The superoxide dismutase1 (SOD1) G93A mutation does not promote neuronal injury after focal brain ischemia and optic nerve transection in mice

Neuroscience

Volumn 128, Issue 2, 2004, Pages 359-364

  Kilic, E ^a   Weishaupt, J H ^b   Kilic, U ^a   Rohde, G ^b   Yulug, B ^b   Peters, K ^b   Hermann, D M ^a   Bahr M ^b  

^a UNIVERSITY HOSPITAL ZURICH   (Switzerland)

^b UNIVERSITY MEDICAL CENTER GÖTTINGEN   (Germany)

Author keywords

familial amyotrophic lateral sclerosis; free radical scavenging; ischemic stroke; oxidative stress

Indexed keywords

COPPER ZINC SUPEROXIDE DISMUTASE; SUPEROXIDE DISMUTASE; UNCLASSIFIED DRUG;

AMYOTROPHIC LATERAL SCLEROSIS; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN ISCHEMIA; CONTROLLED STUDY; ENZYME MODIFICATION; ENZYME SUBUNIT; MOUSE; MUTANT; MUTATIONAL ANALYSIS; NERVE CELL DEGENERATION; NERVE INJURY; NERVE TRANSECTION; NEUROPATHOLOGY; NONHUMAN; OPTIC NERVE; PRIORITY JOURNAL; RETINA GANGLION CELL; WILD TYPE;

ANIMALS; BRAIN ISCHEMIA; CELL SURVIVAL; HUMANS; MICE; MICE, TRANSGENIC; MUTATION; NEURONS; OPTIC NERVE INJURIES; RETINAL GANGLION CELLS; SUPEROXIDE DISMUTASE;

EID: 4444239693     PISSN: 03064522     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neuroscience.2004.06.064     Document Type: Article

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