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Therefore, we tested whether systemic administration of desipramine can rescue aging-related deficit of emotional memory in aged rats.
Furthermore, acute administration of NE repaired the aging-related deficit of surface expression of GluR1 and emotional memory in aged rats.
This study was designed to determine if increasing GluN2B subunit expression in the frontal lobe or hippocampus would improve memory in aged mice.
We have previously shown that pharmacological inhibition of the intracellular glucocorticoid-amplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) improves spatial memory in aged mice.
Old males had significantly fewer platform crossings than young males, indicating that spatial memory is reduced in old males (Fig. 6c), On the other hand, aged C3-treated mice performed significantly better than wild-type old mice, showing that treatment with the SOD mimetic preserves spatial memory in aged mice.
Finally, acute treatment with NE or desipramine rescued the impaired emotional memory in aged rats.
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These results imply a pivotal role for NE in synaptic plasticity and associative fear memory in aging rats and suggest that desipramine is a potential candidate for treating aging-related emotional memory deficit.
Newman, J. C. et al. Ketogenic diet reduces midlife mortality and improves memory in aging mice.
Clapp WC, Gazzaley A. Distinct mechanisms for the impact of distraction and interruption on working memory in aging.
Mander, B.A. et al. Prefrontal atrophy, disrupted NREM slow waves, and impaired hippocampal-dependent memory in aging.
Yaakov Stern, PhD, Taub Institute, will receive $3,896,093 over five years from the National Institute on Aging for "Imaging of Cognition, Learning, and Memory in Aging" in a competitive renewal.
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