Journal
BEHAVIOURAL BRAIN RESEARCH
Volume 216, Issue 1, Pages 255-261Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbr.2010.08.002
Keywords
PPAR gamma; Fear conditioning; Hippocampus-dependent learning and memory; Mouse model; Alzheimer's disease; Glucose tolerance test; Insulin
Categories
Funding
- National Institutes of Health [F31 NS052928, R01- AG031859]
- Mitchell Center for Neurodegenerative Diseases
- Sealy Foundation
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [F31NS052928] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG031859] Funding Source: NIH RePORTER
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Converging lines of evidence associate gluco-regulatory abnormalities and peroxisome-proliferator-activated receptor (PPAR) gamma function with increased risk for Alzheimer's disease (AD). In this study, we used the Tg2576 AD mouse model to test the hypothesis that cognitive improvement following 1 month of PPAR gamma agonism with rosiglitazone (RTZ) correlates with peripheral gluco-regulatory status. We assessed cognition and peripheral gluco-regulatory status of Tg2576 mice following 1 month treatment with RTZ initiated prior to, coincident with, or after, the onset of peripheral gluco-regulatory abnormalities (4, 8, and 12 months of age, respectively). Whereas 5 months old (MO) and 13 MO Tg2576 did not gain cognitive improvement after 1 month treatment with RTZ, 9 MO Tg2576 mice exhibited reversal of associative learning and memory deficits. Peripheral gluco-regulatory abnormalities were improved in 9 and 13 MO Tg2576 with RTZ treatment; RTZ treatment had no effect on the normal glucose status of 5 MO Tg2576 mice. These findings suggest that RTZ-mediated cognitive improvement does not correlate with peripheral gluco-regulatory abnormalities per se, but reflects the age-dependent mechanistic differences that underlie cognitive decline in this mouse model. (C) 2010 Elsevier B.V. All rights reserved.
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