More expertise for a better perspective: Task and strategy-driven adaptive neurofunctional reorganization for word production in high-performing older adults

The suggestion that neurofunctional reorganization may contribute to preserved language abilities is still emerging in aging studies. Some of these abilities, such as verbal fluency (VF), are not unitary but instead rely on different strategic processes that are differentially changed with age. Younger (n = 13) and older adults (n = 13) carried out an overt self-paced semantic and orthographic VF tasks within mixed fMRI design. Our results suggest that patterns of brain activation sustaining equivalent performances could be underpinned by different strategies facing brain changes during healthy aging. These main findings suggest that temporally mediated semantic clustering and frontally mediated orthographic switching were driven by evolutive neurofunctional resources in high-performing older adults. These age-related activation changes can appear to be compatible with the idea that unique neural patterns expressing distinctive cognitive strategies are necessary to support older adults’ performance on VF tasks.     

Hippocampal long-term potentiation, memory, and longevity in mice that overexpress mitochondrial superoxide dismutase

Superoxide has been shown to be critically involved in several pathological manifestations of aging animals. In contrast, superoxide also can act as a signaling molecule to modulate signal transduction cascades required for hippocampal synaptic plasticity. Mitochondrial superoxide dismutase (SOD-2 or Mn-SOD) is a key antioxidant enzyme that scavenges superoxide. Thus, SOD-2 may not only prevent aging-related oxidative stress, but may also regulate redox signaling in young animals. We used transgenic mice overexpressing SOD-2 to study the role of mitochondrial superoxide in aging, synaptic plasticity, and memory-associated behavior. We found that overexpression of SOD-2 had no obvious effect on synaptic plasticity and memory formation in young mice, and could not rescue the age-related impairments in either synaptic plasticity or memory in old mice. However, SOD-2 overexpression did decrease mitochondrial superoxide in hippocampal neurons, and extended the lifespan of the mice. These findings increase our knowledge of the role of mitochondrial superoxide in physiological and pathological processes in the brain.