Gene therapy and neuroprotection for cerebral infarction

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Topical application of GDNF protein greatly reduced the infarct size and brain edema at 24 hr of continuous MCAO in rats. The reduction of the infarct size was not related to a change of cerebral blood flow (CBF), but was accompanied by marked reduction of positive cells for TUNEL and caspases in the affected area. GDNF protein showed a direct protective effect against ischemic brain damage, but not secondary by improving CBF. Pretreatment of animals with Ad-GDNF 24 hr before the subsequent 90 min of transient MCAO effectively reduced infract volume and area without affecting regional CBF compared to the vehicle or Ad-LacZ animal groups. Free radical scavenger edaravone effectively reduced brain edema, infarct size, and peroxidative markers of protein, lipid and DNA. Thus, gene therapy and neuroprotective strategy have a great potential for reducing ischemic brain damage of human stroke patients in the near future.

Original languageEnglish
Pages (from-to)894-896
Number of pages3
JournalClinical Neurology
Volume43
Issue number11
Publication statusPublished - Nov 2003

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Cerebrovascular Circulation
Glial Cell Line-Derived Neurotrophic Factor
Cerebral Infarction
Genetic Therapy
Brain Edema
Free Radical Scavengers
Proteins
Regional Blood Flow
In Situ Nick-End Labeling
Brain
Caspases
Stroke
Lipids
DNA
Neuroprotection

Keywords

  • Cerebral infarction
  • Gene therapy
  • Neuroprotection
  • Neurotrophic factor

ASJC Scopus subject areas

  • Clinical Neurology

Cite this

Gene therapy and neuroprotection for cerebral infarction. / Abe, Koji.

In: Clinical Neurology, Vol. 43, No. 11, 11.2003, p. 894-896.

Research output: Contribution to journalArticle

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