Beta-amyloid precursor polypeptide in SAMP8 mice affects learning and memory.
Senescence accelerated (SAMP8 [P8]) mice develop age-related deficits in memory and learning. We show that increased expression of amyloid precursor protein (APP) and its mRNA in the hippocampus are also age-related. Immunocytochemical data suggest that a critical amount of APP expression may be needed to generate amyloid (Abeta) protein plaques in the hippocampus. Deficits in acquisition and retention test performance were alleviated by administration of antibody to Abeta protein into the cerebral ventricles. This reversal of cognitive deficits provides a link between increased expression of both APP and Abeta protein and learning and memory loss in these mice.
Morley
J E
JE
Geriatric Research, Education and Clinical Center, St. Louis Department of Veterans Affairs Medical Center, 63104, St. Louis, MO, USA. morley@slu.edu
Kumar
V B
VB
Bernardo
A E
AE
Farr
S A
SA
Uezu
K
K
Tumosa
N
N
Flood
J F
JF
D000367:Age Factors; D016564:Amyloid beta-Protein Precursor / Q000096:biosynthesis* / Q000737:chemistry*; D000818:Animals; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D006624:Hippocampus / Q000378:metabolism*; D007074:Immunoglobulin G / Q000378:metabolism; D007150:Immunohistochemistry; D007858:Learning; D008297:Male; D008568:Memory; D051379:Mice; D008817:Mice, Mutant Strains; D012333:RNA, Messenger / Q000378:metabolism; D012260:Ribonucleases / Q000378:metabolism
D016564:Amyloid beta-Protein Precursor; D007074:Immunoglobulin G; D012333:RNA, Messenger; D012260:Ribonucleases