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Senescence‐Accelerated Mouse
Author(s) -
NOMURA YASUYUKI,
YAMANAKA YOJIRO,
KITAMURA YOSHIHISA,
ARIMA TAKASHI,
OHNUKI TOSHIO,
OOMURA YUTAKA,
SASAKI KAZUO,
NAGASHIMA KAZUO,
IHARA YASUO
Publication year - 1996
Publication title -
annals of the new york academy of sciences
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1996.tb39080.x
Subject(s) - pharmaceutical sciences , library science , medicine , pharmacology , computer science
Senescence-accelerated mouse (SAMP8) is known as a murine model of accelerated aging and memory dysfunction. The binding activity of [3H] 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxam ide (PK-11195) as a neurochemical marker of gliosis markedly increased with aging in the cerebral cortex and hippocampus of SAMP8. Immunoreactivity for glial fibrillary acidic protein (GFAP) was also enhanced. A beta-amyloid precursor protein (APP)-like immunoreactivity and 27-kDa-carboxyl terminal fragments of APP increased in SAMP8 brain. In addition, anti-APP antibody stained reactive astrocytes surrounding spongy degeneration in brain stern of SAMP8. These results suggest that astrocytosis and production of APP-derived fragments occur markedly in SAMP8 brains.