Journal Article

DZNE-2021-00551

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Lamin B1 decline underlies age‐related loss of adult hippocampal neurogenesis

Bedrosian, T. A. ; Houtman, J.DZNE* ; Eguiguren, J. S.DZNE* ; Ghassemzadeh, S. ; Rund, N.DZNE* ; Novaresi, N. M. ; Hu, L. ; Parylak, S. L. ; Denli, A. M. ; Randolph-Moore, L. ; Namba, T. ; Gage, F. H. ; Toda, T. (Last author)DZNE*

2021
Wiley Hoboken, NJ [u.a.]

This record in other databases:      

Please use a persistent id in citations: doi:10.15252/embj.2020105819

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.

Keyword(s): Aging: genetics (MeSH) ; Aging: metabolism (MeSH) ; Animals (MeSH) ; Anxiety: genetics (MeSH) ; Cell Differentiation (MeSH) ; Cell Line (MeSH) ; Disease Models, Animal (MeSH) ; Down-Regulation (MeSH) ; Female (MeSH) ; Hippocampus: cytology (MeSH) ; Hippocampus: metabolism (MeSH) ; Lamin Type B: genetics (MeSH) ; Lamin Type B: metabolism (MeSH) ; Male (MeSH) ; Mice (MeSH) ; Neural Stem Cells: cytology (MeSH) ; Neural Stem Cells: metabolism (MeSH) ; Neurogenesis (MeSH) ; Rats (MeSH)

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Contributing Institute(s):

1. Nuclear architecture in neural plasticity and aging (AG Toda)

Research Program(s):

1. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2021

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Database coverage:
; ; ; BIOSIS Previews ; Biological Abstracts ; Clarivate Analytics Master Journal List ; Current Contents - Life Sciences ; DEAL Wiley ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 10 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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Linked articles:

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Dataset Toda, T. (First author)DZNE* ; Linker, S. B. ; Gage, F. H.
Dataset: Lamin B1 dependent transcriptional control in neural progenitor cells
Gene Expression Omnibus (2020)2020   Fulltext BibTeX | EndNote: XML, Text | RIS

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