Oxygen free radical injury is sufficient to cause some Alzheimer-type molecular abnormalities in human CNS neuronal cells

Journal of Alzheimer's Disease

Volumn 2, Issue 3-4, 2000, Pages 261-281

  De La Monte, S M ^a,b   Ganju, N ^a,b   Feroz, N ^a,b   Luong, T ^a,b   Banerjee, K ^a,b   Cannon, J ^a,b   Wands, J R ^a,b  

^a MASSACHUSETTS GENERAL HOSPITAL   (United States)

^b BROWN UNIVERSITY   (United States)

Author keywords

Apoptosis; Free radical; Mitochondria; Neuritic sprouting; Neurodegeneration

Indexed keywords

8 HYDROXYDEOXYGUANOSINE; CYCLIN DEPENDENT KINASE 5; CYCLINE; FAS ANTIGEN; HYDROGEN PEROXIDE; MITOCHONDRIAL DNA; NERVE PROTEIN; NEUROMODULIN; NEURONAL THREAD PROTEIN; NITRIC OXIDE SYNTHASE; OXYGEN RADICAL; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN BCL 2; PROTEIN P25; PROTEIN P35; PROTEIN P53; STRESS ACTIVATED PROTEIN KINASE; TAU PROTEIN; UNCLASSIFIED DRUG;

ALZHEIMER DISEASE; APOPTOSIS; ARTICLE; CELL SURVIVAL; CONCENTRATION RESPONSE; CONTROLLED STUDY; DNA DAMAGE; ENZYME ACTIVITY; GENE EXPRESSION; HUMAN; HUMAN CELL; INCUBATION TIME; NERVE CELL CULTURE; NERVE DEGENERATION; NERVE FIBER GROWTH; OXIDATIVE STRESS; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION;

EID: 0034489359     PISSN: 13872877     EISSN: None     Source Type: Journal    
DOI: 10.3233/JAD-2000-23-406     Document Type: Article

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