Brain Research Bulletin最新文献_第6页

Polyamine pathway in neurological disorders: Potential therapeutic implications based on current evidences 神经系统疾病中的多胺通路：基于现有证据的潜在治疗意义。

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2025.111711

Mengqi Yan , Yingying Tang , Shuo Zhang , Li Yu , Cenglin Xu

Polyamines (PAs) with a positive charge and low molecular weight, are a class of general biogenic amines that are involved in many important cellular processes, including maintaining nucleic acid stability, controlling ion channel activity, regulating transcription and translation, modulating cell cycle, influencing kinase activity, protecting oxidative damage, and maintaining membrane structure. Cumulative studies have shown that in various neurological disorders, the normal synthesis and metabolism of the polyamine pathway would be disrupted. And the changed polyamine system is believed to participate in the pathophysiological process of the disease through various mechanisms, these include down-regulating or up-regulating PA, putrescine, spermidine, spermine, the key enzymes in the polyamine catabolic pathway include ornithine decarboxylase (ODC), spermidine/spermine N1-acetyltransferase (SAT1), and spermine oxidase (SMOX). They also play a role in the disease process by affecting different downstream molecular pathways or mechanisms, resulting in distinct changes under different disease conditions. With such implications of polyamine in the disorder process, targeting the synthesis and metabolism of polyamine system emerges as potential approaches for intervening the neurological disorders. We attempted to explore the potential molecular mechanisms and molecular connections involved in polyamines at first. Then, we describe possible links between polyamines and various neurological disorders, and finally the possible therapeutic implications on targeting the polyamine system for the treatment of various disorders were proposed. This review may provide an up-to-date overview to propose the new perspective about targeting PA for developing potential therapeutic strategies.

多胺（Polyamines, PAs）是一类具有正电荷和低分子量的普通生物胺，参与许多重要的细胞过程，包括维持核酸稳定性、控制离子通道活性、调节转录和翻译、调节细胞周期、影响激酶活性、保护氧化损伤和维持膜结构。累积研究表明，在各种神经系统疾病中，多胺途径的正常合成和代谢会被破坏。而改变后的多胺系统被认为通过下调或上调PA、腐胺、亚精胺、精胺等多种机制参与了该病的病理生理过程，多胺分解代谢途径的关键酶包括鸟氨酸脱羧酶（ODC）、亚精胺/精胺n1 -乙酰转移酶（SAT1）和精胺氧化酶（SMOX）。它们还通过影响不同的下游分子途径或机制在疾病过程中发挥作用，在不同的疾病条件下产生不同的变化。鉴于多胺在神经紊乱过程中的作用，靶向多胺系统的合成和代谢成为干预神经紊乱的潜在途径。我们首先试图探索多胺的潜在分子机制和分子联系。然后，我们描述了多胺与各种神经系统疾病之间可能的联系，最后提出了针对多胺系统治疗各种疾病的可能的治疗意义。本文综述了针对PA靶向治疗的最新进展，并提出了新的研究视角。

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引用次数: 0

Disease-specific network pattern of perinatal depression revealed by Common Orthogonal Basis Extraction 公共正交基提取揭示围产儿抑郁的疾病特异性网络模式

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2026.111719

Yueheng Peng , Jihan Wang , Xianyong Fan , Yue Yu , Guolin He , Dawazhuoma , Lu Jiang , Tingting Zhang , Silangquncuo , Chanlin Yi , Dezhong Yao , Bin Lv , Peng Xu , Kaibo Shi

The clinical diagnosis of perinatal depression (PD) presents considerable challenge, as it is much harder to identify than non-perinatal depression. Psychologically, common emotional fluctuations during pregnancy are easily confounded with depressive symptoms, leading to missed and incorrect diagnoses. Neurologically, pregnancy-induced alterations in brain activity could obscure neuroimaging features specific to PD. Therefore, this study introduced an innovative approach that combined brain network analysis with Common Orthogonal Basis Extraction (COBE) to identify a PD-Specific Network Pattern from resting-state brain networks, as well as validating its efficacy in diagnosis and assessment. Resting-state electroencephalography (EEG) data were collected from 21 patients with PD and 20 healthy pregnant (HP) individuals, from which functional brain networks were constructed. An optimized COBE method was then employed to extract Exclusive Network Pattern for each group, as well as Common Network Pattern shared by all participants (PD + HP). This process enabled the identification of the PD-Specific Network Pattern that most consistent with neural mechanisms of PD. Based on the PD-Specific Network Pattern, PD-Specific Features were derived and applied to train support vector machine and multiple linear regression models, which respectively performed individual-level classification and assessment. This study effectively addressed the limitation of traditional neuroimaging techniques in the diagnosis of PD, providing a new avenue for objective screening and dynamic monitoring of perinatal depression.

围产期抑郁症（PD）的临床诊断提出了相当大的挑战，因为它比非围产期抑郁症更难识别。从心理上讲，怀孕期间常见的情绪波动很容易与抑郁症状混淆，导致漏诊和误诊。神经学上，妊娠引起的脑活动改变可能模糊PD特有的神经影像学特征。因此，本研究引入了一种创新的方法，将脑网络分析与公共正交基提取（COBE）相结合，从静息状态脑网络中识别pd特异性网络模式，并验证其在诊断和评估中的有效性。收集21例PD患者和20例健康孕妇的静息状态脑电图（EEG）数据，构建脑功能网络。然后采用优化的COBE方法提取各组的Exclusive Network Pattern，以及所有参与者共享的Common Network Pattern （PD + HP）。这一过程使PD特异性网络模式的识别与PD的神经机制最一致。基于PD-Specific Network Pattern，导出PD-Specific Features并应用于训练支持向量机和多元线性回归模型，分别进行个体层面的分类和评估。本研究有效解决了传统神经影像学技术在PD诊断中的局限性，为围产期抑郁症的客观筛查和动态监测提供了新的途径。

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引用次数: 0

Exogenous Aβ1–42 monomers rescue memory deficits in presenilin-1 and presenilin-2 conditional double knockout mice 外源性Aβ1-42单体修复早老素-1和早老素-2条件双敲除小鼠的记忆缺陷

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2026.111715

Jinnan Chen , Bo Wang , Zhidong Chen , Fan Ding, Jiayue Wang, Chaoyang Ding, Xiaohua Cao

Emerging evidence challenges the direct causal relationship between amyloid-β (Aβ) deposition and cognitive decline in Alzheimer's disease (AD), as exemplified in presenilin-1 and presenilin-2 conditional double knockout (cDKO) mice which exhibit no amyloid plaques and reduced soluble Aβ_1–42 monomers, but paradoxically display AD-like memory deficits. In this study, we hypothesize that reduced soluble Aβ_1–42 monomers critically underlie memory dysfunction in cDKO mice. Combining behavioral assessments and in vivo multichannel electrophysiology, we show that cDKO mice exhibit impaired spatial and episodic memory, accompanied by reduced theta oscillation power and theta-gamma phase-amplitude coupling in the dorsal hippocampal CA1. Remarkably, exogenous supplementation of physiological level Aβ_1–42 monomers rescued memory deficits and restored neural oscillatory dynamics, while co-administration of the α7-nicotinic acetylcholine receptors (α7-nAChRs) antagonist methyllycaconitine blocked these rescuing effects. Our findings reveal that soluble Aβ_1–42 monomers help to sustain hippocampal memory through α7-nAChRs-dependent pathways, thereby contributing toa revised perspective on the roles of Aβ_1–42 monomers in cognition and suggesting potential avenues for Aβ-targeted AD treatments.

新出现的证据挑战了淀粉样蛋白-β (Aβ)沉积与阿尔茨海默病（AD）认知能力下降之间的直接因果关系，如早老素-1和早老素-2条件双敲除（cDKO）小鼠，它们没有淀粉样斑块，可溶性Aβ1 - 42单体减少，但矛盾的是表现出AD样记忆缺陷。在这项研究中，我们假设可溶性Aβ1-42单体的减少是cDKO小鼠记忆功能障碍的关键基础。结合行为评估和体内多通道电生理学，我们发现cDKO小鼠表现出空间和情景记忆受损，并伴有海马背侧CA1的θ振荡功率和θ - γ相位振幅耦合降低。值得注意的是，外源性补充生理水平的a - β1 - 42单体可以挽救记忆缺陷并恢复神经振荡动力学，而α7-尼古丁乙酰胆碱受体（α7-nAChRs）拮抗剂甲基茄头碱可以阻断这些挽救作用。我们的研究结果表明，可溶性Aβ1-42单体通过α7- nachrs依赖通路帮助维持海马记忆，从而有助于对Aβ1-42单体在认知中的作用进行修订，并为a β靶向AD治疗提供潜在途径。

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引用次数: 0

AD16 as a novel therapeutic agent: Mechanisms and efficacy in chronic inflammatory pain management AD16作为一种新型治疗剂：治疗慢性炎症性疼痛的机制和疗效。

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2025.111707

Zhi-Ping Hu , Hai-Juan Ma , Hui Liu , Zhi-Xian He , Dan-Dan Jia , Ya-Lan Sun , Zhi-Hua Huang , Zhi-dong Yuan , Tao Chen , Cheng Huang

Chronic inflammatory pain is a complex condition marked by enduring pain due to inflammation and central sensitization. Present therapeutic strategies primarily rely on non-steroidal anti-inflammatory drugs (NSAIDs) or opioid-based treatments, which frequently entail considerable adverse effects and demonstrate limited efficacy in managing chronic pain. Therefore, there is a pressing need to identify novel therapeutic strategies that can effectively target and modulate the underlying mechanisms of chronic inflammatory pain. Here, we examined an innovation compound named AD16 in mitigating chronic inflammatory pain and investigated its molecular mechanisms. The findings revealed that AD16 significantly attenuated pain-related behaviors in rat models of chronic inflammatory pain induced by complete Freund's adjuvant (CFA), specifically reducing foot swelling and mechanical allodynia. AD16 was found to be associated with the activation of GABA_B receptors and alterations in the expression ratios of GluN2A/GluN2B subunits, suggesting a potential impact on synaptic plasticity. Furthermore, AD16 was correlated with a reduction in systemic inflammatory markers, as demonstrated by decreased levels of IL-1β and increased levels of IL-10 known to play roles in the modulation of central sensitization in inflammatory pain. These findings suggest that AD16 may counteract CFA-induced central sensitization by restoring two critical pathways: (1) the balance between neuronal excitation and inhibition, and (2) the equilibrium between pro-inflammatory and anti-inflammatory immune responses within the spinal cord. Consequently, AD16 represents a promising therapeutic candidate for chronic inflammatory pain.

慢性炎症性疼痛是一种复杂的疾病，其特征是由于炎症和中枢致敏引起的持久疼痛。目前的治疗策略主要依赖于非甾体抗炎药（NSAIDs）或基于阿片类药物的治疗，这些治疗通常会产生相当大的副作用，并且在治疗慢性疼痛方面疗效有限。因此，迫切需要确定新的治疗策略，可以有效地靶向和调节慢性炎症性疼痛的潜在机制。在这里，我们研究了一种名为AD16的创新化合物，以减轻慢性炎症性疼痛，并研究了其分子机制。结果显示，AD16显著减轻了完全弗氏佐剂（CFA）诱导的慢性炎症性疼痛大鼠模型的疼痛相关行为，特别是减轻足部肿胀和机械异常性痛。AD16被发现与GABAB受体的激活和GluN2A/GluN2B亚基表达比例的改变有关，提示其对突触可塑性有潜在影响。此外，AD16与全身性炎症标志物的减少相关，如IL-1β水平的降低和IL-10水平的升高所证明的那样，IL-1β水平在炎症性疼痛的中枢致敏调节中起作用。这些发现表明，AD16可能通过恢复两个关键途径来抵消cfa诱导的中枢致敏：(1)神经元兴奋和抑制之间的平衡，(2)脊髓内促炎和抗炎免疫反应之间的平衡。因此，AD16是一种治疗慢性炎症性疼痛的有希望的候选药物。

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引用次数: 0

Chronic suppression of monoacylglycerol lipase restores adult neurogenesis in the septal but not the temporal DG in Ts65Dn mouse model of Down syndrome 长期抑制单酰基甘油脂肪酶可恢复Ts65Dn唐氏综合征小鼠中隔的成年神经发生，但不能恢复颞叶DG

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2026.111721

Donya Fozoonmayeh, Mathangi Sankaran, Jessica Yu, Meriel Walsh, Anna Tyrtyshnaia, Alexander M. Kleschevnikov

Down syndrome (DS) is a genetic disorder characterized by cognitive impairment and varying degrees of changes in emotion-related behaviors. A deficiency in adult hippocampal neurogenesis is among the cellular mechanisms implicated in both abnormalities. Previously, we observed that chronic inhibition of monoacylglycerol lipase (MAGL) with the selective inhibitor JZL184 increased brain levels of the endocannabinoid 2-arachidonoylglycerol (2-AG), improved hippocampal synaptic plasticity and long-term memory, but did not affect anxiety-related thigmotactic behavior in Ts65Dn mice, a genetic model of DS. In this study, we tested the hypothesis that these effects of JZL184 might be associated with changes in adult hippocampal neurogenesis. Ts65Dn mice and their normosomic (2 N) littermates were injected daily for 3 weeks with JZL184 or vehicle, and bromodeoxyuridine (BrdU) was co-administered during the chronic phase of the treatment. BrdU-immunopositive cells were quantified in the septal, medial, and temporal segments of the dentate gyrus (DG). It was observed that both the total number and the density of BrdU-positive cells were significantly reduced in Ts65Dn mice compared to their 2 N littermate controls. Strikingly, JZL184 treatment effects exhibited a profound septo-temporal bias: the BrdU-immunopositive cell density was restored to near control levels in the septal DG (a region presumably linked to cognitive function), but it was largely unaffected in the temporal DG (presumably associated with emotion-related behaviors). These results suggest that chronic MAGL inhibition may provide a targeted region-specific therapeutic strategy for cognitive impairment in Down syndrome, potentially independent of its effects on emotional behavior.

唐氏综合症（DS）是一种以认知障碍和不同程度的情绪相关行为改变为特征的遗传性疾病。成人海马神经发生缺陷是导致这两种异常的细胞机制之一。在此之前，我们观察到选择性抑制剂JZL184对单酰基甘油脂肪酶（MAGL）的慢性抑制增加了内源性大麻素2-花生四烯醇甘油（2-AG）的脑水平，改善了海马突触可塑性和长期记忆，但不影响Ts65Dn小鼠（一种退行性痴呆的遗传模型）焦虑相关的促动行为。在本研究中，我们验证了JZL184的这些作用可能与成人海马神经发生变化有关的假设。每天给Ts65Dn小鼠及其正常（2 N）窝仔注射JZL184或对照剂，连续3周，在治疗的慢性阶段同时给药溴脱氧尿苷（BrdU）。在齿状回（DG）的间隔、内侧和颞段定量检测brdu免疫阳性细胞。结果发现，与对照组2 N相比，Ts65Dn小鼠brdu阳性细胞的总数和密度均显著降低。引人注意的是，JZL184治疗效果表现出深刻的中隔-颞叶偏倚：brdu免疫阳性细胞密度在中隔DG（一个可能与认知功能有关的区域）恢复到接近控制水平，但在颞区DG（可能与情绪相关行为有关）中基本未受影响。这些结果表明，慢性MAGL抑制可能为唐氏综合征的认知障碍提供了一种有针对性的区域特异性治疗策略，可能独立于其对情绪行为的影响。

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引用次数: 0

TRIM37 regulates HMGB1 ubiquitination to inhibit ferroptosis in Schwann cells and alleviate peripheral nerve injury TRIM37调节HMGB1泛素化，抑制雪旺细胞铁凋亡，减轻周围神经损伤。

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2025.111701

Xiang Zhou , Yazhu You , Liangying Zhong , Wenfu Peng , Yi Yang , Jian Qi

Peripheral nerve injury (PNI) is a common neurological disorder. Despite advances in surgical and non-surgical interventions, therapeutic outcomes remain suboptimal, necessitating the identification of novel molecular targets. TRIM37, an E3 ubiquitin ligase, has not been investigated in the context of peripheral nerve injury. To address this gap, we first established a rat sciatic nerve injury model to explore whether PNI is associated with ferroptosis and to characterize TRIM37 expression levels in this context. Using DHE staining, immunofluorescence, and ELISA, we quantified ROS levels, GPX4 expression, and oxidative stress markers. Meanwhile, TRIM37 expression was analyzed via qPCR, Western blot, and immunofluorescence. To clarify the direct role of TRIM37 in ferroptosis, we further performed in vitro experiments using H₂O₂-induced ferroptosis in RSC96 cells. Given that TRIM37 functions as an E3 ubiquitin ligase, we then used co-immunoprecipitation and ubiquitination assays to investigate its potential interaction with HMGB1 and the underlying mechanism. Finally, to validate the in vivo relevance, SFI, von Frey test, and histopathological analyses were used to evaluate the impact of TRIM37 on functional recovery after nerve injury. In summary, PNI significantly induced ferroptosis, which was accompanied by reduced TRIM37 expression. Mechanistically, TRIM37 directly interacted with HMGB1 and promoted its ubiquitination and degradation, thereby inhibiting ferroptosis. TRIM37 overexpression reversed these pathological changes by alleviating ferroptosis, enhancing functional recovery, reducing structural damage, and modulating oxidative stress markers in injured sciatic nerves. Thus, TRIM37 is a potential therapeutic target for improving functional recovery in PNI.

周围神经损伤是一种常见的神经系统疾病。尽管在手术和非手术干预方面取得了进展，但治疗效果仍然不理想，因此需要确定新的分子靶点。TRIM37是一种E3泛素连接酶，尚未在周围神经损伤的背景下进行研究。为了解决这一空白，我们首先建立了一个大鼠坐骨神经损伤模型，以探索PNI是否与铁下垂有关，并表征TRIM37在这种情况下的表达水平。通过DHE染色、免疫荧光和ELISA，我们量化了ROS水平、GPX4表达和氧化应激标志物。同时，通过qPCR、Western blot和免疫荧光分析TRIM37的表达。为了明确TRIM37在铁凋亡中的直接作用，我们进一步在RSC96细胞中进行了h2o2诱导铁凋亡的体外实验。考虑到TRIM37作为E3泛素连接酶的功能，我们随后使用共免疫沉淀和泛素化分析来研究它与HMGB1的潜在相互作用及其潜在机制。最后，为了验证其体内相关性，我们采用SFI、von Frey试验和组织病理学分析来评估TRIM37对神经损伤后功能恢复的影响。综上所述，PNI显著诱导铁下垂，并伴有TRIM37表达降低。机制上，TRIM37直接与HMGB1相互作用，促进其泛素化和降解，从而抑制铁凋亡。TRIM37过表达通过减轻铁下垂、促进功能恢复、减少结构损伤和调节损伤坐骨神经氧化应激标志物来逆转这些病理变化。因此，TRIM37是改善PNI患者功能恢复的潜在治疗靶点。

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引用次数: 0

Research on the syntax of EEG microstates: A comprehensive analysis of epilepsy and psychosis of epilepsy 脑电微态句法研究：癫痫与癫痫精神病的综合分析

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2026.111720

Wei Shi , Fangni Chen , Yina Cao , Lei Zhang , Jian Wan

Growing evidence suggests that abnormalities within the microstate sequence are associated with a wide range of mental illnesses. In this study, we aimed to evaluate the impact of higher-order microstate sequence syntax on brain cognitive processes. We first refined the microstate sequences obtained from the EEG recordings of individuals with epilepsy (EP) and those with psychosis of epilepsy (POE) into subdivisions in terms of microstate words. Subsequently, the microstate word characteristics and clustering degree features of different microstate word sizes were computed and compared. Finally, the correlation between word characteristics and the severity of POE was analyzed using Pearson's correlation coefficient and linear regression analysis. Our study showed that microstate B and the combined microstates {C, D} switch frequently in patients with POE compared to those with EP, whereas microstate A rarely switches directly with the combination {B, D}. In patients with higher Positive and Negative Syndrome Scale (PANSS) negative factor scores, we observed numerous continuous transitions involving {B, D}, {A, D}, and microstate C. Conversely, fewer continuous transitions of {B, C}, {C, D}, and microstate A could exacerbate psychiatric symptoms. Furthermore, while verifying the high-cohesion properties of microstate words on the time scale, patterns of "binary loop words" and "mirror word pairs" within brain microstate sequences were observed. Overall, the results demonstrate that mining higher-order syntax within microstate sequences provides novel methodological tools to understand brain cognitive processes and POE’s pathological mechanisms, while offering clinical biomarkers for POE severity assessment.

越来越多的证据表明，微态序列的异常与多种精神疾病有关。在这项研究中，我们旨在评估高阶微状态序列句法对大脑认知过程的影响。我们首先将从癫痫（EP）和癫痫精神病（POE）患者的脑电图记录中获得的微状态序列根据微状态词进行细分。随后，计算并比较了不同微态词大小的微态词特征和聚类度特征。最后，通过Pearson相关系数和线性回归分析，分析单词特征与POE严重程度的相关性。我们的研究表明，与EP患者相比，POE患者的微状态B和组合微状态{C， D}频繁切换，而微状态A很少直接切换组合{B， D}。在阳性和阴性综合征量表（PANSS）负因子得分较高的患者中，我们观察到许多涉及{B， D}, {A， D}和微状态C的连续转变。相反，较少的{B， C}, {C， D}和微状态A的连续转变会加重精神症状。此外，在验证微状态词在时间尺度上的高内聚特性的同时，观察了脑微状态序列中“二元循环词”和“镜像词对”的模式。总体而言，研究结果表明，在微状态序列中挖掘高阶语法为理解大脑认知过程和POE的病理机制提供了新的方法工具，同时为POE的严重程度评估提供了临床生物标志物。

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引用次数: 0

Alternations of gray matter lateralization and structural covariation in the children with developmental dyslexia and isolated spelling deficit 发展性阅读障碍和孤立性拼写缺陷儿童脑灰质侧化和结构共变的变化

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2026.111718

Huanhuan Liu , Qian Shen , Xiaodong He , Jiaxin Ding , Bing Xiong , Feng Li

Background

Spelling components in developmental dyslexia (DD) have been marginally reported, and there has been controversy over to what extent reading and spelling deficits share a common neuroanatomical mechanism. This study aims to explore the pattern of gray matter alteration in children with dyslexia and isolated spelling disorders (SpD).

Method

This study included 22 children with typically developing (TD), 20 children with DD, and 16 children with SpD. Voxel-based lateralization analysis was performed to calculate lateralization index (LI) and investigate the structural asymmetry of gray matter. Furthermore, the structural covariance network (SCN) was utilized to describe the changes of structural covariation network in the brain regions of interest among the DD, SpD and TD groups.

Result

The results demonstrated that compared with the TD group, the lateralization patterns of the middle frontal gyrus (MFG) and superior frontal gyrus (SFG) in the DD and SpD groups were changed. Additionally, SCN results revealed that compared with the TD group, the structural covariation of the left MFG to the Frontal_Mid_L, Occipital_Sup_R, Lingual_R, Precuneus_L and Cuneus_R were weakened in the DD group. The structural covariation between the left SFG and the Occipital_Mid_L and Occipital_Sup_L was enhanced. In contrast, the structural covariance between the left SFG and the Cuneus_R, Cingulum_Ant_R, Precuneus_L, and Precentral_L was weakened. In addition, the structural covariation of left MFG with the Supp_Motor_Area_R was increased and the structural covariation with Temporal_Sup_L was decreased in the SpD group. The structural covariation between left SFG and bilateral postcentral gyrus was increased, while that between left SFG and Parietal_Sup_L was decreased.

Conclusion

This study displayed lateralization patterns of gray matter in children with DD and SpD, and proved that both types of dysfunctions have shared and distinct neural signatures.

关于发展性阅读障碍（DD）的拼写成分的报道很少，关于阅读和拼写缺陷在多大程度上具有共同的神经解剖学机制一直存在争议。本研究旨在探讨阅读障碍和孤立拼写障碍（SpD）儿童的灰质改变模式。方法选取典型发育儿童22例，DD儿童20例，SpD儿童16例。通过体素侧化分析计算脑灰质侧化指数（LI），研究脑灰质结构的不对称性。此外，我们还利用结构协方差网络（SCN）来描述DD、SpD和TD组感兴趣脑区结构协方差网络的变化。结果与TD组比较，DD组和SpD组的额上回和额中回的侧化模式发生了改变。此外，SCN结果显示，与TD组相比，DD组左侧MFG对Frontal_Mid_L、Occipital_Sup_R、Lingual_R、Precuneus_L和Cuneus_R的结构共变异减弱。左SFG与Occipital_Mid_L和Occipital_Sup_L的结构共变异增强。左侧SFG与Cuneus_R、Cingulum_Ant_R、Precuneus_L和Precentral_L之间的结构协方差减弱。SpD组左MFG与Supp_Motor_Area_R的结构共变异增加，与Temporal_Sup_L的结构共变异减少。左侧SFG与双侧中央后回之间的结构共变增加，而左侧SFG与顶叶- sup_l之间的结构共变减少。结论本研究显示了DD和SpD儿童的灰质偏侧模式，并证明了这两种功能障碍具有共同和不同的神经特征。

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引用次数: 0

Resting-state fMRI reveals cerebellar-temporal lobe network remodeling in hyperlipidemia: A graph theoretical analysis 静息状态fMRI揭示高脂血症小脑-颞叶网络重构：图理论分析。

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2025.111697

Jian-Hui He , Jia-Jia Wu , Ling-Ling Li , Shuang He , Xin Xue , Jie Ma , Mou-Xiong Zheng , Yu-Xin Zheng , Jian-Guang Xu

Hyperlipidemia (HLP) is a major risk factor for cardiovascular diseases and has a significant impact on the nervous system, potentially leading to cognitive decline. This study uses resting-state functional magnetic resonance imaging (fMRI) to analyze the brain network characteristics of HLP patients and explore their relationship with cognitive performance.This study collected fMRI data from 50 patients with HLP and 54 healthy controls. Graph theory analysis was employed to examine differences in brain functional networks between the two groups. Compared with the healthy control group, the HLP group did not exhibit abnormal global properties at the whole-brain level (all P > 0.05). At the nodal level, patients showed abnormal local network topology, characterized by decreased local efficiency, degree centrality, and clustering coefficient in several brain regions, while increased local efficiency, nodal efficiency, degree centrality (P < 0.05), and clustering coefficient were observed in multiple nodes located in the cerebellum (P < 0.05). Patients with hyperlipidemia demonstrate cognitive decline and aberrant activity in several brain regions, most prominently in areas essential for cognition and memory, such as the cerebellum, temporal lobe, and basal ganglia. These findings enhance understanding of brain function in hyperlipidemia and offer a novel framework for exploring disease progression.

高脂血症（HLP）是心血管疾病的主要危险因素，对神经系统有重大影响，可能导致认知能力下降。本研究利用静息状态功能磁共振成像（fMRI）分析HLP患者的脑网络特征，探讨其与认知表现的关系。本研究收集了50名HLP患者和54名健康对照者的功能磁共振成像数据。采用图论分析分析两组脑功能网络的差异。与健康对照组相比，HLP组在全脑水平上未表现出异常的整体特性（P < 0.05）。在节点水平，患者局部网络拓扑结构出现异常，表现为局部效率、度中心性和多个脑区聚类系数下降，而局部效率、节点效率和度中心性升高(P

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引用次数: 0

The functional connectivity status of DMN and its anti-correlated networks across cognitive loads in clinical high risk for psychosis 临床精神病高危人群认知负荷中DMN及其反相关网络的功能连通性状况

IF 3.7 3区医学 Q2 NEUROSCIENCES

Brain Research Bulletin

Pub Date : 2026-01-01 DOI: 10.1016/j.brainresbull.2025.111709

Ling Quan , Xiaoying Sun , Chuan He , Xiao Guo , Ting Ye , Hanxi Wu , Gujing Li , Maria Luisa Bringas-Vega , Sisi Jiang , Dezhong Yao , Cheng Luo

The abnormal functional integration of DMN was widely observed in the psychosis. However, few studies focused on DMN in individuals at Clinical High Risk for Psychosis (CHR), especially under different cognitive loads. The present research predominantly focused on DMN and its antagonism with other networks using the functional MRI. To characterize the specificity of cognitive load-dependent antagonism between DMN and its anti-correlated networks in CHR, this study simulated a graded cognitive load continuum by implementing resting-state fMRI (Minimal cognitive load), passive SSVEP task (low cognitive load), and Emotional Face-Matching Task (high cognitive load). There were 36 CHR individuals and 39 healthy controls (HC) enrolled. Static and dynamic functional connectivity (sFC and dFC) were analyzed. The CHR subjects exhibited significantly reduced antagonism between higher-order cortices and DMN under low cognitive condition. Conversely, they demonstrated enhanced antagonism with greater fluctuation under high cognitive condition, likely a compensatory mechanism to maintain cognitive performance. Concurrently, the primary cortex demonstrated compensatory fluctuations during low cognitive load task. The neural signature reflects inefficient neural resource allocation and cognitive flexibility deficits, suggesting that dynamic brain network indicators based on cognitive load may become sensitive biomarkers for the early identification and intervention of CHR.

DMN功能整合异常在精神病患者中广泛存在。然而，很少有研究关注临床精神病高危人群（CHR）的DMN，特别是不同认知负荷下的DMN。目前的研究主要集中在DMN及其与其他网络的拮抗作用上。为了表征CHR中DMN及其反相关网络之间认知负荷依赖性拮抗的特异性，本研究通过静息状态fMRI（最小认知负荷）、被动SSVEP任务（低认知负荷）和情绪面孔匹配任务（高认知负荷）模拟了分级认知负荷连续体。共纳入36例CHR个体和39例健康对照（HC）。分析了静态和动态功能连通性（sFC和dFC）。在低认知状态下，CHR受试者的高阶皮质与DMN之间的拮抗作用显著降低。相反，在高认知条件下，他们表现出更强的拮抗性和更大的波动，可能是维持认知表现的代偿机制。同时，初级皮层在低认知负荷任务中表现出代偿性波动。神经特征反映了神经资源分配效率低下和认知灵活性缺陷，提示基于认知负荷的动态脑网络指标可能成为早期识别和干预CHR的敏感生物标志物。

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引用次数: 0