Peroxiredoxin II preserves cognitive function against age-linked hippocampal oxidative damage

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• 作者：Sun-Uk Kim^a ; Mei-Hua Jin^a ; ^h ; Yoon Sik Kim^j ; Sang-Hee Lee^e ; Yee Sook Cho^b ; Kyoung-Joo Cho^k ; Kyu-Sun Lee^a ; Yang In Kim^j ; Gyung Whan Kim^k ; Jin-Man Kim^f ; Tae-Hoon Leeⁱ ; Young-Ho Lee^g ; Minho Shong^h ; Hyung-Chun Kim^d ; Kyu-Tae Chang^c ; Dae-Yeul Yu^a ; ^{dyyu10@kribb.re.kr"" rel=""nofollow} ; Dong-Seok Lee^l ; ^{lee1@knu.ac.kr"" rel=""nofollow}
• 关键词：Reactive oxygen species ; Peroxiredoxin ; Hippocampus ; Aging ; Mitochondria ; Long-term potentiation
• 刊名：Neurobiology of Aging
• 出版年：2011
• 出版时间：June 2011
• 年：2011
• 卷：32
• 期：6
• 页码：1054-1068
• 全文大小：4167 K

文摘

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.