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

Sun Uk Kim, Mei Hua Jin, Yoon Sik Kim, Sang Hee Lee, Yee Sook Cho, Kyoung Joo Cho, Kyu Sun Lee, Yang In Kim, Gyung Whan Kim, Jin Man Kim, Tae Hoon Lee, Young Ho Lee, Minho Shong, Hyung Chun Kim, Kyu Tae Chang, Dae Yeul Yu, Dong Seok Lee

Research output: Contribution to journalArticlepeer-review

43 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)1054-1068
Number of pages15
JournalNeurobiology of Aging
Issue number6
Publication statusPublished - 2011 Jun


  • Aging
  • Hippocampus
  • Long-term potentiation
  • Mitochondria
  • Peroxiredoxin
  • Reactive oxygen species

ASJC Scopus subject areas

  • Neuroscience(all)
  • Ageing
  • Developmental Biology
  • Clinical Neurology
  • Geriatrics and Gerontology


Dive into the research topics of 'Peroxiredoxin II preserves cognitive function against age-linked hippocampal oxidative damage'. Together they form a unique fingerprint.

Cite this