Translocation of amyloid precursor protein C-terminal fragment(s) to the nucleus precedes neuronal death due to thiamine deficiency-induced mild impairment of oxidative metabolism

Neurochemical Research

Volumn 33, Issue 7, 2008, Pages 1365-1372

  Karuppagounder, Saravanan S ^a   Xu, Hui ^a   Pechman, David ^a   Chen, Lian H ^a   DeGiorgio, Lorraine A ^a   Gibson, Gary E ^a  

^a WEILL CORNELL MEDICAL COLLEGE   (United States)

Author keywords

Amyloid precursor protein; Inflammation; Neurodegeneration; Oxidative stress; Sub medial thalamic nucleus

Indexed keywords

AMYLOID PRECURSOR PROTEIN;

AEROBIC METABOLISM; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; BRAIN REGION; CARBOXY TERMINAL SEQUENCE; CONTROLLED STUDY; IMMUNOREACTIVITY; MALE; MOUSE; NERVE CELL NECROSIS; NERVE DEGENERATION; NONHUMAN; PRIORITY JOURNAL; THALAMUS NUCLEUS; THIAMINE DEFICIENCY;

AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; BLOTTING, WESTERN; CELL DEATH; CELL NUCLEUS; CEREBRAL CORTEX; IMMUNOHISTOCHEMISTRY; MALE; MICE; MICE, INBRED C57BL; NERVE DEGENERATION; NEURONS; OXIDATION-REDUCTION; PEPTIDE FRAGMENTS; SUBTHALAMIC NUCLEUS; THIAMINE DEFICIENCY; TRANSLOCATION, GENETIC;

EID: 44549083055     PISSN: 03643190     EISSN: None     Source Type: Journal    
DOI: 10.1007/s11064-008-9594-z     Document Type: Article

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