Transgenic mice overexpressing amyloid beta protein are an incomplete model of Alzheimer disease

Experimental Neurology

Volumn 188, Issue 1, 2004, Pages 52-64

  Schwab, Claudia ^a   Hosokawa, Masato ^a   McGeer, Patrick L ^a  

^a UNIVERSITY OF BRITISH COLUMBIA   (Canada)

Author keywords

Complement; Complement receptors; Inflammation; Microglia; Neurofibrillary tangles; Tau; Vaccination

Indexed keywords

AMYLOID BETA PROTEIN; APOLIPOPROTEIN E; COMPLEMENT COMPONENT CD11B RECEPTOR; COMPLEMENT RECEPTOR; CONGO RED; PROTEIN ANTIBODY; TAU PROTEIN; UNCLASSIFIED DRUG;

ALZHEIMER DISEASE; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ASTROCYTE; BIREFRINGENCE; CELL ACTIVATION; CONTROLLED STUDY; GENE MUTATION; IMMUNOHISTOCHEMISTRY; MICROGLIA; MOUSE; NEUROFIBRILLARY TANGLE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SILVER STAINING; STAINING; TRANSGENIC MOUSE;

AGE FACTORS; ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN; ANIMALS; ANTIGENS, CD11B; APOLIPOPROTEINS E; ASTROCYTES; BRAIN; COMPLEMENT SYSTEM PROTEINS; DISEASE MODELS, ANIMAL; GLIOSIS; IMMUNOHISTOCHEMISTRY; MICE; MICE, TRANSGENIC; MICROGLIA; MUTATION; NEURITES; NEUROFIBRILLARY TANGLES; REPRODUCIBILITY OF RESULTS; SENILE PLAQUES; TAU PROTEINS;

EID: 2942611429     PISSN: 00144886     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.expneurol.2004.03.016     Document Type: Article

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