Journal
BRAIN RESEARCH
Volume 1368, Issue -, Pages 65-70Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2010.11.009
Keywords
Aging; Short-term memory; Superoxide; NADPH oxidase; Mitochondria; Synaptosome
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Funding
- Stein Institute on Research on Aging
- Veterans Affairs Center of Excellence for Stress and Mental Health
- National Institute of Mental Health [R01 MH074697, MH66248]
- National Institute on Aging [R21AG030320, K25AG026379]
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Unregulated production of reactive oxygen species (ROS) is a marker of cellular and organismal aging linked to cognitive decline in humans and rodents. The sources of elevated ROS contributing to cognitive decline are unknown. Because NADPH oxidase (Nox) inhibition may prevent memory decline with age, we hypothesized that Nox and not mitochondrial sources of synaptic ROS production are linked to individual variance in cognitive performance in aged mice. Young (8 months) and aged (26 months) mice were tested in the novel object recognition task (NORT). Mitochondrial and Nox ROS production was assayed in isolated synaptosomes using spin trapping electron paramagnetic resonance (EPR) spectroscopy. Aged mice exhibited variance in NORT performance, with some performing similar to young mice while others exhibited poorer short-term memory. EPR studies indicated that Nox rather than mitochondria was the major ROS source at the synapse, and Nox-induced but not mitochondrial-induced ROS levels correlated with NORT performance in aged mice. Our findings support the hypothesis that variance in Nox-specific synaptic ROS production may predict short-term memory deficits with age. Published by Elsevier B.V.
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