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Mitochondrial permeability transition in acute neurodegeneration.

Friberg, Hans LU and Wieloch, Tadeusz LU (2002) In Biochimie 84(2-3). p.241-250
Abstract
Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here... (More)
Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here we present data that strongly imply the mtPT in acute neurodegeneration in vivo. Compounds that readily pass the blood-brain-barrier (BBB) and block the mtPT may be neuroprotective in stroke. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biochimie
volume
84
issue
2-3
pages
241 - 250
publisher
Elsevier
external identifiers
  • wos:000175648600016
  • scopus:0036479054
ISSN
1638-6183
language
English
LU publication?
yes
id
3e6cdc87-e3a4-4e50-8aa3-88991b4f0d97 (old id 108348)
alternative location
http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12022955&dopt=Abstract
date added to LUP
2007-07-23 15:43:03
date last changed
2017-12-10 03:49:04
@article{3e6cdc87-e3a4-4e50-8aa3-88991b4f0d97,
  abstract     = {Acute neurodegeneration in man is encountered during and following stroke, transient cardiac arrest, brain trauma, insulin-induced hypoglycemia and status epilepticus. All these severe clinical conditions are characterized by neuronal calcium overload, aberrant cell signaling, generation of free radicals and elevation of cellular free fatty acids, conditions that favor activation of the mitochondrial permeability transition pore (mtPTP). Cyclosporin A (CsA) and its analog N-methyl-valine-4-cyclosporin A (MeValCsA) are potent blockers of the mtPTP and protect against neuronal death following excitotoxicity and oxygen glucose deprivation. Also, CsA and MeValCsA diminish cell death following cerebral ischemia, trauma, and hypoglycemia. Here we present data that strongly imply the mtPT in acute neurodegeneration in vivo. Compounds that readily pass the blood-brain-barrier (BBB) and block the mtPT may be neuroprotective in stroke.},
  author       = {Friberg, Hans and Wieloch, Tadeusz},
  issn         = {1638-6183},
  language     = {eng},
  number       = {2-3},
  pages        = {241--250},
  publisher    = {Elsevier},
  series       = {Biochimie},
  title        = {Mitochondrial permeability transition in acute neurodegeneration.},
  volume       = {84},
  year         = {2002},
}