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Neuronal replacement from endogenous precursors in the adult brain after stroke.

Arvidsson, Andreas LU ; Collin, Tove LU ; Kirik, Deniz LU ; Kokaia, Zaal LU and Lindvall, Olle LU (2002) In Nature Medicine 8(9). p.963-970
Abstract
In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we... (More)
In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans. (Less)
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author
organization
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type
Contribution to journal
publication status
published
subject
in
Nature Medicine
volume
8
issue
9
pages
963 - 970
publisher
Nature Publishing Group
external identifiers
  • pmid:12161747
  • wos:000177757900031
  • scopus:0036735672
ISSN
1546-170X
DOI
10.1038/nm747
language
English
LU publication?
yes
id
c3087779-d5a3-493f-9bb1-91bbc8b08a98 (old id 109740)
alternative location
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12161747&dopt=Abstract
date added to LUP
2007-07-23 15:37:44
date last changed
2017-12-10 04:35:39
@article{c3087779-d5a3-493f-9bb1-91bbc8b08a98,
  abstract     = {In the adult brain, new neurons are continuously generated in the subventricular zone and dentate gyrus, but it is unknown whether these neurons can replace those lost following damage or disease. Here we show that stroke, caused by transient middle cerebral artery occlusion in adult rats, leads to a marked increase of cell proliferation in the subventricular zone. Stroke-generated new neurons, as well as neuroblasts probably already formed before the insult, migrate into the severely damaged area of the striatum, where they express markers of developing and mature, striatal medium-sized spiny neurons. Thus, stroke induces differentiation of new neurons into the phenotype of most of the neurons destroyed by the ischemic lesion. Here we show that the adult brain has the capacity for self-repair after insults causing extensive neuronal death. If the new neurons are functional and their formation can be stimulated, a novel therapeutic strategy might be developed for stroke in humans.},
  author       = {Arvidsson, Andreas and Collin, Tove and Kirik, Deniz and Kokaia, Zaal and Lindvall, Olle},
  issn         = {1546-170X},
  language     = {eng},
  number       = {9},
  pages        = {963--970},
  publisher    = {Nature Publishing Group},
  series       = {Nature Medicine},
  title        = {Neuronal replacement from endogenous precursors in the adult brain after stroke.},
  url          = {http://dx.doi.org/10.1038/nm747},
  volume       = {8},
  year         = {2002},
}