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Perturbed cellular response to brain injury during aging

Popa-Wagner, Aurel; Buga, Ana-Maria and Kokaia, Zaal LU (2011) In Ageing Research Reviews 10(1). p.71-79
Abstract
Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only partly understood. Therefore, studying the basic mechanisms underlying structural and functional recovery after brain injury in aged subjects is of considerable clinical interest. Behavioral and cytological analyses of rodents that have undergone experimental injury show that: (a) behaviorally, aged rodents are more severely impaired by ischemia than are young animals, and older rodents also show diminished functional recovery; (b) compared to young animals, aged animals develop a larger infarct area, as well as a necrotic zone characterized by a higher rate of cellular... (More)
Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only partly understood. Therefore, studying the basic mechanisms underlying structural and functional recovery after brain injury in aged subjects is of considerable clinical interest. Behavioral and cytological analyses of rodents that have undergone experimental injury show that: (a) behaviorally, aged rodents are more severely impaired by ischemia than are young animals, and older rodents also show diminished functional recovery; (b) compared to young animals, aged animals develop a larger infarct area, as well as a necrotic zone characterized by a higher rate of cellular degeneration and a larger number of apoptotic cells; (c) both astrocytes and macrophages are activated strongly and early following stroke in aged rodents; (d) in older animals, the premature, intense cytoproliferative activity following brain injury leads to the precipitous formation of growth-inhibiting scar tissue, a phenomenon amplified by the persistent expression of neurotoxic factors; (e) though the timing is altered, the regenerative capability of the brain is largely preserved in rats, at least into early old age. Whether endogenous neurogenesis contributes to spontaneous recovery after stroke has not yet been established. If neurogenesis from endogenous neuronal stem cells is to be used therapeutically, an individual approach will be required to assess the possible extent of neurogenic response as well as the possibilities to alter this response for functional improvement or prevention of further loss of brain function. (C) 2009 Elsevier Ireland Ltd. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Brain injury, Stroke, Aging, Recuperation, Glial scar, Degeneration, Apoptosis, Microglia activation, Cytoproliferation, Regeneration, Neurogenesis, Stem cells
in
Ageing Research Reviews
volume
10
issue
1
pages
71 - 79
publisher
Elsevier
external identifiers
  • wos:000287068900008
  • scopus:78650230589
ISSN
1872-9649
DOI
10.1016/j.arr.2009.10.008
language
English
LU publication?
yes
id
cd88a800-473f-4e51-9e68-020bcec1e08a (old id 1878199)
date added to LUP
2011-04-01 08:34:28
date last changed
2017-10-22 03:22:47
@article{cd88a800-473f-4e51-9e68-020bcec1e08a,
  abstract     = {Old age is associated with an enhanced susceptibility to stroke and poor recovery from brain injury, but the cellular processes underlying these phenomena are only partly understood. Therefore, studying the basic mechanisms underlying structural and functional recovery after brain injury in aged subjects is of considerable clinical interest. Behavioral and cytological analyses of rodents that have undergone experimental injury show that: (a) behaviorally, aged rodents are more severely impaired by ischemia than are young animals, and older rodents also show diminished functional recovery; (b) compared to young animals, aged animals develop a larger infarct area, as well as a necrotic zone characterized by a higher rate of cellular degeneration and a larger number of apoptotic cells; (c) both astrocytes and macrophages are activated strongly and early following stroke in aged rodents; (d) in older animals, the premature, intense cytoproliferative activity following brain injury leads to the precipitous formation of growth-inhibiting scar tissue, a phenomenon amplified by the persistent expression of neurotoxic factors; (e) though the timing is altered, the regenerative capability of the brain is largely preserved in rats, at least into early old age. Whether endogenous neurogenesis contributes to spontaneous recovery after stroke has not yet been established. If neurogenesis from endogenous neuronal stem cells is to be used therapeutically, an individual approach will be required to assess the possible extent of neurogenic response as well as the possibilities to alter this response for functional improvement or prevention of further loss of brain function. (C) 2009 Elsevier Ireland Ltd. All rights reserved.},
  author       = {Popa-Wagner, Aurel and Buga, Ana-Maria and Kokaia, Zaal},
  issn         = {1872-9649},
  keyword      = {Brain injury,Stroke,Aging,Recuperation,Glial scar,Degeneration,Apoptosis,Microglia activation,Cytoproliferation,Regeneration,Neurogenesis,Stem cells},
  language     = {eng},
  number       = {1},
  pages        = {71--79},
  publisher    = {Elsevier},
  series       = {Ageing Research Reviews},
  title        = {Perturbed cellular response to brain injury during aging},
  url          = {http://dx.doi.org/10.1016/j.arr.2009.10.008},
  volume       = {10},
  year         = {2011},
}