Disruption of corticocortical connections ameliorates amyloid burden in terminal fields in a transgenic model of Aβ amyloidosis

Journal of Neuroscience

Volumn 22, Issue 22, 2002, Pages 9794-9799

  Sheng, Jin G ^a   Price, Donald L ^a   Koliatsos, Vassilis E ^a  

^a JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Alzheimer's disease; APP; Axonal transport; A ; Entorhinal cortex; Perforant pathway; Senile plaques

Indexed keywords

AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN; THIOFLAVINE;

ALZHEIMER DISEASE; AMYLOIDOSIS; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DENTATE GYRUS; ENTORHINAL CORTEX; HIPPOCAMPUS; IMMUNOASSAY; MOUSE; NERVE FIBER; NERVE FIBER TRANSPORT; NEURITE; NONHUMAN; PERFORANT NERVE TRACT; PRIORITY JOURNAL; PROTEIN DEGRADATION; PROTEIN TRANSPORT; SENILE PLAQUE; SILVER STAINING; WESTERN BLOTTING;

EID: 0037111838     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.22-22-09794.2002     Document Type: Article

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