High levels of education, occupational complexity and/or premorbid intelligence are associated with lower levels of cognitive impairment than would be expected from a given brain pathology. This has been observed across a range of conditions including Alzheimer's Disease (Roe, et al., 2010), stroke (Ojala-Oksala, et al., 2012), traumatic brain injury (Kesler, et al., 2003), and penetrating brain injury (Grafman, 1986). This cluster of factors, which seemingly protect the brain from expressing symptoms of damage, has been termed 'cognitive reserve' (Stern, 2012). The current review considers one possible neural network which may contribute to cognitive reserve. Based on evidence that the neurotransmitter noradrenaline mediates cognitive reserve's protective effects (Robertson, 2013) this review identifies the neurocognitive correlates of noradrenergic (NA) activity. These involve a set of inter-related cognitive processes (arousal, sustained attention, response to novelty and awareness) with a strongly right hemisphere, fronto-parietal localization, along with working memory which is also strongly modulated by NA. It is proposed that this set of processes is one plausible candidate for partially mediating the protective effects of cognitive reserve. In addition to its biological effects on brain structure and function, NA function may also facilitate networks for arousal, novelty, attention, awareness and working memory which collectively provide for a set of additional, cognitive, mechanisms that help the brain adapt to age-related changes and disease. It is hypothesized that to the extent that the lateral surface of the right prefrontal lobe and/or the right inferior parietal lobe maintain structural (white and grey matter) and functional integrity and connectivity, cognitive reserve should benefit and behavioral expression of pathological damage should thus be mitigated.