Cited 43 time in
- Peroxiredoxin II preserves cognitive function against age-linked hippocampal oxidative damage
- Sun-Uk Kim; M H Jin; Y S Kim; S H Lee; Yeesook Cho; K J Cho; Kyu-Sun Lee; Y I Kim; G W Kim; J M Kim; T H Lee; Y H Lee; M Shong; H C Kim; Kyu Tae Chang; Dae Yeul Yu; D S Lee
- Bibliographic Citation
- Neurobiology of Aging, vol. 32, no. 6, pp. 1054-1068
- Publication Year
- Reactive oxygen species (ROS), routinely produced in biological reactions, contribute to both normal aging and age-related decline in cognitive function. However, little is known regarding the involvement of specific antioxidants in the underlying mechanism(s). Here, we examined if peroxiredoxin II (Prx II) scavenges intracellular ROS that cause age-dependent mitochondrial decay in hippocampal CA1 pyramidal neurons and subsequent impairment of learning and memory. Age-dependent mitochondrial ROS generation and long-term potentiation (LTP) decline were more prominent in hippocampal neurons in Prx II-/- than in wild-type mice. Additionally, Prx II-/- mice failed to activate synaptic plasticity-related cellular signaling pathways involving CREB, CaMKII, and ERK, or to maintain functional integrity of their mitochondria. Dietary vitamin E alleviated Prx II deficiency-related deficits, including mitochondrial decay and CREB signaling, resulting in restoration of the abrupt cognitive decline in aged Prx II-/- mice. These results suggest that Prx II help maintain hippocampal synaptic plasticity against age-related oxidative damage.
- AgingHippocampusLong-term potentiationMitochondriaPeroxiredoxinReactive oxygen species
- Appears in Collections:
- Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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