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Single-cell pan-omics, environmental neurology, and artificial intelligence: the time for holistic brain health research. 单细胞泛组学、环境神经学和人工智能:全面脑健康研究的时代。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00324
Paolo Abondio, Francesco Bruno
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引用次数: 0
Role of the globus pallidus in motor and non-motor symptoms of Parkinson's disease. 苍白球在帕金森病运动和非运动症状中的作用。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-23-01660
Yimiao Jiang, Zengxin Qi, Huixian Zhu, Kangli Shen, Ruiqi Liu, Chenxin Fang, Weiwei Lou, Yifan Jiang, Wangrui Yuan, Xin Cao, Liang Chen, Qianxing Zhuang

The globus pallidus plays a pivotal role in the basal ganglia circuit. Parkinson's disease is characterized by degeneration of dopamine-producing cells in the substantia nigra, which leads to dopamine deficiency in the brain that subsequently manifests as various motor and non-motor symptoms. This review aims to summarize the involvement of the globus pallidus in both motor and non-motor manifestations of Parkinson's disease. The firing activities of parvalbumin neurons in the medial globus pallidus, including both the firing rate and pattern, exhibit strong correlations with the bradykinesia and rigidity associated with Parkinson's disease. Increased beta oscillations, which are highly correlated with bradykinesia and rigidity, are regulated by the lateral globus pallidus. Furthermore, bradykinesia and rigidity are strongly linked to the loss of dopaminergic projections within the cortical-basal ganglia-thalamocortical loop. Resting tremors are attributed to the transmission of pathological signals from the basal ganglia through the motor cortex to the cerebellum-ventral intermediate nucleus circuit. The cortico-striato-pallidal loop is responsible for mediating pallidi-associated sleep disorders. Medication and deep brain stimulation are the primary therapeutic strategies addressing the globus pallidus in Parkinson's disease. Medication is the primary treatment for motor symptoms in the early stages of Parkinson's disease, while deep brain stimulation has been clinically proven to be effective in alleviating symptoms in patients with advanced Parkinson's disease, particularly for the movement disorders caused by levodopa. Deep brain stimulation targeting the globus pallidus internus can improve motor function in patients with tremor-dominant and non-tremor-dominant Parkinson's disease, while deep brain stimulation targeting the globus pallidus externus can alter the temporal pattern of neural activity throughout the basal ganglia-thalamus network. Therefore, the composition of the globus pallidus neurons, the neurotransmitters that act on them, their electrical activity, and the neural circuits they form can guide the search for new multi-target drugs to treat Parkinson's disease in clinical practice. Examining the potential intra-nuclear and neural circuit mechanisms of deep brain stimulation associated with the globus pallidus can facilitate the management of both motor and non-motor symptoms while minimizing the side effects caused by deep brain stimulation.

摘要:苍白球在基底神经节回路中起着关键作用。帕金森病的特征是黑质中产生多巴胺的细胞发生变性,导致脑内多巴胺缺乏,进而表现为各种运动和非运动症状。本综述旨在总结球状苍白球在帕金森病的运动和非运动表现中的参与情况。内侧苍白球旁神经元的发射活动,包括发射率和模式,与帕金森病相关的运动迟缓和僵直表现出很强的相关性。与运动迟缓和僵直高度相关的贝塔振荡增加是由外侧丘脑调节的。此外,运动迟缓和僵直与皮质-基底节-丘脑皮质环路内多巴胺能投射的丧失密切相关。静止性震颤是由于病理信号从基底节通过运动皮层传递到小脑-腹侧中间核回路。皮质-纹状体-苍白球环路负责介导苍白球相关睡眠障碍。药物治疗和脑深部刺激是针对帕金森病苍白球的主要治疗策略。药物治疗是帕金森病早期运动症状的主要治疗方法,而深部脑刺激经临床证实可有效缓解晚期帕金森病患者的症状,尤其是左旋多巴引起的运动障碍。针对苍白球内侧的深部脑刺激可以改善震颤为主型和非震颤为主型帕金森病患者的运动功能,而针对苍白球外侧的深部脑刺激可以改变整个基底节-丘脑网络的神经活动时间模式。因此,研究苍白球神经元的组成、作用于这些神经元的神经递质、神经元的电活动及其形成的神经回路,可以为临床实践中寻找治疗帕金森病的多靶点新药提供指导。研究与苍白球相关的深部脑刺激的潜在核内机制和神经回路机制有助于治疗运动和非运动症状,同时最大限度地减少深部脑刺激引起的副作用。
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引用次数: 0
Neurogenesis dynamics in the olfactory bulb: deciphering circuitry organization, function, and adaptive plasticity. 嗅球的神经发生动态:破译电路组织、功能和适应性可塑性。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00312
Moawiah M Naffaa

Adult neurogenesis persists after birth in the subventricular zone, with new neurons migrating to the granule cell layer and glomerular layers of the olfactory bulb, where they integrate into existing circuitry as inhibitory interneurons. The generation of these new neurons in the olfactory bulb supports both structural and functional plasticity, aiding in circuit remodeling triggered by memory and learning processes. However, the presence of these neurons, coupled with the cellular diversity within the olfactory bulb, presents an ongoing challenge in understanding its network organization and function. Moreover, the continuous integration of new neurons in the olfactory bulb plays a pivotal role in regulating olfactory information processing. This adaptive process responds to changes in epithelial composition and contributes to the formation of olfactory memories by modulating cellular connectivity within the olfactory bulb and interacting intricately with higher-order brain regions. The role of adult neurogenesis in olfactory bulb functions remains a topic of debate. Nevertheless, the functionality of the olfactory bulb is intricately linked to the organization of granule cells around mitral and tufted cells. This organizational pattern significantly impacts output, network behavior, and synaptic plasticity, which are crucial for olfactory perception and memory. Additionally, this organization is further shaped by axon terminals originating from cortical and subcortical regions. Despite the crucial role of olfactory bulb in brain functions and behaviors related to olfaction, these complex and highly interconnected processes have not been comprehensively studied as a whole. Therefore, this manuscript aims to discuss our current understanding and explore how neural plasticity and olfactory neurogenesis contribute to enhancing the adaptability of the olfactory system. These mechanisms are thought to support olfactory learning and memory, potentially through increased complexity and restructuring of neural network structures, as well as the addition of new granule granule cells that aid in olfactory adaptation. Additionally, the manuscript underscores the importance of employing precise methodologies to elucidate the specific roles of adult neurogenesis amidst conflicting data and varying experimental paradigms. Understanding these processes is essential for gaining insights into the complexities of olfactory function and behavior.

摘要:成人神经发生在出生后持续存在于室管膜下区,新神经元迁移到嗅球的颗粒细胞层和团粒层,在那里作为抑制性中间神经元整合到现有的电路中。嗅球中这些新神经元的生成支持结构和功能的可塑性,有助于记忆和学习过程引发的电路重塑。然而,这些神经元的存在,加上嗅球内细胞的多样性,为了解其网络组织和功能带来了持续的挑战。此外,嗅球中新神经元的不断整合在调节嗅觉信息处理方面起着关键作用。这一适应过程会对上皮成分的变化做出反应,并通过调节嗅球内的细胞连接以及与高阶脑区的复杂互动,促进嗅觉记忆的形成。成人神经发生在嗅球功能中的作用仍是一个争论不休的话题。然而,嗅球的功能与围绕有丝细胞和簇细胞的颗粒细胞的组织密切相关。这种组织模式对输出、网络行为和突触可塑性有重大影响,而这些对嗅觉感知和记忆至关重要。此外,来自皮层和皮层下区域的轴突终端也进一步塑造了这种组织结构。尽管嗅球在与嗅觉相关的大脑功能和行为中起着至关重要的作用,但这些复杂且高度相互关联的过程尚未作为一个整体得到全面研究。因此,本手稿旨在讨论我们目前的理解,并探讨神经可塑性和嗅觉神经发生如何有助于增强嗅觉系统的适应性。这些机制可能通过增加神经网络结构的复杂性和重组,以及增加有助于嗅觉适应的新颗粒细胞,来支持嗅觉学习和记忆。此外,手稿还强调了采用精确方法在相互矛盾的数据和不同的实验范式中阐明成体神经发生的具体作用的重要性。要深入了解嗅觉功能和行为的复杂性,了解这些过程至关重要。
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引用次数: 0
Peripheral mitochondrial DNA as a neuroinflammatory biomarker for major depressive disorder. 外周线粒体 DNA 作为重度抑郁症的神经炎症生物标志物。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-23-01878
Jinmei Ye, Cong Duan, Jiaxin Han, Jinrong Chen, Ning Sun, Yuan Li, Tifei Yuan, Daihui Peng

In the pathogenesis of major depressive disorder, chronic stress-related neuroinflammation hinders favorable prognosis and antidepressant response. Mitochondrial DNA may be an inflammatory trigger, after its release from stress-induced dysfunctional central nervous system mitochondria into peripheral circulation. This evidence supports the potential use of peripheral mitochondrial DNA as a neuroinflammatory biomarker for the diagnosis and treatment of major depressive disorder. Herein, we critically review the neuroinflammation theory in major depressive disorder, providing compelling evidence that mitochondrial DNA release acts as a critical biological substrate, and that it constitutes the neuroinflammatory disease pathway. After its release, mitochondrial DNA can be carried in the exosomes and transported to extracellular spaces in the central nervous system and peripheral circulation. Detectable exosomes render encaged mitochondrial DNA relatively stable. This mitochondrial DNA in peripheral circulation can thus be directly detected in clinical practice. These characteristics illustrate the potential for mitochondrial DNA to serve as an innovative clinical biomarker and molecular treatment target for major depressive disorder. This review also highlights the future potential value of clinical applications combining mitochondrial DNA with a panel of other biomarkers, to improve diagnostic precision in major depressive disorder.

摘要:在重度抑郁症的发病机制中,与应激相关的慢性神经炎症阻碍了良好的预后和抗抑郁反应。线粒体 DNA 从应激引起的中枢神经系统功能失调的线粒体释放到外周循环后,可能成为炎症的触发因素。这些证据支持将外周线粒体 DNA 作为神经炎症生物标志物用于重度抑郁障碍的诊断和治疗。在此,我们对重度抑郁障碍中的神经炎症理论进行了批判性回顾,提供了令人信服的证据,证明线粒体 DNA 的释放是一种关键的生物基质,它构成了神经炎症疾病的途径。线粒体 DNA 释放后可被外泌体携带并运送到中枢神经系统和外周循环的细胞外空间。可检测的外泌体使包裹的线粒体 DNA 相对稳定。因此,在临床实践中可以直接检测外周循环中的线粒体 DNA。这些特点说明线粒体 DNA 有潜力成为重度抑郁障碍的创新临床生物标志物和分子治疗靶点。本综述还强调了将线粒体 DNA 与其他生物标记物组合在一起的临床应用的未来潜在价值,以提高重度抑郁障碍的诊断精确度。
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引用次数: 0
Decline and fall of aging astrocytes: the human perspective. 衰老星形胶质细胞的衰退与衰亡:人类视角。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00418
Alexei Verkhratsky, Alexey Semyanov
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引用次数: 0
Dendritic spine degeneration: a primary mechanism in the aging process. 树突棘退化:衰老过程的主要机制。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-06-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00311
Gonzalo Flores, Leonardo Aguilar-Hernández, Fernado García-Dolores, Humberto Nicolini, Andrea Judith Vázquez-Hernández, Hiram Tendilla-Beltrán
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引用次数: 0
How dopamine tunes parvalbumin interneurons in the hippocampus: new experimental observations in Alzheimer's disease. 多巴胺如何调节海马中的副发光体中间神经元:对阿尔茨海默病的新实验观察。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00322
Livia La Barbera, Paraskevi Krashia, Annalisa Nobili
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引用次数: 0
Microglial dysfunction and genetic risk for neurodegenerative disease. 小胶质细胞功能障碍与神经退行性疾病的遗传风险
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00146
Debra S MacDonald, Jay Penney
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引用次数: 0
Complement-dependent neuroinflammation in spinal cord injury: from pathology to therapeutic implications. 脊髓损伤中的补体依赖性神经炎症:从病理学到治疗意义。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-24-00116
Hassan Saad, Bachar El Baba, Ali Tfaily, Firas Kobeissy, Juanmarco Gutierrez Gonzalez, Daniel Refai, Gerald R Rodts, Christian Mustroph, David Gimbel, Jonathan Grossberg, Daniel L Barrow, Matthew F Gary, Ali M Alawieh

Spinal cord injury remains a major cause of disability in young adults, and beyond acute decompression and rehabilitation, there are no pharmacological treatments to limit the progression of injury and optimize recovery in this population. Following the thorough investigation of the complement system in triggering and propagating cerebral neuroinflammation, a similar role for complement in spinal neuroinflammation is a focus of ongoing research. In this work, we survey the current literature investigating the role of complement in spinal cord injury including the sources of complement proteins, triggers of complement activation, and role of effector functions in the pathology. We study relevant data demonstrating the different triggers of complement activation after spinal cord injury including direct binding to cellular debris, and or activation via antibody binding to damage-associated molecular patterns. Several effector functions of complement have been implicated in spinal cord injury, and we critically evaluate recent studies on the dual role of complement anaphylatoxins in spinal cord injury while emphasizing the lack of pathophysiological understanding of the role of opsonins in spinal cord injury. Following this pathophysiological review, we systematically review the different translational approaches used in preclinical models of spinal cord injury and discuss the challenges for future translation into human subjects. This review emphasizes the need for future studies to dissect the roles of different complement pathways in the pathology of spinal cord injury, to evaluate the phases of involvement of opsonins and anaphylatoxins, and to study the role of complement in white matter degeneration and regeneration using translational strategies to supplement genetic models.

摘要:脊髓损伤仍是青壮年致残的一个主要原因,除了急性减压和康复治疗外,目前还没有药物治疗方法来限制损伤的进展和优化这一人群的康复。在对补体系统引发和传播脑神经炎症进行深入研究之后,补体在脊髓神经炎症中的类似作用也成为当前研究的重点。在这项工作中,我们调查了目前研究补体在脊髓损伤中作用的文献,包括补体蛋白的来源、补体激活的触发因素以及效应功能在病理中的作用。我们研究了证明脊髓损伤后补体激活的不同触发因素的相关数据,包括与细胞碎片的直接结合,或通过抗体与损伤相关分子模式的结合激活。补体的几种效应功能与脊髓损伤有关联,我们对近期关于补体无氨毒素在脊髓损伤中的双重作用的研究进行了认真评估,同时强调了对氨蛋白在脊髓损伤中的作用缺乏病理生理学认识。在病理生理学综述之后,我们系统地回顾了在脊髓损伤临床前模型中使用的不同转化方法,并讨论了未来转化为人类受试者所面临的挑战。本综述强调,未来的研究需要剖析不同补体途径在脊髓损伤病理学中的作用,评估蛋白溶解素和无氨毒素的参与阶段,并利用转化策略研究补体在白质变性和再生中的作用,以补充遗传模型。
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引用次数: 0
The complex effects of miR-146a in the pathogenesis of Alzheimer's disease. miR-146a 在阿尔茨海默病发病机制中的复杂作用。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-23-01566
Yunfan Long, Jiajia Liu, Yu Wang, Haidong Guo, Guohong Cui

Alzheimer's disease is a neurodegenerative disorder characterized by cognitive dysfunction and behavioral abnormalities. Neuroinflammatory plaques formed through the extracellular deposition of amyloid-β proteins, as well as neurofibrillary tangles formed by the intracellular deposition of hyperphosphorylated tau proteins, comprise two typical pathological features of Alzheimer's disease. Besides symptomatic treatment, there are no effective therapies for delaying Alzheimer's disease progression. MicroRNAs (miR) are small, non-coding RNAs that negatively regulate gene expression at the transcriptional and translational levels and play important roles in multiple physiological and pathological processes. Indeed, miR-146a, a NF-κB-regulated gene, has been extensively implicated in the development of Alzheimer's disease through several pathways. Research has demonstrated substantial dysregulation of miR-146a both during the initial phases and throughout the progression of this disorder. MiR-146a is believed to reduce amyloid-β deposition and tau protein hyperphosphorylation through the TLR/IRAK1/TRAF6 pathway; however, there is also evidence supporting that it can promote these processes through many other pathways, thus exacerbating the pathological manifestations of Alzheimer's disease. It has been widely reported that miR-146a mediates synaptic dysfunction, mitochondrial dysfunction, and neuronal death by targeting mRNAs encoding synaptic-related proteins, mitochondrial-related proteins, and membrane proteins, as well as other mRNAs. Regarding the impact on glial cells, miR-146a also exhibits differential effects. On one hand, it causes widespread and sustained inflammation through certain pathways, while on the other hand, it can reverse the polarization of astrocytes and microglia, alleviate neuroinflammation, and promote oligodendrocyte progenitor cell differentiation, thus maintaining the normal function of the myelin sheath and exerting a protective effect on neurons. In this review, we provide a comprehensive analysis of the involvement of miR-146a in the pathogenesis of Alzheimer's disease. We aim to elucidate the relationship between miR-146a and the key pathological manifestations of Alzheimer's disease, such as amyloid-β deposition, tau protein hyperphosphorylation, neuronal death, mitochondrial dysfunction, synaptic dysfunction, and glial cell dysfunction, as well as summarize recent relevant studies that have highlighted the potential of miR-146a as a clinical diagnostic marker and therapeutic target for Alzheimer's disease.

阿尔茨海默病是一种以认知功能障碍和行为异常为特征的神经退行性疾病。淀粉样蛋白-β在细胞外沉积形成的神经炎症斑块和高磷酸化 tau 蛋白在细胞内沉积形成的神经纤维缠结是阿尔茨海默病的两个典型病理特征。除了对症治疗外,目前还没有有效的疗法来延缓阿尔茨海默病的进展。微RNA(miR)是一种小型非编码RNA,可在转录和翻译水平上负向调节基因表达,在多种生理和病理过程中发挥重要作用。事实上,miR-146a 作为一种 NF-κB 调控基因,已被广泛认为通过多种途径与阿尔茨海默病的发病有关。研究表明,miR-146a 在这种疾病的初始阶段和整个发展过程中都存在严重的失调。据信,miR-146a 可通过 TLR/IRAK1/TRAF6 途径减少淀粉样蛋白-β 的沉积和 tau 蛋白的过度磷酸化;但也有证据表明,它可通过许多其他途径促进这些过程,从而加剧阿尔茨海默病的病理表现。有广泛报道称,miR-146a 通过靶向编码突触相关蛋白、线粒体相关蛋白和膜蛋白的 mRNA 及其他 mRNA,介导突触功能障碍、线粒体功能障碍和神经元死亡。关于对神经胶质细胞的影响,miR-146a 也表现出不同的效应。一方面,它通过某些途径引起广泛而持续的炎症;另一方面,它又能逆转星形胶质细胞和小胶质细胞的极化,缓解神经炎症,促进少突胶质祖细胞分化,从而维持髓鞘的正常功能,对神经元起到保护作用。在这篇综述中,我们全面分析了 miR-146a 参与阿尔茨海默病发病机制的情况。我们旨在阐明 miR-146a 与阿尔茨海默病的主要病理表现(如淀粉样蛋白-β沉积、tau 蛋白高磷酸化、神经元死亡、线粒体功能障碍、突触功能障碍和神经胶质细胞功能障碍)之间的关系,并总结最近的相关研究,这些研究强调了 miR-146a 作为阿尔茨海默病临床诊断标志物和治疗靶点的潜力。
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