The fetal basis of amyloidogenesis: Exposure to lead and latent overexpression of amyloid precursor protein and β-amyloid in the aging brain

Journal of Neuroscience

Volumn 25, Issue 4, 2005, Pages 823-829

  Basha, M Riyaz ^a   Wei, Wei ^a   Bakheet, Saleh A ^a   Benitez, Nathalie ^a   Siddiqi, Hasan K ^a   Ge, Yuan Wen ^b   Lahiri, Debomoy K ^b   Zawia, Nasser H ^a  

^a UNIVERSITY OF RHODE ISLAND   (United States)

^b INDIANA UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

peptide; Alzheimer; CNS; Dementia; Development; Environment; Latency; Transcription

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN; LEAD; MESSENGER RNA; SMALL INTERFERING RNA; TRANSCRIPTION FACTOR SP1;

AGED; AGING; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BRAIN DEVELOPMENT; CONTROLLED STUDY; DISEASE COURSE; DNA BINDING; ENVIRONMENTAL EXPOSURE; GENE CONTROL; GENE EXPRESSION; LIFESPAN; NERVE DEGENERATION; NEWBORN; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; UPREGULATION;

AGING; AMYLOID BETA-PROTEIN; AMYLOID BETA-PROTEIN PRECURSOR; ANIMALS; ANIMALS, NEWBORN; BRAIN; FEMALE; GENE EXPRESSION REGULATION, DEVELOPMENTAL; HUMANS; LEAD; MALE; PC12 CELLS; PROMOTER REGIONS (GENETICS); RATS; RATS, LONG-EVANS; RNA, SMALL INTERFERING; SP1 TRANSCRIPTION FACTOR;

EID: 12844273354     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/JNEUROSCI.4335-04.2005     Document Type: Article

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