Cognitive aging, a pivotal domain at the intersection of neuroscience and psychology, exhibits a strong association with neurodegenerative disorders; however, its comprehensive underlying mechanisms remain incompletely elucidated. This review aims to provide a thorough synthesis of recent advancements in the investigation of cognitive aging in the brain, highlighting multidimensional assessment techniques, neurobiological foundations, molecular regulatory pathways, systemic changes, environmental-gene interactions, and intervention strategies. Evidence suggests that cognitive aging is marked not only by widespread neuronal loss but also by subtle modifications within neural networks, protein homeostasis, mitochondrial functionality, and epigenetic regulation. The integration of various technological methodologies has shed light on the continuum that exists between cognitive aging and neurodegenerative disorders. Concurrently, multidimensional intervention strategies are being proposed; however, current research frameworks face challenges due to limitations in biomarker systems, indicating a need for a paradigm shift. Future investigations should leverage emerging technologies to develop more precise regulatory frameworks and personalized intervention strategies aimed at addressing the global challenges associated with aging, thereby enhancing the prevention and treatment of related pathologies.

BackgroundAutism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interaction and restricted, repetitive behaviors (RRBs). These symptoms may stem from cognitive flexibility deficits, with dysfunction in the prefrontal cortex (PFC) and related neural circuits proposed as underlying mechanisms.ObjectivesThis study examined whether transcranial direct current stimulation (tDCS) could enhance PFC activity and functional connectivity, thereby improving cognitive flexibility in a valproic acid (VPA)-induced ASD rat model.MethodsPregnant Sprague-Dawley rats were administered VPA (600 mg/kg, E12.5) or saline. VPA-exposed offspring exhibiting curved tails received tDCS and underwent behavioral tests, including the three-chamber social interaction test and cross-maze rule-shifting task, while local field potentials (LFPs) were recorded. Immunohistochemistry was performed to evaluate microglial activation (Iba1 +) and synaptic density (PSD95).ResultsValproic acid -exposed offspring displayed significant social interaction deficits and impaired cognitive flexibility, alongside disrupted functional connectivity in frontal-striato-hippocampal circuits. Neuroinflammatory analysis revealed elevated Iba1+ microglial density (p < 0.05) and increased PSD95 expression (p < 0.05). After tDCS intervention, VPA rats exhibited restored sociability and cognitive performance, normalized functional connectivity, and significantly reduced microglial activation (p < 0.05), though PSD95 levels were unaffected.ConclusionOur results indicate that tDCS ameliorates ASD-like phenotypes in VPA rats, potentially through microglial suppression and PFC network synchronization. These findings support neuromodulation as a promising therapeutic approach for ASD-related cognitive dysfunction.

Ginkgo biloba extracts (GBE) have been shown to effectively improve cognitive function in patients with Alzheimer’s disease (AD). One potential therapeutic strategy for AD is to prevent loss of adult hippocampal neurons. While recent studies have reported that GBE protects against oxidative stress in neurons, the underlying mechanisms remain unclear. In this study, an AD-like rat model was established via bidirectional injection of amyloid beta 25–35 (Aβ25–35; 20 μg) in the hippocampal CA1 region. Learning and memory abilities of experimental rats were AD assessed in response to oral administration of 7.5 g/L or 15 g/L Ginkgo biloba extract 50 (GBE50) solution and the peroxidation phenomenon of hippocampal mitochondria determined via analysis of mitochondrial H2O2 and several related enzymes. Levels of the oxidative stress-related signaling factor cytochrome C (Cyto C), apoptosis-related proteins (Bax, Bcl-2 and caspase-3) and caspase-activated DNase (CAD) were further detected via western blot. 8-Hydroxydeoxyguanosine (8-OHdG), the major product of DNA oxidative stress, was evaluated to analyze DNA status. Our results showed elevated H2O2 levels and monoamine oxidase (MAO) activity, and conversely, a decrease in the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in the hippocampus of AD rats. Administration of GBE50 regulated the activities of these three enzymes and induced a decrease in H2O2. GBE50 exerted regulatory effects on abnormally expressed apoptotic proteins in the AD rat hippocampus, enhancing the expression of Bcl-2, inhibiting release of Cyto C from mitochondria, and suppressing the level of caspase-3 (excluding cleaved caspase-3). Furthermore, GBE50 inhibited DNA damage by lowering the generation of 8-OHdG rather than influencing expression of CAD. The collective findings support a protective role of GBE50 in hippocampal neurons of AD-like animals against mitochondrial oxidative stress.

Autism Spectrum Disorder (ASD) often co-occurs with sleep disorders, which can exacerbate core symptoms such as social impairments and repetitive stereotyped behaviors. Sleep is crucial for brain function, as it enhances cerebrospinal fluid circulation, clears metabolic toxins, and consolidates memories. Despite the high prevalence of these sleep issues in individuals with autism, the specific brain networks involved remain poorly understood. This study reviews recent advancements in identifying the brain network mechanisms underlying sleep disorders in ASD. By focusing on the interplay between autism-related sleep disturbances and brain network functionality, we synthesize current findings to highlight key mechanisms involved. Our research provides a preliminary theoretical framework that advances understanding of how sleep disorders impact brain networks in autism, offering a valuable reference for future investigations in this area.

脑性瘫痪是由于发育中的胎儿或婴幼儿脑部非进行性损伤所致的一组持续存在的中枢性运动和姿势发育障碍及活动受限症候群,而胆红素脑病是导致脑性瘫痪发生的主要原因之一.本文从脑瘫患儿三级损伤机制的角度出发,对胆红素脑病致脑性瘫痪发病机制各环节及早期诊断等方面进行综述,旨在为胆红素脑病相关性脑性瘫痪的早期防治提供参考.

Abstract Background Autism spectrum disorder (ASD) is a neurodevelopmental disorder that is correlated with anxiety behavior. This study aimed to investigate the effect of Xiaoyaosan (XYS) on anxiety behavior in autism rats and its potential mechanism. Materials and Methods The autistic rat model was established by intraperitoneal injection of pregnant rats with sodium valproic acid (VPA) at 12.5 days of pregnancy. The newborn rats (n = 15 in each group) were given XYS solution gavage daily for 21 days. The autistic behaviors were identified by the marble-burying behavior test (MBT), ultrasonic vocalization (USV) test, three-chamber social interaction task (TCT), and novel object recognition (NOR) task. The anxiety behaviors were detected by open field test (OFT), elevated plus maze (EPM), and sucrose preference test (SPT). Heart rate variability (HRV) was used to detect the changes in the autonomic nerve. The expression of Ionized calcium-binding adaptor molecule 1 (Iba-1) in microglia of the hippocampus and amygdala was detected by immunohistochemistry. Results Compared with the control group, the number of buried marbles in MBT was increased, the number of vocalizations at 50 kHz in the USV test was reduced, the social ability in the TST was reduced, and the exploration time and distance of new objects in NOR task were reduced in the VPA group. In the OFT, the activity time in the central zone was reduced, the open arm activity time in EPM was reduced, and the sucrose consumption rate in SPT was reduced in autistic rats. The autonomic sympathetic balance of autistic rats was impaired. In hippocampus and amygdala regions, the number of Iba-1 positive cells was increased in VPA-induced rats. After XYS treatment, the above effects caused by VPA were reversed. Conclusion XYS could improve autism and anxiety behaviors. It could also maintain the balance of sympathetic and parasympathetic nerves in autistic rats. Its mechanism may be related to the inhibition of the activation of microglia in the hippocampus and amygdala.

简要介绍了国内康复机器人应用于脑卒中领域的研究现状,以中国知网数据库为数据源,检索了 2004 年 1月至2022年5 月31 日收录的康复机器人应用于脑卒中领域的相关文献,基于CiteSpace软件对纳入文献的作者、关键词、研究热点及趋势进行了可视化分析,指出了康复机器人应用于脑卒中领域的发文量总体呈逐年增长趋势,发文作者分布较为分散且研究团队之间缺乏深度合作研究,康复训练、运动功能、平衡功能、主动训练等为目前的研究热点,人机交互、运动仿真以及虚拟现实为研究前沿,为我国开展相关研究提供了参考.

BACKGROUND:Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders characterized by deficits in social communication and restrictive behaviors. Mouse nerve growth factor (mNGF), a neurotrophic factor, is critical for neuronal growth and survival, and the mNGF treatment is considered a promising therapy for neurodegeneration. In light of this, we aimed to evaluate the effect of mNGF on neurological function in ASD.METHODS:An ASD rat model was established by intraperitoneal injection of valproic acid (VPA). Social behavior, learning, and memory of the rats were measured. TdT-mediated dUTP Nick-end labeling and Nissl assays were performed to detect neuronal apoptosis and survival in the hippocampus and prefrontal cortex. Apoptosis-related proteins and oxidative stress markers were detected.RESULTS:mNGF improved locomotor activity, exploratory behavior, social interaction, and spatial learning and memory in VPA-induced ASD rats. In the hippocampus and prefrontal cortex, mNGF suppressed neuronal apoptosis, increased the number of neurons, superoxide dismutase, and glutathione levels, and decreased reactive oxygen species, nitric oxide, TNF-α, and IL-1β levels compared with the VPA group. In addition, mNGF increased the levels of Bcl-2, p-phosphoinositide-3-kinase (PI3K), and p-serine/threonine kinase (Akt), and decreased the levels of Bax and cleaved caspase-3, while the PI3K inhibitor LY294002 reversed these effects.CONCLUSION:These data suggest that mNGF suppressed neuronal apoptosis and ameliorated the abnormal behaviors in VPA-induced ASD rats, in part, by activating the PI3K/Akt signaling pathway.

Autism spectrum disorder (ASD) is a multifactorial disease, with social difficulties and repetitive behaviors as its core symptoms. With the improvement of diagnostic methods, the detection rate of ASD is increasing year by year.Cognitive flexibility impairment is very obvious in most autistic patients.More and more studies have shown that cognitive flexibility impairment is related to the occurrence and development of core symptoms. However, the mechanism of cognitive flexibility impairment in autism remains unclear. The frontal lobe plays an important role in advanced cognition, and its complete development is related to cognitive function. Recent studies have shown that frontal lobe dysfunction is closely related to cognitive flexibility deficits in autistic patients, and the abnormal changes in the frontal lobe, the associated default mode network dysfunction and frontal striatal circuit defects may be the important mechanisms of cognitive flexibility impairment. Based on the recent clinical and basic studies on cognitive flexibility in autism, this article reviews the mechanisms of frontal lobe and related circuits involved in the impairment of cognitive flexibility in autism.

事件相关电位(ERP)是认知神经科学领域中评价大脑信息处理过程相关电活动的一种无创性检测手段,是研究认知等心理加工过程的有力工具.近年来,ERP在自闭症谱系障碍(ASD)中的应用研究逐年增多,其有望成为检测ASD的有前途的生物标志物.该文就ERP在ASD中的应用研究进展进行综述.

目的 探究孤独症谱系障碍(ASD)儿童重复刻板行为的发育轨迹,明确其与大脑感觉门控之间的相关性,以期进一步为临床诊疗提供参考.方法 选取2018年8月—2021年5月就诊于郑州大学第五附属医院儿童康复科门诊符合ASD诊断儿童89例,符合全面性发育迟缓(GDD)诊断儿童76例,采用重复行为量表-修订版(RBS-R)评价患儿重复刻板行为,采用感觉门控P50比值评价患儿大脑感觉门控,并分析二者的相关性.结果 ASD及GDD儿童的重复刻板行为总分、低阶及高阶与感觉门控均无相关性(P＞0.05).ASD儿童重复刻板行为总分、低阶及高阶得分随年龄增长未见明显下降趋势(P＞0.05),GDD儿童重复刻板行为与年龄呈明显负相关(r=-0.43～-0.23,P＜0.05).结论 ASD儿童重复刻板行为发育轨迹并非简单的负性线性关系,其重复刻板行为与大脑感觉门控无明显相关性,P50可能不是一个有效预测重复刻板行为的指标.

目的 研究4～16岁正常儿童事件相关电位(event-related potentials,ERPs)中的经典成分失匹配负波(MMN)、认知电位P300及感觉门控P50的发育规律.方法 收集2019年4月 ～2021年6月在郑州大学第五附属医院门诊招募的正常儿童130例,按年龄分为4～6岁、7～9岁、10～12岁和13～16岁共4个组.ERPs成分包括MMN、P300及P50各波潜伏期及波幅.结果 MMN潜伏期与年龄未见明显相关性,组间比较差异无统计学意义(P>0.05);波幅与年龄呈负相关,组间比较差异有统计学意义(P<0.05);P300外源性反应电位及P3a潜伏期与年龄呈负相关(P<0.05),P3b潜伏期及波幅变化不显著(P>0.05);P50比值随年龄增长而下降(P<0.05).结论 ERPs各波潜伏期及波幅与年龄具有一定相关性,与儿童理解、注意、认知等能力的提高密不可分,适宜在临床上广泛应用.

Troxerutin is known for its anti-inflammatory and antioxidative effects in nerve impairment. The purpose of this study is to investi-gate the effect of troxerutin and cerebroprotein hydrolysate injections (TCHis) on prenatal valproic acid (VPA)-exposed rats. The VPA was administered to pregnant rats on gestational day 12.5 to induce a model of autism. The offspring were given the treat-ment of TCHis on postnatal day (PND) 21-50. On PND 43-50, the behavioral analysis of offspring was performed after the treat-ment of TCHis for 1 h. On PND 50, the offspring were harvested and the brains were collected. The hippocampus and prefrontal cortex were isolated for relevant biochemical detections. The administration of TCHis increased pain sensitivity and improved abnormal social behaviors in prenatal VPA-exposed rats. Prenatal exposure of VPA induced neuronal loss and apoptosis, enhanced reactive oxygen species (ROS) production, and promoted oxidative stress in hippocampus and prefrontal cortex, whereas these effects were reversed by the postnatal treatment of TCHis. In addition, postnatal administration of TCHis amelio-rated mitochondrial function in hippocampus and prefrontal cortex of prenatal VPA-exposed rats. This study concluded that post-natal treatment of TCHis reduced oxidative stress and ameliorated abnormal behavior in a prenatal VPA-induced rat model of autism.

Objectives Guizhi Fuling Formulation (GZFL), a traditional Chinese medical formulation, consists of Cinnamomi Ramulus, Paeoniae Radix Alba (or Paeoniae Radix Rubra), Moutan Cortex, Persicae Semen, and Poria, with multiple therapeutic functions such as sedation, antitumor activity, anti-inflammation, and neuroprotection. However, its clinical applications remain relatively fragmented, and the underlying mechanisms of GZFL in different diseases are still not very certain. Further research and summary in both application and mechanisms remain to be needed for human health and the best use of GZFL. Therefore, we summarized the multiple pharmacologic effects and possible mechanisms of action of GZFL according to recent 17 years of research. Methods We retrieved four English and two Chinese databases using these keywords (the formulation name or its synonyms) and searched articles written in English from January 2006 up to February 2022. Key Findings. GZFL exhibits multiple pharmacologic advantages in gynecologic diseases and other expanding diseases such as cancer, blood, and vascular disease, renal failure, inflammation, and brain injury. Possibly due to its diverse bioactive components and pharmacologic activities, GZFL could target the multiple signaling pathways involved in regulating blood circulation, inflammatory and immune factors, proliferation, apoptosis, and so on. Conclusion This review suggests that GZFL displays promising therapeutic effects for many kinds of diseases, which have been beyond the scope of the original prescription for gynecologic diseases. In this way, we wish to provide a reference and recommendation for further preclinic and clinic studies.

焦虑或焦虑障碍是自闭症谱系障碍(autism spectrum disorder,ASD)最常见的合并症之一,该文通过归纳国内外自闭症谱系障碍共患焦虑文献,分析自闭症和焦虑之间的关系、自闭症儿童焦虑的影响因素、自闭症与焦虑患儿的脑功能、自闭症及焦虑的干预方式等方面,便于未来的患病率研究使用明确定义和有效的诊断评估及干预.

重复刻板行为是孤独症谱系障碍的核心症状之一,病因复杂,表现形式多样.其形成机制假说众多,近年来有研究显示纹状体功能异常可能参与了孤独症重复刻板行为演变过程.本文拟对纹状体及其环路参与孤独症重复刻板行为相关机制研究进展进行综述,期望推动孤独症重复刻板行为机制研究.

自闭症谱系障碍是一种儿童早期发病的严重神经发育障碍性疾病,临床特征主要表现为社交障碍、刻板行为、兴趣狭窄和感知觉方面的异常.研究发现自闭症儿童会出现技能倒退现象,该文对倒退型自闭症概念、患病率、病因学、临床特点及预后等进行了综述.

目的:研制具有无创、集成、移动便携、可家用特征的孤独症智能治疗头盔.方法:开发了能够集成模拟电针刺激模块、药物离子导入模块、生物反馈模块和网络信息模块功能.结果:头盔安全性高,疗效佳,可实现家庭化、便携化.结论:现代科技与先进通讯技术将传统针刺技术广泛传播,为广大孤独症患儿提供有效、便捷的治疗与帮助,使更多患儿及家庭获益.

目的 通过对0～1岁婴儿神经心理发育状况调查,探讨影响其神经心理发育的因素,以及大运动、精细动作、适应能力、语言及社交能力之间的相关性.方法 收集2019年1月～2020年1月在郑州大学第五附属医院儿童康复医学科就诊,并经0～6岁儿童神经心理发育量表评估的109例0～1岁婴儿为研究对象,用单因素分析(t检验、方差分析)、Spearman相关性分析研究婴儿性别、高危因素及胎产方式对神经心理发育的影响,用Spearman相关性分析及散点图分析109例婴儿的大运动、精细动作、适应能力、语言、社交能力、智龄及发育商之间的关系.?结果 通过单因素分析,婴儿的大运动、精细动作、适应能力、语言、社交能力及智龄与婴儿性别、高危因素及胎产方式之间差异无统计学意义(P>0.05),发育商与高危因素、胎产方式之间差异有统计学意义(P<0.05).与早产并顺产比较,足月并顺产及足月并剖宫产出生的婴儿发育商均较高,差异有统计学意义(P<0.05).通过Spearman相关性分析,胎产方式与发育商之间,差异有统计学意义(r=-0.231,P=0.016),高危因素与发育商之间,差异有统计学意义(r=-0.298,P=0.002).而大运动、精细动作、适应能力、语言及社交能力之间相关性显著,差异有统计学意义(P<0.05).通过散点图分析,大运动、精细动作、适应能力、语言及社交能力之间存在线性正相关.结论 高危因素是影响婴儿发育水平的危险因素,大运动、精细动作、适应能力、语言及社交能力之间相互影响,并呈正相关.

A chronic neuroinflammatory response has been considered as a critical pathogenesis promoting neurodegenerative progression in Alzheimer's disease (AD). During neuroinflammatory process, microglia are excessively activated and simultaneously release numerous pro-inflammatory mediators that cause synaptic dysfunction in the forebrain prior to neuronal degeneration and memory deficits in AD. Thus, prevention of neuroinflammation-mediated synaptic dysfunction may be a potential therapeutic approach against neurodegenerative disorders. Trans-cinnamaldehyde (TCA) is a primary bioactive component derived from the stem bark of Cinnamomum cassia, and it possesses potent anti-inflammatory and neuroprotective activities in in vivo and in vitro experiments. However, the in-depth molecular mechanisms of TCA underlying anti-neuroinflammatory and neuroprotective effects on memory deficits in AD are still unclear. The presenilin 1 and 2 conditional double knockout (PS cDKO) mice exhibit AD-like phenotypes including obvious neuroinflammatory responses and synaptic dysfunction and memory deficits. Here, PS cDKO were used to evaluate the potential neuroprotective effects of TCA against neuroinflammation-mediated dementia by performing behavioral tests, electrophysiological recordings and molecular biology analyses. We observed that TCA treatment reversed abnormal expression of synaptic proteins and tau hyperphosphorylation in the hippocampus and prefrontal cortex of PS cDKO mice. TCA treatment also ameliorated NMDA receptor (NMDAR) dysfunction including impaired NMDAR-mediated responses and long-term potentiation (LTP) induction in the hippocampus of PS cDKO mice. Moreover, TCA possesses an ability to suppress neuroinflammatory responses by diminishing microglial activation and levels of pro-inflammatory mediators in the hippocampus and prefrontal cortex of PS cDKO mice. Importantly, improving NMDAR dysfunction and memory deficits of PS cDKO mice was due to the inhibition of neuroinflammatory responses through TCA's interruptive effect on the nuclear factor kappa B (NF-κB) signaling pathway. Therefore, TCA may be a potential anti-neuroinflammatory agent for deterring neurodegenerative progression of AD.