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Targeting the intracellular neurexin interactome by in vivo proximity ligation. 通过体内近距离连接瞄准细胞内神经毒素相互作用组。
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-06 DOI: 10.1016/j.tins.2024.02.007
Ming-Han Wang, Yue Hao, Xia-Jing Tong

In a recent study, Profes, Tiroumalechetty, and colleagues used the in vivo proximity ligation technique TurboID to scrupulously characterize the interactome of the intracellular domain (ICD) of neurexin, revealing that this domain may be involved in presynaptic actin assembly by interacting with actin-associated proteins.

在最近的一项研究中,Proves、Tiroumalechett 及其同事利用体内近距离连接技术 TurboID 仔细分析了神经肽胞内结构域 (ICD) 的相互作用组,发现该结构域可能通过与肌动蛋白相关蛋白相互作用而参与突触前肌动蛋白组装。
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引用次数: 0
Embracing sleep-onset complexity. 迎接睡眠发病的复杂性。
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-21 DOI: 10.1016/j.tins.2024.02.002
Célia Lacaux, Mélanie Strauss, Tristan A Bekinschtein, Delphine Oudiette

Sleep is crucial for many vital functions and has been extensively studied. By contrast, the sleep-onset period (SOP), often portrayed as a mere prelude to sleep, has been largely overlooked and remains poorly characterized. Recent findings, however, have reignited interest in this transitional period and have shed light on its neural mechanisms, cognitive dynamics, and clinical implications. This review synthesizes the existing knowledge about the SOP in humans. We first examine the current definition of the SOP and its limits, and consider the dynamic and complex electrophysiological changes that accompany the descent to sleep. We then describe the interplay between internal and external processing during the wake-to-sleep transition. Finally, we discuss the putative cognitive benefits of the SOP and identify novel directions to better diagnose sleep-onset disorders.

睡眠对许多生命机能至关重要,对它的研究也非常广泛。相比之下,睡眠启动期(SOP)通常被认为只是睡眠的前奏,却在很大程度上被忽视了,其特征也不甚明了。然而,最近的研究结果重新点燃了人们对这一过渡时期的兴趣,并揭示了其神经机制、认知动态和临床影响。本综述综合了有关人类 SOP 的现有知识。我们首先探讨了 SOP 的现有定义及其局限性,并考虑了伴随着进入睡眠的动态和复杂的电生理变化。然后,我们描述了在从唤醒到睡眠的转变过程中内部和外部处理之间的相互作用。最后,我们讨论了 SOP 可能带来的认知益处,并确定了更好地诊断睡眠障碍的新方向。
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引用次数: 0
Astrocytes in selective vulnerability to neurodegenerative disease. 选择性易患神经退行性疾病的星形胶质细胞
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-22 DOI: 10.1016/j.tins.2024.02.008
Till S Zimmer, Adam L Orr, Anna G Orr

Selective vulnerability of specific brain regions and cell populations is a hallmark of neurodegenerative disorders. Mechanisms of selective vulnerability involve neuronal heterogeneity, functional specializations, and differential sensitivities to stressors and pathogenic factors. In this review we discuss the growing body of literature suggesting that, like neurons, astrocytes are heterogeneous and specialized, respond to and integrate diverse inputs, and induce selective effects on brain function. In disease, astrocytes undergo specific, context-dependent changes that promote different pathogenic trajectories and functional outcomes. We propose that astrocytes contribute to selective vulnerability through maladaptive transitions to context-divergent phenotypes that impair specific brain regions and functions. Further studies on the multifaceted roles of astrocytes in disease may provide new therapeutic approaches to enhance resilience against neurodegenerative disorders.

特定脑区和细胞群的选择性易损性是神经退行性疾病的一个特征。选择性易损性的机制涉及神经元的异质性、功能特化以及对压力和致病因素的不同敏感性。在这篇综述中,我们将讨论越来越多的文献表明,星形胶质细胞与神经元一样,具有异质性和特化性,能对不同的输入做出反应并进行整合,并对大脑功能产生选择性影响。在疾病中,星形胶质细胞会发生特定的、依赖于环境的变化,从而促进不同的致病轨迹和功能结果。我们提出,星形胶质细胞通过向损害特定脑区和功能的情境差异表型的不适应性转变,促成了选择性脆弱性。对星形胶质细胞在疾病中的多方面作用的进一步研究可能会提供新的治疗方法,以增强对神经退行性疾病的复原力。
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引用次数: 0
The emergence of multiscale connectomics-based approaches in stroke recovery. 基于多尺度连接组学的中风康复方法的出现。
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-02-23 DOI: 10.1016/j.tins.2024.01.003
Shahrzad Latifi, S Thomas Carmichael

Stroke is a leading cause of adult disability. Understanding stroke damage and recovery requires deciphering changes in complex brain networks across different spatiotemporal scales. While recent developments in brain readout technologies and progress in complex network modeling have revolutionized current understanding of the effects of stroke on brain networks at a macroscale, reorganization of smaller scale brain networks remains incompletely understood. In this review, we use a conceptual framework of graph theory to define brain networks from nano- to macroscales. Highlighting stroke-related brain connectivity studies at multiple scales, we argue that multiscale connectomics-based approaches may provide new routes to better evaluate brain structural and functional remapping after stroke and during recovery.

中风是导致成人残疾的主要原因。要了解脑卒中的损伤和恢复情况,需要破译复杂脑网络在不同时空尺度上的变化。尽管最近脑读出技术的发展和复杂网络建模的进步彻底改变了目前对中风对宏观脑网络影响的理解,但对较小尺度脑网络重组的理解仍然不全面。在本综述中,我们使用图论的概念框架来定义从纳米到宏观尺度的脑网络。通过强调与脑卒中相关的多尺度脑连接研究,我们认为基于多尺度连接组学的方法可为更好地评估脑卒中后和恢复期的脑结构和功能重映射提供新的途径。
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引用次数: 0
Supermultipotency and unpredictability in the developing superior colliculus. 发育中上丘的超多重性和不可预测性
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-20 DOI: 10.1016/j.tins.2024.03.001
Andrii Rudenko, In-Jung Kim

A recent study by Cheung, Pauler, Koppensteiner et al. combining lineage tracing with single-cell RNA sequencing (scRNA-seq) has revealed unexpected features of the developing superior colliculus (SC). Extremely multipotent individual progenitors generate all types of SC neurons and glial cells that were found to localize in a non-predetermined pattern, demonstrating a remarkable degree of unpredictability in SC development.

Cheung、Pauler、Koppensteiner 等人最近的一项研究将系追踪与单细胞 RNA 测序(scRNA-seq)相结合,揭示了发育中的上丘脑(SC)的意外特征。极具多能性的单个祖细胞产生了所有类型的上丘脑神经元和胶质细胞,这些细胞以一种非预定的模式定位,显示了上丘脑发育过程中显著的不可预测性。
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引用次数: 0
Balancing neuronal activity to fight neurodevelopmental disorders. 平衡神经元活动,对抗神经发育障碍。
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-22 DOI: 10.1016/j.tins.2024.03.002
Stephanie Le, Carmen Menacho, Alessandro Prigione

In a recent study, Rylaarsdam and colleagues revealed that mutant PACS1 gene, which causes a rare neurodevelopmental syndrome, affects the firing ability of human neurons without dysregulating the cellular architecture of brain organoids. These findings suggest aberrant neuronal electrophysiology as a possible interventional target for pediatric diseases impairing brain development.

在最近的一项研究中,Rylaarsdam 及其同事发现,导致一种罕见神经发育综合征的突变 PACS1 基因会影响人类神经元的发射能力,但不会导致脑器官组织的细胞结构失调。这些研究结果表明,神经元电生理学异常可能成为影响大脑发育的儿科疾病的干预目标。
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引用次数: 0
The 'middle-aging' brain. 中年 "大脑
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-19 DOI: 10.1016/j.tins.2024.02.001
Sebastian Dohm-Hansen, Jane A English, Aonghus Lavelle, Carlos P Fitzsimons, Paul J Lucassen, Yvonne M Nolan

Middle age has historically been an understudied period of life compared to older age, when cognitive and brain health decline are most pronounced, but the scope for intervention may be limited. However, recent research suggests that middle age could mark a shift in brain aging. We review emerging evidence on multiple levels of analysis indicating that midlife is a period defined by unique central and peripheral processes that shape future cognitive trajectories and brain health. Informed by recent developments in aging research and lifespan studies in humans and animal models, we highlight the utility of modeling non-linear changes in study samples with wide subject age ranges to distinguish life stage-specific processes from those acting linearly throughout the lifespan.

与老年期相比,中年期的认知能力和大脑健康衰退最为明显,但干预范围可能有限。然而,最近的研究表明,中年可能标志着大脑衰老的转变。我们回顾了多层次分析的新证据,这些证据表明,中年是一个由独特的中枢和外周过程所定义的时期,这些过程塑造了未来的认知轨迹和大脑健康。根据人类和动物模型在衰老研究和寿命研究方面的最新进展,我们强调了在研究对象年龄范围较广的样本中建立非线性变化模型的实用性,以区分特定生命阶段的过程和在整个生命周期中线性作用的过程。
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引用次数: 0
The selfish network: how the brain preserves behavioral function through shifts in neuronal network state. 自私的网络:大脑如何通过神经元网络状态的变化来保持行为功能。
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-04-01 Epub Date: 2024-03-13 DOI: 10.1016/j.tins.2024.02.005
Albrecht Stroh, Susann Schweiger, Jan-Marino Ramirez, Oliver Tüscher

Neuronal networks possess the ability to regulate their activity states in response to disruptions. How and when neuronal networks turn from physiological into pathological states, leading to the manifestation of neuropsychiatric disorders, remains largely unknown. Here, we propose that neuronal networks intrinsically maintain network stability even at the cost of neuronal loss. Despite the new stable state being potentially maladaptive, neural networks may not reverse back to states associated with better long-term outcomes. These maladaptive states are often associated with hyperactive neurons, marking the starting point for activity-dependent neurodegeneration. Transitions between network states may occur rapidly, and in discrete steps rather than continuously, particularly in neurodegenerative disorders. The self-stabilizing, metastable, and noncontinuous characteristics of these network states can be mathematically described as attractors. Maladaptive attractors may represent a distinct pathophysiological entity that could serve as a target for new therapies and for fostering resilience.

神经元网络具有调节其活动状态以应对干扰的能力。神经元网络如何以及何时从生理状态转变为病理状态,从而导致神经精神疾病的出现,这在很大程度上仍是未知数。在这里,我们提出,神经元网络即使以神经元丢失为代价,也能从本质上保持网络的稳定性。尽管新的稳定状态可能是不适应的,但神经网络可能不会逆转回与更好的长期结果相关的状态。这些不适应状态通常与神经元过度活跃有关,是活动依赖性神经退化的起点。网络状态之间的转换可能发生得很快,而且是以离散的步骤而不是连续的方式进行,尤其是在神经退行性疾病中。这些网络状态的自稳定、易变和非连续特性可以用吸引子来进行数学描述。不适应性吸引子可能代表一种独特的病理生理学实体,可作为新疗法和促进恢复力的目标。
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引用次数: 0
Protein-protein interactions regulating α-synuclein pathology. 调节α-突触核蛋白病理学的蛋白质间相互作用
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-03-01 Epub Date: 2024-02-13 DOI: 10.1016/j.tins.2024.01.002
Jiannan Wang, Lijun Dai, Sichun Chen, Zhaohui Zhang, Xin Fang, Zhentao Zhang

Parkinson's disease (PD) is a neurodegenerative disease characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the formation of Lewy bodies (LBs). The main proteinaceous component of LBs is aggregated α-synuclein (α-syn). However, the mechanisms underlying α-syn aggregation are not yet fully understood. Converging lines of evidence indicate that, under certain pathological conditions, various proteins can interact with α-syn and regulate its aggregation. Understanding these protein-protein interactions is crucial for unraveling the molecular mechanisms contributing to PD pathogenesis. In this review we provide an overview of the current knowledge on protein-protein interactions that regulate α-syn aggregation. Additionally, we briefly summarize the methods used to investigate the influence of protein-protein interactions on α-syn aggregation and propagation.

帕金森病(Parkinson's disease,PD)是一种神经退行性疾病,其特征是黑质上皮(substantia nigra pars compacta,SNpc)中的多巴胺能神经元变性并形成路易体(Lewy bodies,LBs)。路易体的主要蛋白成分是聚集的α-突触核蛋白(α-syn)。然而,α-syn聚集的机制尚未完全明了。越来越多的证据表明,在某些病理条件下,各种蛋白质可与α-syn相互作用并调节其聚集。了解这些蛋白质之间的相互作用对于揭示导致帕金森病发病的分子机制至关重要。在这篇综述中,我们概述了目前有关调控α-syn聚集的蛋白-蛋白相互作用的知识。此外,我们还简要总结了用于研究蛋白-蛋白相互作用对α-syn聚集和传播的影响的方法。
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引用次数: 0
A noncoding role of coding mRNA in monogenic olfactory receptor choice. 编码 mRNA 在单基因嗅觉受体选择中的非编码作用
IF 15.9 1区 医学 Q1 Neuroscience Pub Date : 2024-03-01 Epub Date: 2024-02-19 DOI: 10.1016/j.tins.2024.02.004
Yue Hao, Kang-Ying Qian, Qian Li

In a recent study, Pourmorady and colleagues uncovered a noncoding role for olfactory receptor (OR)-coding mRNA in mediating nuclear architecture and singular OR choice. The OR mRNAs reinforce the prevailing enhancer hub and inhibit other competitors, facilitating transition from polygenic to singular OR expression.

在最近的一项研究中,Pourmorady 及其同事发现了嗅觉受体(OR)编码 mRNA 在介导核结构和单一 OR 选择方面的非编码作用。嗅觉受体编码 mRNA 强化了主要的增强子枢纽,抑制了其他竞争者,促进了从多基因到单一嗅觉受体表达的过渡。
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引用次数: 0
期刊
Trends in Neurosciences
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