The aged nervous system displays impaired cognitive functions, and these impairments are exacerbated in several neurodegenerative diseases. A role for oxidative stress has been suggested for several of these age-3associated dysfunctions. In addition, recovery from more acute traumatic insults that also generate oxidative stress is impaired in the aged. Here we examine the response of aged rat hippocampi to normobaric hyperoxia treatments and demonstrate an attenuation in the DNA binding activity of the AP-1 and nuclear factor-κB transcription factors, which are important components of stress response signal transduction pathways and can determine shifts in cellular commitments to necrosis, apoptosis, or functional recovery in the central nervous system.
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience