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PMID: 10513583 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Progressive and gender-dependent cognitive impairment in the APP(SW) transgenic mouse model for Alzheimer's disease.

Behavioural brain research ·Vol. 103 ·No. 2 ·1999-09-00 ·Pages 145-62

King DL, Arendash GW, Crawford F, Sterk T, Menendez J, Mullan MJ

Abstract

To determine if early cognitive sensorimotor deficits exist in APP(SW) transgenic mice overexpressing human amyloid precursor protein (APP). Tg+ and Tg- animals at both 3 and 9 months of age (3M and 9M, respectively) were evaluated in a comprehensive battery of measures. The performance of all Tg+ mice at both ages was no different from all Tg- controls in Y-maze alternations, water maze acquisition, passive avoidance, and active avoidance testing. By contrast, results from other tasks revealed substantive cognitive deficits in Tg+ mice that were usually gender-dependent and sometimes progressive in nature. Between 3M and 9M, a progressive impairment was observed in circular platform performance by Tg+ males, as was a progressive deficit in visible platform testing for all Tg+ animals. Other transgenic effects included both impaired water maze retention and circular platform performance in 3M Tg+ females; this later effect was responsible for an overall (males + females) Tg+ deficit in circular platform performance at 3M. Sensorimotor testing revealed several Tg+ effects, most notably an increased activity of Tg+ males in both open field and Y-maze at 3M. Significant correlations between a number of behavioral measures were observed, although factor analysis suggests that each task measured components of sensorimotor/cognitive function not measured by other tasks. Finally, Tg+ mice had lower survivability than Tg- animals through 9M (85 vs. 96%). In summary, these results demonstrate the presence of gender-related and progressive cognitive deficits in APP(SW) transgenic mice at a relatively early age (i.e., prior to overt, beta-amyloid deposition in the brain), suggesting a pathophysiologic role for elevated levels of 'soluble' beta-amyloid in such impairments.

MeSH Terms
Alzheimer Disease/genetics,psychology Amyloid beta-Protein Precursor/genetics Animals Avoidance Learning/physiology Cognition/physiology Cognition Disorders/genetics,psychology Exploratory Behavior Female Humans Male Maze Learning/physiology Mice Mice, Inbred C57BL Mice, Transgenic Motor Activity Plaque, Amyloid/pathology Psychomotor Performance/physiology Sex Characteristics Survival Analysis
Chemicals
Amyloid beta-Protein Precursor
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
King D L
Alzheimer's Research Laboratory, Department of Biology, University of South Florida, Tampa 33620, USA.
Arendash G W
Crawford F
Sterk T
Menendez J
Mullan M J
Article Info
Journal
Behavioural brain research
Abbr.
Behav Brain Res
ISSN
0166-4328
Published
1999-09-00
Pages
145-62
Language
English
Region
Netherlands
NLM ID
8004872
Subset
IM
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