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Lamin B1 decline underlies age‐related loss of adult hippocampal neurogenesis
Author(s) -
Bedrosian Tracy A,
Houtman Judith,
Eguiguren Juan Sebastian,
Ghassemzadeh Saeed,
Rund Nicole,
Novaresi Nicole M,
Hu Lauren,
Parylak Sarah L.,
Denli Ahmet M,
RandolphMoore Lynne,
Namba Takashi,
Gage Fred H,
Toda Tomohisa
Publication year - 2020
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.2020105819
Subject(s) - biology , lamin , gerontology , german , library science , neuroscience , medicine , history , nucleus , archaeology , computer science
Abstract Neurogenesis in the adult hippocampus declines with age, a process that has been implicated in cognitive and emotional impairments. However, the mechanisms underlying this decline have remained elusive. Here, we show that the age‐dependent downregulation of lamin B1, one of the nuclear lamins in adult neural stem/progenitor cells (ANSPCs), underlies age‐related alterations in adult hippocampal neurogenesis. Our results indicate that higher levels of lamin B1 in ANSPCs safeguard against premature differentiation and regulate the maintenance of ANSPCs. However, the level of lamin B1 in ANSPCs declines during aging. Precocious loss of lamin B1 in ANSPCs transiently promotes neurogenesis but eventually depletes it. Furthermore, the reduction of lamin B1 in ANSPCs recapitulates age‐related anxiety‐like behavior in mice. Our results indicate that the decline in lamin B1 underlies stem cell aging and impacts the homeostasis of adult neurogenesis and mood regulation.