stroke in China: A decomposition analysis investigating the driven factors 中国脑卒中负担：驱动因素的分解分析

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-27 DOI: 10.1016/j.ibneur.2026.01.012

Lijuan Fu , Wencai Jiang , Yanhua Peng , Xianjie Zhang , Rui Zhou

Background

While the degree of population aging is increasing, a nationwide stroke program was started in 2011. We analyzed how population aging outpaced gains in stroke care in China.

Methods

The number of deaths, incidence, prevalence, Disability-Adjusted Life Years (DALYs) attributable to stroke and its subtypes from 2012 to 2021 were extracted from the Global Health Data Exchange database. The total populations of age groups in 2012 and 2021 were extracted from the National Bureau of Statistics of China. The Das Gupta Decomposition method was applied to identify the contributions of population growth, population aging, and the changes in the incidence, mortality, prevalence, and DALYs.

Result

From 2012–2021, the total stroke incidence increased by 38.4 % (from 2.95 to 4.09 million), deaths by 17.6 % (from 2.20 to 2.59 million), and prevalence by 34.2 % (from 19.62 to 26.34 million) in China. Decomposition analysis identified rapid population aging as the predominant driver, accounting for 78.1 % of the incidence increase and even exceeding the total death increase (197.6 %), overwhelming the benefits from improved stroke care. The stroke subtype profile shifted markedly, with ischemic stroke's share of incidence rising from 62 % to 68 % and deaths from 41 % to 46 %, while intracerebral hemorrhage's contribution declined.

Conclusion

The escalating stroke burden in China is primarily driven by population aging, followed by population growth, creating a paradox where healthcare improvements are offset demographically. The epidemic is increasingly characterized by ischemic stroke, leading to a growing population of survivors requiring long-term care. This necessitates a paradigm shift in health policy from a focus solely on reducing acute mortality towards building cost-effective, integrated systems for lifelong stroke management, chronic care, and secondary prevention tailored for an aging society.

随着人口老龄化程度的加剧，2011年开始了全国范围内的中风防治计划。我们分析了中国人口老龄化如何超过中风护理的增长。方法从全球健康数据交换数据库中提取2012年至2021年脑卒中及其亚型的死亡人数、发病率、患病率、残疾调整生命年（DALYs）。2012年和2021年各年龄组人口总数取自中国国家统计局数据。采用Das Gupta分解方法确定人口增长、人口老龄化以及发病率、死亡率、患病率和DALYs变化的贡献。结果2012-2021年，中国脑卒中总发病率增加38.4% %（从295万增加到409万），死亡人数增加17.6% %（从220万增加到259万），患病率增加34.2% %（从1962万增加到2634万）。分解分析发现，人口快速老龄化是主要驱动因素，占发病率增加的78.1 %，甚至超过总死亡增加（197.6 %），压倒了改善卒中护理的好处。脑卒中的亚型特征发生了显著变化，缺血性脑卒中的发病率从62% %上升到68% %，死亡从41% %上升到46% %，而脑出血的发病率下降。结论中国脑卒中负担的增加主要是由人口老龄化驱动的，其次是人口增长，造成了医疗保健改善被人口统计学抵消的悖论。这种流行病越来越多地以缺血性中风为特征，导致越来越多的幸存者需要长期护理。这就需要在卫生政策方面进行范式转变，从只注重降低急性死亡率转向为老龄化社会量身打造具有成本效益的终身卒中管理、慢性护理和二级预防综合系统。

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引用次数: 0

TNKS1 mediates the PTEN-PI3K/AKT pathway to regulate glycolysis and proliferation in gliomas TNKS1介导PTEN-PI3K/AKT通路调节胶质瘤中的糖酵解和增殖

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-21 DOI: 10.1016/j.ibneur.2026.01.007

Zhenyan Shi , Danke Shen , Jie Wu, Hai Luo, Shenhao Xie, Duanzheng Cao, Yong Cao, Bin Tang

Objective

To explore the mechanisms by which TNKS1 regulates glycolysis and proliferation in glioma.

Methods

Cell viability was assessed using the CCK-8 assay. Levels of glucose and lactate were measured using biochemical detection kits. Western blotting was used to detect the expression levels of glycolysis-related proteins, and qPCR was employed to measure the mRNA expression of GLUT1 and HK2. A subcutaneous xenograft tumor model in nude mice was established. After intratumoral injection of drugs, the effects of TNKS1 knockdown on tumor tissues were observed using HE staining and immunohistochemical staining. Western blotting was also used to detect the expression of PTEN and other proteins in glioma tissues.

Results

Compared with the control group, TNKS1 knockdown resulted in increased expression of PTEN, decreased expression of PI3K and p-AKT/AKT proteins, reduced cell proliferation capacity, and lower glucose uptake and lactate production. The results were opposite in the TNKS1 overexpression group. In the group treated with a PI3K agonist compared with the untreated group, the expression of PI3K and p-AKT/AKT proteins increased, and cell proliferation capacity, glucose uptake, and lactate production also increased to varying degrees. In the TNKS1 overexpression + PI3K inhibitor group compared with the TNKS1 overexpression group, the expression of PI3K and p-AKT/AKT proteins decreased, and cell proliferation capacity, glucose uptake, and lactate production also decreased to varying degrees. In the in vivo experiments, compared with the control group, the TNKS1 knockdown group showed increased tumor cell apoptosis and necrosis. Immunohistochemical and Western blotting analyses indicated that compared with the TNKS1-siRNA empty vector group, the TNKS1-siRNA group had significantly increased PTEN protein expression. The expression levels of PI3K, p-AKT/AKT proteins, and Ki67 were significantly lower in the TNKS1-siRNA group, inhibitor group, and TNKS1-siRNA + inhibitor group.

Conclusion

TNKS1 regulates glycolysis and proliferation in glioma by mediating the PTEN-PI3K/AKT pathway.

目的探讨TNKS1调控胶质瘤糖酵解和增殖的机制。方法采用CCK-8法测定细胞活力。采用生化检测试剂盒测定葡萄糖和乳酸水平。Western blotting检测糖酵解相关蛋白表达水平，qPCR检测GLUT1、HK2 mRNA表达水平。建立裸鼠皮下异种移植瘤模型。瘤内注射药物后，采用HE染色和免疫组化染色观察TNKS1敲低对肿瘤组织的影响。Western blotting检测胶质瘤组织中PTEN等蛋白的表达。结果与对照组相比，TNKS1敲低导致PTEN表达升高，PI3K和p-AKT/AKT蛋白表达降低，细胞增殖能力降低，葡萄糖摄取和乳酸生成降低。TNKS1过表达组则相反。PI3K激动剂治疗组与未治疗组相比，PI3K和p-AKT/AKT蛋白表达增加，细胞增殖能力、葡萄糖摄取和乳酸生成也有不同程度的增加。TNKS1过表达+ PI3K抑制剂组与TNKS1过表达组相比，PI3K和p-AKT/AKT蛋白表达降低，细胞增殖能力、葡萄糖摄取、乳酸生成均不同程度降低。在体内实验中，与对照组相比，TNKS1敲低组肿瘤细胞凋亡和坏死增加。免疫组织化学和Western blotting分析显示，与TNKS1-siRNA空载体组相比，TNKS1-siRNA组PTEN蛋白表达显著升高。在TNKS1-siRNA组、抑制剂组和TNKS1-siRNA + 抑制剂组中，PI3K、p-AKT/AKT蛋白和Ki67的表达水平均显著降低。结论tnks1通过PTEN-PI3K/AKT通路调控胶质瘤的糖酵解和增殖。

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引用次数: 0

Prefrontal TDCS does not improve working memory performance in individuals with chronic alcohol and tobacco use 前额叶TDCS不能改善长期饮酒和吸烟个体的工作记忆表现

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-21 DOI: 10.1016/j.ibneur.2026.01.011

Franziska Göttgens , Ute Habel , Paul Wallheinke , Julie A. Blendy , Carmen Weidler

Working memory (WM) deficits are common in psychiatric disorders that are associated with decreased prefrontal cortex activity. As WM is essential for cognitive functions, deficits interfere with daily life and treatment. The lateralization of WM components remains unclear, but stimuli matching, often assessed using the n-back task, has been associated with right-hemispheric dominance. This study examines whether anodal transcranial direct current stimulation (tDCS) targeting the right dorsolateral prefrontal cortex (DLPFC) could enhance WM performance in alcohol-dependent patients (AD), tobacco users (TU) and healthy controls (HC). In a double-blind, sham-controlled study, tDCS was applied to upregulate right DLPFC activity. A total of 46 participants received anodal tDCS with a current intensity of 1.5 mA for 20 min or sham stimulation. In addition to the 7x5cm anode, a large reference electrode (10x10cm) was situated over the contralateral supraorbital area. While being stimulated, participants performed the n-back task as a measure of WM performance. Results revealed no significant differences in WM performance between active and sham stimulated participants, nor between groups, and no significant interaction between stimulation condition and group. Bayesian analysis supported the null effects. These findings do not provide evidence that single-session right DLPFC stimulation reliably enhances working memory across all stimulus types. The outcomes may have been influenced by task–stimulation mismatch, sample heterogeneity, small sample size, and stimulation parameters, which could limit the ability to detect subtle tDCS effects in both clinical and healthy populations.

工作记忆（WM）缺陷在与前额皮质活动减少相关的精神疾病中很常见。由于WM对认知功能至关重要，因此缺陷会干扰日常生活和治疗。WM成分的偏侧化尚不清楚，但刺激匹配（通常使用n-back任务进行评估）与右半球优势有关。本研究探讨了针对右背外侧前额叶皮质（DLPFC）的阳极经颅直流电刺激（tDCS）是否可以提高酒精依赖患者（AD）、烟草使用者（TU）和健康对照（HC）的WM表现。在一项双盲、假对照研究中，tDCS被用于上调右侧DLPFC的活性。共有46名参与者接受了电流强度为1.5 mA的阳极tDCS，持续20 min或假刺激。除了7x5cm的阳极外，一个大的参考电极（10x10cm）位于对侧眶上区域。在受到刺激的情况下，参与者执行n-back任务，以衡量WM的表现。结果显示，刺激条件与组间无显著性差异，刺激条件与组间无显著交互作用。贝叶斯分析支持零效应。这些发现并没有提供证据证明单次的右侧DLPFC刺激在所有刺激类型中都能可靠地增强工作记忆。结果可能受到任务-刺激不匹配、样本异质性、小样本量和刺激参数的影响，这可能限制了在临床和健康人群中检测微妙tDCS效应的能力。

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引用次数: 0

Sleep deprivation and memory: A neurobiological perspective 睡眠剥夺和记忆：一个神经生物学的观点

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-18 DOI: 10.1016/j.ibneur.2026.01.010

Kehinde O. Adeniji BSc, MSc , Olumayowa O. Igado DVM, MSc, PhD , Funmilayo E. Olopade MBBS, MPH, MSc, PhD , Omowumi M. Femi-Akinlosotu BDS, MSc, PhD

Memory consolidation and the preservation of cognitive function are fundamentally influenced by sleep. Lack of sleep affects synaptic plasticity and neurogenesis, as well as oxidative stress and neuroinflammation, all of which impair memory accuracy, cognitive flexibility, and attention. The behavioural repercussions include decreased learning ability, attentional problems, emotional dysregulation, and heightened vulnerability to false memories. This review examines the neurobiological impact of sleep deprivation on memory and cognition, emphasising how the brain systems performing these functions are disrupted by insufficient sleep. The distinct sleep stages that are in support of declarative, procedural, and emotional memory, drawing on contemporary concepts such as the synaptic homeostasis hypothesis and the active system consolidation theory, were emphasised. We highlighted how sleep deprivation can affect important areas, especially the hippocampus, and cause problems with neurotransmitter systems and immune regulation. Preventative and therapeutic approaches, such as pharmacological supports, behavioural interventions, and the cognitive advantages of recovery sleep and naps, were also enumerated. These insights on how sleep and memory interact are vital for enhancing learning outcomes, mental health, and long-term brain resilience.

记忆的巩固和认知功能的保持从根本上受到睡眠的影响。睡眠不足会影响突触可塑性和神经发生，以及氧化应激和神经炎症，所有这些都会损害记忆的准确性、认知的灵活性和注意力。行为反应包括学习能力下降、注意力问题、情绪失调以及对错误记忆的脆弱性增加。这篇综述探讨了睡眠剥夺对记忆和认知的神经生物学影响，强调了执行这些功能的大脑系统是如何被睡眠不足扰乱的。强调了支持陈述性、程序性和情绪性记忆的不同睡眠阶段，并借鉴了突触稳态假说和主动系统巩固理论等当代概念。我们强调了睡眠剥夺如何影响重要区域，特别是海马体，并导致神经递质系统和免疫调节问题。预防和治疗方法，如药物支持，行为干预，以及恢复睡眠和小睡的认知优势，也被列举出来。这些关于睡眠和记忆如何相互作用的见解对于提高学习成果、心理健康和长期大脑恢复能力至关重要。

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引用次数: 0

Behavioral effects of a chronic envy-like stress paradigm in mice using an adjacent cage model 使用相邻笼模型的小鼠慢性嫉妒样应激范式的行为影响

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-17 DOI: 10.1016/j.ibneur.2026.01.008

Hiroshi Ueno , Yoshihiro Tanaka , Eriko Kitano , Yu Takahashi , Sachiko Mori , Shinji Murakami , Kenta Wani , Yosuke Matsumoto , Motoi Okamoto , Takeshi Ishihara

Background

Social comparison and envy are significant psychosocial stressors in humans and are known to be involved in the onset and persistence of psychiatric disorders. However, animal models capable of experimentally reproducing the effects of indirect social comparison without physical contact are limited. In this study, we used a newly developed "adjacent-cage paradigm" to investigate whether chronic vicarious exposure to conspecifics in different environments induces envy-like stress in mice.

Methods

Male C57BL/6 N mice served as observers, while demonstrator mice were assigned to one of four conditions: (1) an environment enriched with objects, (2) an igloo, (3) a tube, or (4) social isolation. Observers were continuously exposed to these adjacent cages for 21 days. Subsequently, a comprehensive battery of behavioral tests was conducted to assess general health, anxiety-like behavior, spatial memory, social behavior, and depression-like behavior.

Results

In the objects condition, a decrease in time spent in the light compartment of the light/dark box indicated an increase in anxiety-like behavior. In the isolation condition, the mean duration per social interaction was shortened, suggesting a qualitative change in social behavior. The igloo condition resulted in reduced immobility time in the forced swim test, suggesting a possible alteration in stress coping behavior. Furthermore, increased nociceptive sensitivity was observed in the hot plate test under both the objects and isolation conditions.

Conclusion

Although the envy-like stress paradigm did not affect many behavioral indices, it did cause condition-dependent and limited behavioral changes. This suggests that the paradigm may serve as a novel model for capturing psychological and context-dependent social stress, which differs from conventional physical stress models. Elucidating the neural basis of this paradigm is expected to contribute to the understanding of how social comparison affects mental health in modern society.

社会比较和嫉妒是人类重要的社会心理压力源，已知与精神疾病的发病和持续有关。然而，能够在实验中再现没有身体接触的间接社会比较效果的动物模型是有限的。在这项研究中，我们使用了一种新开发的“邻接笼子范式”来研究小鼠在不同环境中慢性替代暴露于同种物质是否会引起嫉妒样应激。方法C57BL/6 N只小鼠作为观察小鼠，示范小鼠被分配到四种条件中的一种：(1)充满物体的环境，(2)冰屋，(3)管道，或(4)社会隔离。观察人员在这些相邻的笼子中连续暴露21天。随后，进行了一系列全面的行为测试，以评估一般健康状况、焦虑样行为、空间记忆、社会行为和抑郁样行为。结果在物体条件下，在明暗箱的光室中待的时间减少表明焦虑样行为增加。在隔离条件下，每次社会互动的平均持续时间缩短，表明社会行为发生了质的变化。冰屋条件导致强迫游泳测试中静止时间减少，表明压力应对行为可能发生改变。此外，在热板实验中，在物体和隔离条件下均观察到伤害敏感性的增加。结论羡慕型应激模式虽然对许多行为指标没有影响，但会引起条件依赖性和限制性的行为改变。这表明该范式可以作为一种新的模型来捕捉心理和情境依赖的社会压力，这与传统的物理压力模型不同。阐明这一范式的神经基础有望有助于理解社会比较如何影响现代社会的心理健康。

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引用次数: 0

Acupuncture-induced changes in locus coeruleus connectivity and memory improvement in patients with amnestic cognitive impairment 针刺诱导的遗忘性认知障碍患者蓝斑连通性和记忆改善的变化

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-15 DOI: 10.1016/j.ibneur.2026.01.005

Liyu Hu , Xinbei Li , Juan Ou , Ting Liu , Xingxian Huang , Xingchen Liu , Yingqi Lu , Nan Yang , Jinhuan Zhang

Background

An increasing number of neuroimaging studies have consistently indicated that the locus coeruleus is associated with cognitive impairment in the early stages of Alzheimer's disease, and the locus coeruleus plays a critical role in cognition, including memory encoding, consolidation, and retrieval.

Objective

To investigate whether and how acupuncture modulates the functional connectivity patterns of the locus coeruleus, and offer a new perspective on the mechanism through which acupuncture exerts its efficacy.

Methods

Resting-state functional magnetic resonance imaging (fMRI) data were collected from 50 patients with amnestic cognitive impairment (aMCI) before and after verum or sham acupuncture. Seed-based whole-brain functional connectivity (FC) was calculated and compared to explore the changing patterns of the locus coeruleus in aMCI patients following acupuncture.

Results

Increased FCs were observed between the left locus coeruleus and the left inferior parietal lobule, and between the right locus coeruleus and the right posterior cerebellum in aMCI patients after verum acupuncture. Further analyses revealed a correlation between FC of the left locus coeruleus and the left inferior parietal lobule before acupuncture and improvement in immediate recall in aMCI patients.

Conclusions

These results suggest that acupuncture could enhance FC between the locus coeruleus and the inferior parietal lobule/the posterior cerebellum. These functional alterations appear to be linked to the efficacy of acupuncture, particularly in ameliorating memory deficits.

越来越多的神经影像学研究一致表明，蓝斑位点与阿尔茨海默病早期阶段的认知障碍有关，蓝斑位点在认知中起着关键作用，包括记忆编码、巩固和检索。目的探讨针刺是否以及如何调节蓝斑的功能连接模式，为针刺的作用机制提供新的视角。方法收集50例遗忘性认知障碍（aMCI）患者静息状态功能磁共振成像（fMRI）数据。计算并比较基于种子的全脑功能连通性（FC），探讨针刺后aMCI患者蓝斑座的变化模式。结果经verum针刺后，aMCI患者左侧蓝斑与左侧顶叶下小叶、右侧蓝斑与右侧小脑后叶之间的FCs增加。进一步的分析显示，针灸前左蓝斑和左顶叶下小叶的FC与aMCI患者即时回忆的改善之间存在相关性。结论针刺可增强蓝斑与顶叶下小叶/小脑后叶之间的FC。这些功能改变似乎与针灸的功效有关，尤其是在改善记忆缺陷方面。

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引用次数: 0

Endurance training mitigates obesity-induced hippocampal impairment by enhancing neurotrophin signalling, synaptic plasticity, and cellular responses in a female rat model 在雌性大鼠模型中，耐力训练通过增强神经营养因子信号传导、突触可塑性和细胞反应来减轻肥胖诱导的海马损伤

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-14 DOI: 10.1016/j.ibneur.2026.01.006

Tomáš Kuruc , Karolína Kuchárová , Alexandra Kisucká , Mária Ileninová , Lenka Ihnátová , Katarína Kiss Bimbová , Martina Magurová , Ján Gálik , Nadežda Lukáčová

Obesity-related health issues, including cognitive decline linked to hippocampal neurogenesis and neuroplasticity, are gaining more attention as obesity rates rise worldwide. Physical activity is recognized as a potent stimulator of neurotrophic factors. This study examined the impact of six weeks of treadmill training on hippocampal molecular pathways in adult female Zucker diabetic fatty (obese) and Zucker lean rats. Animals were assigned to either treadmill exercise (n = 10) or sedentary control (n = 10) groups. Endurance training (ET) markedly upregulated mRNA expression of brain-derived neurotrophic factor and its receptor. The PI3K/Akt pathway was upregulated only in the trained lean rats and downregulated in the trained obese group compared with sedentary controls. ET elicited divergent effects on neurotrophin-associated PLCγ/PKC/CAMKII signalling between lean and obese groups. Sedentary obese rats primarily utilized the PLCγ/PKC axis, while both trained groups (lean and obese) showed increased CAMKII expression, associated with enhanced synaptic plasticity and memory. Enhanced synaptophysin mRNA indicated improved synaptogenesis and plasticity following ET. Trained obese rats also exhibited reduced expression of the microglial pro-inflammatory marker Iba1, alongside increased markers of oligodendrocyte regeneration and neurofilament expression. Behavioral assessment via the passive avoidance test demonstrated improved learning and memory in trained obese animals. Collectively, these findings suggest that ET may mitigate obesity-induced hippocampal damage, exert neuroprotection, and enhance hippocampal function.

随着全球肥胖率的上升，与肥胖相关的健康问题，包括与海马神经发生和神经可塑性有关的认知能力下降，正受到越来越多的关注。体育活动被认为是神经营养因子的有力刺激物。本研究检测了6周的跑步机训练对成年雌性Zucker糖尿病肥胖大鼠和Zucker瘦大鼠海马分子通路的影响。动物被分配到跑步机运动组（n = 10）或久坐对照组（n = 10）。耐力训练显著上调脑源性神经营养因子及其受体mRNA表达。与久坐不动的对照组相比，PI3K/Akt通路仅在训练过的瘦大鼠中上调，而在训练过的肥胖组中下调。在瘦和肥胖组中，ET对神经营养因子相关的PLCγ/PKC/CAMKII信号传导的影响不同。久坐肥胖大鼠主要利用PLCγ/PKC轴，而两个训练组（瘦和肥胖）均显示CAMKII表达增加，与突触可塑性和记忆增强有关。突触素mRNA的增强表明，ET后突触发生和可塑性得到改善。训练过的肥胖大鼠还表现出小胶质促炎标志物Iba1的表达减少，少突胶质细胞再生和神经丝表达标志物增加。通过被动回避测试的行为评估表明，经过训练的肥胖动物的学习和记忆得到了改善。综上所述，这些发现表明ET可能减轻肥胖引起的海马损伤，发挥神经保护作用，并增强海马功能。

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引用次数: 0

Structural remodeling of medium spiny neurons in the tail of the striatum and stress-related behavioral alterations after early handling and adolescent stress in male rats 雄性大鼠纹状体尾部中棘神经元结构重塑及早期处理和青春期应激后应激相关行为改变

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-08 DOI: 10.1016/j.ibneur.2026.01.004

Negar Kayedi-Bakhtiari, Jafar Vatanparast

The tail of the striatum (TS), the most distal part of the striatum, integrates sensory and value-based information and plays a critical role in threat responses. However, its vulnerability to stress remains underexplored. Here, we examined the effects of early handling (EH), chronic social defeat stress (SD) in late adolescence, and their combination (EH-SD) on anxiety- and depression-like behaviors, as well as dendritic morphology and spine density of TS medium spiny neurons (MSNs) in male rats. SD induced anxiety- and depression-like behaviors in the elevated plus maze and forced swim test, whereas EH conferred resilience against these effects. Structural analysis of Golgi-Cox–stained MSNs revealed that EH and EH-SD increased average dendritic process length without affecting branching or total dendritic length. SD markedly elevated dendritic spine density, while EH reduced it; combined EH-SD prevented the SD-induced increase. Although the changes in the total length of dendritic spines in MSNs did not reach a significant level between groups, there was a trend towards increase in the EH and EH-SD groups and a decrease in the SD group, leading to an estimate of the total number of MSN spines did not differ between groups. It seems that EH promotes structural adaptations linked to circuit stabilization, whereas SD enhances excitatory connectivity of TS MSNs, potentially heightening sensitivity to stress-related sensory inputs. Together, the findings identify the TS as a critical site of structural plasticity in stress and early-life experience, and suggest a link between MSN morphology and resilience or vulnerability to stress-related behavioral outcomes.

纹状体尾部（tail of striatum， TS）是纹状体的最末端，整合了感觉和基于价值的信息，在威胁反应中起着关键作用。然而，它对压力的脆弱性仍未得到充分研究。在此，我们研究了早期处理（EH）、青春期后期慢性社会失败压力（SD）及其组合（EH-SD）对雄性大鼠焦虑和抑郁样行为以及TS中棘神经元（msn）树突形态和脊柱密度的影响。在迷宫和强迫游泳测试中，SD诱导焦虑和抑郁样行为，而EH则赋予抗这些影响的弹性。高尔基氧化酶染色msn的结构分析显示，EH和EH- sd增加了平均树突过程长度，但不影响分枝或总树突长度。SD显著提高树突棘密度，EH显著降低树突棘密度；EH-SD联合用药可抑制sd诱导的增高。虽然微MSN树突棘总长度的变化在组间没有达到显著水平，但EH组和EH-SD组有增加的趋势，SD组有减少的趋势，因此对微MSN棘总数的估计在组间没有差异。EH似乎促进了与电路稳定相关的结构适应，而SD则增强了TS msn的兴奋性连接，潜在地提高了对压力相关感官输入的敏感性。总之，这些发现确定了TS是压力和早期生活经历中结构可塑性的关键部位，并提出了MSN形态与弹性或对压力相关行为结果的脆弱性之间的联系。

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引用次数: 0

Chronic stress alters neurotransmitter co-expression and disrupts context discrimination in a sex-dependent manner 慢性应激改变神经递质共表达，并以性别依赖的方式破坏环境歧视

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-06 DOI: 10.1016/j.ibneur.2026.01.003

Christopher Mazon , Ryan Betters , Gabriella Salmeron-Ceballos , Anthony Tomaziefski , Cristina Coffman , Renae Simonson , Elif Tunc-Ozcan

Stress contributes to neuropsychiatric disorders by altering brain circuits and neurotransmitter signaling, often in a sex-dependent manner. The specifics of these stress-induced changes and their role in the development and perseverance of conditions like depression are largely unknown. We examined how context discrimination and neurotransmitter co-expression in the medial septum (MS) changes in response to unpredictable chronic mild stress (uCMS). Female mice subjected to uCMS showed significant context discrimination impairments compared to female controls, while male mice showed no differences in context discrimination as a result of uCMS. We conducted immunolabeling in the MS and found that in females, uCMS reduced the number of cholinergic (ChAT+) neurons while increasing the percent of neurons co-expressing ChAT & GAD67 (marker for GABAergic neurons). These changes suggest a link between chronic stress, neurotransmitter phenotype plasticity in the MS, and hippocampal dysfunction. These differences were observed in the absence of changes to apoptosis and overall neuron number and were specific to female mice; no significant changes to MS neurotransmitter expression was observed in males. Our future work will focus on further dissecting the specific molecular mechanisms behind these changes.

压力通过改变大脑回路和神经递质信号，通常以性别依赖的方式，导致神经精神疾病。这些压力引起的变化的细节及其在抑郁症等疾病的发展和坚持中的作用在很大程度上是未知的。我们研究了在不可预测的慢性轻度应激（uCMS）下，中隔（MS）的环境歧视和神经递质共同表达是如何变化的。与雌性对照组相比，经uCMS处理的雌性小鼠表现出明显的背景辨别障碍，而雄性小鼠在uCMS处理后的背景辨别方面没有差异。我们在MS中进行了免疫标记，发现在女性中，uCMS减少了胆碱能（ChAT+）神经元的数量，同时增加了共表达ChAT & GAD67 （gaba能神经元的标记物）的神经元的百分比。这些变化表明慢性应激、多发性硬化症神经递质表型可塑性和海马功能障碍之间存在联系。这些差异是在没有细胞凋亡和总神经元数量变化的情况下观察到的，并且是雌性小鼠特有的；男性MS神经递质表达无明显变化。我们未来的工作将集中在进一步剖析这些变化背后的具体分子机制。

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引用次数: 0

Case report of stiff - person syndrome and literature review 僵直者综合征1例报告及文献复习

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2026-01-03 DOI: 10.1016/j.ibneur.2025.12.006

Qiongfang Zhang , MengJie Xia , Dan Gui , Jia Wei , Yongfeng Liu , Yanhua Gou

Objective

Currently, there is no objective evaluation method to measure muscle tension and therapeutic effects in patients with stiff person syndrome (SPS). We aimed to investigate objective evaluation criteria for diagnosis and treatment. We used needle electromyography (EMG) to record muscle electrical signals before and after the diazepam drug trial to diagnose a patient with SPS.

Method

We present a patient who was misdiagnosed as having an "anxiety state" for more than a decade because of recurrent tension, worry, and intermittent fear, resulting in generalized muscle stiffness and even falls. Conventional needle EMG was performed on the limbs and axial muscles. The changes in muscle electrical signals before and after diazepam drug trials were recorded.

Results

EMG revealed a significant increase in spontaneous motor unit potentials in the patient's limbs and axial muscles at rest. After intravenous injection of diazepam, the spontaneous motor unit gradually reduced and ultimately disappeared. Based on these results, anti-antibody testing for SPS was performed one week later. The results revealed a high titer of anti-glutamic acid decarboxylase 65 antibodies (GAD65-Abs) in serum, while anti-amphiphysin antibodies were negative. The diagnosis was confirmed as SPS.

Conclusion

Needle EMG is a convenient tool that can provide diagnostic direction for SPS before genetic testing, enabling clinicians to select specific genes for testing and thereby shortening the time required for clinical examination and diagnosis for patients. Additionally, it can be used to verify the efficacy of experimental medications during testing.

目的目前尚无客观的评价方法来衡量僵直人综合征（SPS）患者的肌肉张力和治疗效果。我们旨在探讨客观的诊断和治疗评价标准。我们用针肌电图（EMG）记录地西泮药物试验前后的肌电信号来诊断SPS患者。方法我们报告一位因反复出现紧张、担忧和间歇性恐惧而被误诊为“焦虑状态”长达十多年，导致全身肌肉僵硬甚至跌倒的患者。常规针刺肌电图对四肢和轴向肌进行观察。记录地西泮药物试验前后肌肉电信号的变化。结果肌电图显示，在静止状态下，患者四肢和轴肌的自发运动单位电位明显增加。静脉注射地西泮后，自发性运动单位逐渐减少，最终消失。根据这些结果，一周后进行SPS抗抗体检测。结果显示，血清中抗谷氨酸脱羧酶65抗体（GAD65-Abs）滴度高，而抗amphiphysin抗体呈阴性。诊断为SPS。结论针肌电图是一种方便的工具，可以在基因检测前为SPS提供诊断方向，使临床医生能够选择特定的基因进行检测，从而缩短患者临床检查和诊断所需的时间。此外，它还可以在测试过程中用于验证实验性药物的疗效。

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引用次数: 0