Locally reduced levels of acidic FGF lead to decreased expression of 28-kDa calbindin and contribute to the selective vulnerability of the neurons in the entorhinal cortex in Alzheimer's disease

Neuropathology

Volumn 21, Issue 3, 2001, Pages 203-211

  Thorns, Veronika ^a   Licastro, Federico ^b   Masliah, Eliezer ^c  

^a HANNOVER MEDICAL SCHOOL   (Germany)

^b UNIVERSITY OF BOLOGNA   (Italy)

^c UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

aFGF; Alzheimer's disease; Calbindin D28k; NT2N cells; Selective vulnerability

Indexed keywords

ACIDIC FIBROBLAST GROWTH FACTOR; CALBINDIN; EXCITOTOXIN;

ADULT; AGED; ALZHEIMER DISEASE; ARTICLE; CALCIUM HOMEOSTASIS; CLINICAL ARTICLE; CONTROLLED STUDY; DISEASE PREDISPOSITION; ENTORHINAL CORTEX; FEMALE; HIPPOCAMPUS; HUMAN; HUMAN TISSUE; MALE; NEUROPROTECTION; PRIORITY JOURNAL; PROTEIN BINDING; PROTEIN EXPRESSION; PROTEIN INTERACTION;

AGED; ALZHEIMER DISEASE; CALCIUM; CALCIUM-BINDING PROTEIN, VITAMIN D-DEPENDENT; CELL SURVIVAL; DOWN-REGULATION; ENTORHINAL CORTEX; FEMALE; FIBROBLAST GROWTH FACTOR 1; HOMEOSTASIS; HUMANS; IMMUNOHISTOCHEMISTRY; MALE; NEURITES; NEUROGLIA; NEURONS; PROTEIN-TYROSINE KINASES; PYRAMIDAL CELLS; RECEPTOR, FIBROBLAST GROWTH FACTOR, TYPE 3; RECEPTORS, FIBROBLAST GROWTH FACTOR; TUMOR CELLS, CULTURED; UP-REGULATION;

EID: 0034784073     PISSN: 09196544     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1440-1789.2001.00399.x     Document Type: Article

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