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A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse.

Magnusson, Jens P ; Göritz, Christian ; Tatarishvili, Jemal LU ; Dias, David LU ; Smith, Emma LU ; Lindvall, Olle LU ; Kokaia, Zaal LU orcid and Frisén, Jonas (2014) In Science 346(6206). p.237-241
Abstract
Neurogenesis is restricted in the adult mammalian brain; most neurons are neither exchanged during normal life nor replaced in pathological situations. We report that stroke elicits a latent neurogenic program in striatal astrocytes in mice. Notch1 signaling is reduced in astrocytes after stroke, and attenuated Notch1 signaling is necessary for neurogenesis by striatal astrocytes. Blocking Notch signaling triggers astrocytes in the striatum and the medial cortex to enter a neurogenic program, even in the absence of stroke, resulting in 850 ± 210 (mean ± SEM) new neurons in a mouse striatum. Thus, under Notch signaling regulation, astrocytes in the adult mouse brain parenchyma carry a latent neurogenic program that may potentially be useful... (More)
Neurogenesis is restricted in the adult mammalian brain; most neurons are neither exchanged during normal life nor replaced in pathological situations. We report that stroke elicits a latent neurogenic program in striatal astrocytes in mice. Notch1 signaling is reduced in astrocytes after stroke, and attenuated Notch1 signaling is necessary for neurogenesis by striatal astrocytes. Blocking Notch signaling triggers astrocytes in the striatum and the medial cortex to enter a neurogenic program, even in the absence of stroke, resulting in 850 ± 210 (mean ± SEM) new neurons in a mouse striatum. Thus, under Notch signaling regulation, astrocytes in the adult mouse brain parenchyma carry a latent neurogenic program that may potentially be useful for neuronal replacement strategies. (Less)
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author
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Science
volume
346
issue
6206
pages
237 - 241
publisher
American Association for the Advancement of Science (AAAS)
external identifiers
  • pmid:25301628
  • wos:000342721500048
  • scopus:84907857863
ISSN
1095-9203
DOI
10.1126/science.1257791
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neurology, Lund (013027000), Neuronal Survival (013212041), Division of Translational Cancer Research (013250500)
id
08b1a2dd-cbfd-42ae-86ae-6bd531469d42 (old id 4737184)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/25301628?dopt=Abstract
date added to LUP
2016-04-01 10:43:02
date last changed
2022-04-20 05:24:16
@article{08b1a2dd-cbfd-42ae-86ae-6bd531469d42,
  abstract     = {{Neurogenesis is restricted in the adult mammalian brain; most neurons are neither exchanged during normal life nor replaced in pathological situations. We report that stroke elicits a latent neurogenic program in striatal astrocytes in mice. Notch1 signaling is reduced in astrocytes after stroke, and attenuated Notch1 signaling is necessary for neurogenesis by striatal astrocytes. Blocking Notch signaling triggers astrocytes in the striatum and the medial cortex to enter a neurogenic program, even in the absence of stroke, resulting in 850 ± 210 (mean ± SEM) new neurons in a mouse striatum. Thus, under Notch signaling regulation, astrocytes in the adult mouse brain parenchyma carry a latent neurogenic program that may potentially be useful for neuronal replacement strategies.}},
  author       = {{Magnusson, Jens P and Göritz, Christian and Tatarishvili, Jemal and Dias, David and Smith, Emma and Lindvall, Olle and Kokaia, Zaal and Frisén, Jonas}},
  issn         = {{1095-9203}},
  language     = {{eng}},
  number       = {{6206}},
  pages        = {{237--241}},
  publisher    = {{American Association for the Advancement of Science (AAAS)}},
  series       = {{Science}},
  title        = {{A latent neurogenic program in astrocytes regulated by Notch signaling in the mouse.}},
  url          = {{http://dx.doi.org/10.1126/science.1257791}},
  doi          = {{10.1126/science.1257791}},
  volume       = {{346}},
  year         = {{2014}},
}