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作 者:Melania Capasso N.Ahmad Aziz
机构地区:[1]Immune Regulation,German Center for Neurodegenerative Diseases(DZNE),Bonn,Germany [2]Population and Clinical Neuroepidemiology,German Center for Neurodegenerative Diseases(DZNE),Bonn,Germany [3]Department of Neurology,Faculty of Medicine,University of Bonn,Bonn,Germany
出 处:《Signal Transduction and Targeted Therapy》2024年第9期3544-3545,共2页信号转导与靶向治疗(英文)
基 金:supported by DZNE core funding,the Helmholtz-Gemeinschaft Innovation Pool,Deutsche Forschungsgemeinschaft(DFG,German Research Foundation)under Germany’s Excellence Strategy XC2151-390873048;CANTAR.The project“CANTAR”is receiving funding from the program“Netzwerke 2021,”an initiative of the Ministry of Culture and Science of the State of North Rhine-Westphalia.The sole responsibility for the content of this publication lies with the authors;funding from the European Union’s Horizon Europe research and innovation program under the MSCA Doctoral Networks 2021,No.101072759(FuEl ThE bRaiN In healtThY aging and age-related diseases,ETERNITY);supported by DZNE core funding,a European Research Council Starting Grant(#101041677);Alzheimer’s Association Research Grant(AARG-19-616534);the project“InVirtuo 4.0”by the Ministry of Culture and Science of the State of North Rhine-Westphalia.
摘 要:In a recent study published in Cell,Ganz et al.shed new light on the mutational landscape of brain cells,particularly neurons and oligodendrocytes(OLs).1 Utilizing a combination of optimized single-cell whole-genome sequencing with single-nucleus chromatin accessibility and gene expression analysis,they profiled somatic mutations in 86 OLs from 13 neurotypical individuals,spanning in age from infants to elderly.Neurons investigated were 56,derived from 19(including 12 overlapping)individuals(Fig.1).
分 类 号:R329.2[医药卫生—人体解剖和组织胚胎学]
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