Nature Reviews Neuroscience最新文献_第4页

Thirsty work for the cerebellum 小脑的饥渴工作

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-24 DOI: 10.1038/s41583-024-00848-4

Katherine Whalley

引用次数: 0

Schizophrenia genomics: genetic complexity and functional insights 精神分裂症基因组学：遗传复杂性和功能性见解。

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-19 DOI: 10.1038/s41583-024-00837-7

Patrick F. Sullivan, Shuyang Yao, Jens Hjerling-Leffler

{"title":"Schizophrenia genomics: genetic complexity and functional insights","authors":"Patrick F. Sullivan, Shuyang Yao, Jens Hjerling-Leffler","doi":"10.1038/s41583-024-00837-7","DOIUrl":"10.1038/s41583-024-00837-7","url":null,"abstract":"Determining the causes of schizophrenia has been a notoriously intractable problem, resistant to a multitude of investigative approaches over centuries. In recent decades, genomic studies have delivered hundreds of robust findings that implicate nearly 300 common genetic variants (via genome-wide association studies) and more than 20 rare variants (via whole-exome sequencing and copy number variant studies) as risk factors for schizophrenia. In parallel, functional genomic and neurobiological studies have provided exceptionally detailed information about the cellular composition of the brain and its interconnections in neurotypical individuals and, increasingly, in those with schizophrenia. Taken together, these results suggest unexpected complexity in the mechanisms that drive schizophrenia, pointing to the involvement of ensembles of genes (polygenicity) rather than single-gene causation. In this Review, we describe what we now know about the genetics of schizophrenia and consider the neurobiological implications of this information. In recent years, genomic studies have identified numerous genetic variants as risk factors for schizophrenia. Sullivan et al. describe our current understanding of the complex genetic architecture of schizophrenia and consider how the genomic findings can be interrogated to boost our understanding of the neurobiology of the disorder.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"611-624"},"PeriodicalIF":28.7,"publicationDate":"2024-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Publisher Correction: Macroscopic gradients of synaptic excitation and inhibition in the neocortex 出版商更正：新皮层中突触兴奋和抑制的宏观梯度。

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-16 DOI: 10.1038/s41583-024-00847-5

Xiao-Jing Wang

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Neurogenic exacerbation of psoriasis 银屑病的神经源性加重

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-08 DOI: 10.1038/s41583-024-00844-8

Darran Yates

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Predicting natural behaviour by perturbation 通过扰动预测自然行为

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-02 DOI: 10.1038/s41583-024-00842-w

Jake Rogers

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Indirect neurogenesis in space and time 空间和时间上的间接神经发生。

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-01 DOI: 10.1038/s41583-024-00833-x

Stefan Thor

{"title":"Indirect neurogenesis in space and time","authors":"Stefan Thor","doi":"10.1038/s41583-024-00833-x","DOIUrl":"10.1038/s41583-024-00833-x","url":null,"abstract":"During central nervous system (CNS) development, neural progenitor cells (NPCs) generate neurons and glia in two different ways. In direct neurogenesis, daughter cells differentiate directly into neurons or glia, whereas in indirect neurogenesis, neurons or glia are generated after one or more daughter cell divisions. Intriguingly, indirect neurogenesis is not stochastically deployed and plays instructive roles during CNS development: increased generation of cells from specific lineages; increased generation of early or late-born cell types within a lineage; and increased cell diversification. Increased indirect neurogenesis might contribute to the anterior CNS expansion evident throughout the Bilateria and help to modify brain-region size without requiring increased NPC numbers or extended neurogenesis. Increased indirect neurogenesis could be an evolutionary driver of the gyrencephalic (that is, folded) cortex that emerged during mammalian evolution and might even have increased during hominid evolution. Thus, selection of indirect versus direct neurogenesis provides a powerful developmental and evolutionary instrument that drives not only the evolution of CNS complexity but also brain expansion and modulation of brain-region size, and thereby the evolution of increasingly advanced cognitive abilities. This Review describes indirect neurogenesis in several model species and humans, and highlights some of the molecular genetic mechanisms that control this important process. Central nervous system (CNS) neurons and glial cells are generated by both direct and indirect neurogenesis. In this Review, Thor outlines the landscape of indirect neurogenesis during CNS development in key species, including humans, and describes the main genetic mechanisms that contribute to its region-specific, neural progenitor cell-specific and temporal control.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"519-534"},"PeriodicalIF":28.7,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141477031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Wrapping up reward 总结奖励。

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-01 DOI: 10.1038/s41583-024-00841-x

Sian Lewis

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Mapping the cell-type-specific effects of ageing in the human cortex 绘制人类大脑皮层老化对细胞类型特异性影响的图谱

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-07-01 DOI: 10.1038/s41583-024-00843-9

Katherine Whalley

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Timescales of learning in prefrontal cortex 前额叶皮层的学习时标

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-06-27 DOI: 10.1038/s41583-024-00836-8

Jacob A. Miller, Christos Constantinidis

{"title":"Timescales of learning in prefrontal cortex","authors":"Jacob A. Miller, Christos Constantinidis","doi":"10.1038/s41583-024-00836-8","DOIUrl":"10.1038/s41583-024-00836-8","url":null,"abstract":"The lateral prefrontal cortex (PFC) in humans and other primates is critical for immediate, goal-directed behaviour and working memory, which are classically considered distinct from the cognitive and neural circuits that support long-term learning and memory. Over the past few years, a reconsideration of this textbook perspective has emerged, in that different timescales of memory-guided behaviour are in constant interaction during the pursuit of immediate goals. Here, we will first detail how neural activity related to the shortest timescales of goal-directed behaviour (which requires maintenance of current states and goals in working memory) is sculpted by long-term knowledge and learning — that is, how the past informs present behaviour. Then, we will outline how learning across different timescales (from seconds to years) drives plasticity in the primate lateral PFC, from single neuron firing rates to mesoscale neuroimaging activity patterns. Finally, we will review how, over days and months of learning, dense local and long-range connectivity patterns in PFC facilitate longer-lasting changes in population activity by changing synaptic weights and recruiting additional neural resources to inform future behaviour. Our Review sheds light on how the machinery of plasticity in PFC circuits facilitates the integration of learned experiences across time to best guide adaptive behaviour. The prefrontal cortex is critical for working memory, over a timescale of seconds. In this Review, Miller and Constantinidis examine how the prefrontal cortex facilitates the integration of memory systems across other timescales as well. In this framework of prefrontal learning, short-term memory and long-term memory interact to serve goal-directed behaviour.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 9","pages":"597-610"},"PeriodicalIF":28.7,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141461782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Why so slow? Models of parkinsonian bradykinesia 为何如此缓慢？帕金森病运动迟缓的模型

IF 28.7 1区医学

Nature Reviews Neuroscience Pub Date : 2024-06-27 DOI: 10.1038/s41583-024-00830-0

David Williams

{"title":"Why so slow? Models of parkinsonian bradykinesia","authors":"David Williams","doi":"10.1038/s41583-024-00830-0","DOIUrl":"10.1038/s41583-024-00830-0","url":null,"abstract":"Bradykinesia, or slowness of movement, is a defining feature of Parkinson disease (PD) and a major contributor to the negative effects on quality of life associated with this disorder and related conditions. A dominant pathophysiological model of bradykinesia in PD has existed for approximately 30 years and has been the basis for the development of several therapeutic interventions, but accumulating evidence has made this model increasingly untenable. Although more recent models have been proposed, they also appear to be flawed. In this Perspective, I consider the leading prior models of bradykinesia in PD and argue that a more functionally related model is required, one that considers changes that disrupt the fundamental process of accurate information transmission. In doing so, I review emerging evidence of network level functional connectivity changes, information transfer dysfunction and potential motor code transmission error and present a novel model of bradykinesia in PD that incorporates this evidence. I hope that this model may reconcile inconsistencies in its predecessors and encourage further development of therapeutic interventions. There are a number of models that have attempted to explain why people with Parkinson disease move slowly. In this Perspective, Williams identifies the inconsistencies in these models and suggests that these may be addressed by a different model that considers disordered information transmission as fundamental to slow movement development.","PeriodicalId":49142,"journal":{"name":"Nature Reviews Neuroscience","volume":"25 8","pages":"573-586"},"PeriodicalIF":28.7,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141462375","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0