Cue-directed shifts of spatial attention were examined for a letter-discrimination task in 15 patients with mild to moderate dementia of the Alzheimer type (DAT) and 15 healthy, age-matched controls. Spatial cues were valid, invalid or neutral in indicating probable target location and were presented either centrally at fixation or peripherally 6.7 degrees to the left or right of fixation. Stimulus-onset asynchrony (SOA) between cue and target was varied between 200 ms and 2000 ms. Reaction time (RT) benefits conferred by valid cues did not differ between the DAT group and the controls. However, RT costs incurred by invalid cues were significantly greater in the DAT group than in the control group. Group differences in RT costs plus benefits occurred at short SOAs (less than 500 ms) for peripheral cues and at long SOAs (greater than 500 ms) for central cues. Reaction time costs plus benefits were correlated with right-left asymmetry in resting levels of cerebral glucose metabolism in the superior parietal lobe for DAT patients but not for controls. The results indicate that focusing of attention to spatial location is intact in early DAT, whereas the disengagement of visuospatial attention is impaired. Automatic attention shifts elicited by peripheral cues reveal abnormalities earlier than attention shifts initiated 'effortfully' by central cues. Intact focusing and impaired disengagement of visuospatial attention may be linked to dysfunction in early DAT of cortico-cortical networks linking the posterior parietal and frontal lobes.

Cognitive aging reflects not only loss but also adaptation to loss. The adult brain is capable of plastic change, including change in cortical representation. This has been seen in association not only with frank lesions but also in healthy individuals as a function of experience and training. This review considers the potential for adult plasticity together with evidence of a relation in old age between regional cortical atrophy/shrinkage and increased activation in neuroimaging. Those cortical regions shown most consistently to shrink in adulthood--prefrontal and parietal cortices--are the same regions showing increased regional activation in aging. Combining several strands of behavioral and neuroimaging evidence, the author argues that functional plasticity alters the course of cognitive aging. The author advances the hypothesis that losses in regional brain integrity drive functional reorganization through changes in processing strategy and makes specific predictions from that hypothesis.

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That the human frontal lobes are particularly vulnerable to age-related deterioration has been frequently invoked as an explanation of functional decline in aging. This “frontal aging hypothesis” is evaluated in this review by examining evidence of selectively reduced frontal lobe function in aging. The frontal aging hypothesis predicts that functions largely dependent on frontal regions would decline in aging, while functions largely independent of frontal lobes would remain relatively spared. The hypothesis further predicts that age-related brain change would selectively impact frontal regions. The literatures on working memory, visuospatial attention, face recognition, and implicit memory were reviewed as exemplars of functions dependent on prefrontal, parietal, temporal and occipitotemporal cortices, respectively, with a view to establishing mediating structures and effects of aging. Age sensitivity was seen both in functions dependent on frontal integrity as well as in functions apparently independent of frontal integrity. Further, although prefrontal areas exhibit age-related decreases in regional volume, blood flow and metabolism, nonfrontal cortical regions undergo similar declines. It is concluded that while the frontal lobes are subject to age-related changes reflected in both behavior and pathology, there is only weak and conflicting evidence that frontal regions are selectively and differentially affected by aging. It is argued that a network-based theory of cognitive aging has advantages over the localizationist approach inherent in the frontal aging hypothesis. (JINS, 2000, 6, 705–726.)

Executive function declines with age, but engaging in aerobic exercise may attenuate decline. One mechanism by which aerobic exercise may preserve executive function is through the up-regulation of brain-derived neurotropic factor (BDNF), which also declines with age. The present study examined BDNF as a mediator of the effects of a 1-year walking intervention on executive function in 90 older adults (mean age = 66.82). Participants were randomized to a stretching and toning control group or a moderate intensity walking intervention group. BDNF serum levels and performance on a task-switching paradigm were collected at baseline and follow-up. We found that age moderated the effect of intervention group on changes in BDNF levels, with those in the highest age quartile showing the greatest increase in BDNF after 1-year of moderate intensity walking exercise (p = 0.036). The mediation analyses revealed that BDNF mediated the effect of the intervention on task-switch accuracy, but did so as a function of age, such that exercise-induced changes in BDNF mediated the effect of exercise on task-switch performance only for individuals over the age of 71. These results demonstrate that both age and BDNF serum levels are important factors to consider when investigating the mechanisms by which exercise interventions influence cognitive outcomes, particularly in elderly populations.