The precise mechanisms that give rise to the blood-oxygen-level-dependent (BOLD) activation differences that accompany age-related cognitive slowing remain fundamentally unknown. We sought to isolate the origin of age-related BOLD changes by comparing blood-flow and oxygen-metabolic constituents of the BOLD response using dual-echo arterial spin labeling during visual stimulation and CO2 ingestion. We hypothesized, and our results confirmed, that age-related changes in the ratio of fractional cerebral blood flow to fractional cerebral metabolic rate of oxygen consumption (ΔCBF/ΔCMRO2) lead to the BOLD changes that are observed in older adults. ΔCBF/ΔCMRO2 was also significantly related to performance, suggesting that age-related cognitive slowing results from neural cell assemblies that operate less efficiently, requiring greater oxygen metabolism that is not matched by blood-flow changes relative to younger adults. Age-related changes in ΔCBF/ΔCMRO2 are sufficient to explain variations in BOLD responding and performance cited throughout the literature, assuming no bias based on physiological baseline CMRO2.

A view of a scene is often remembered as containing information that might have been present just beyond the actual boundaries of that view, and this is referred to as boundary extension. Characteristics of the view (e.g., scene or nonscene; close-up or wide-angle; whether objects are cropped, static, or in motion, emotionally neutral or emotionally charged), display (e.g., aperture shape and size; target duration; retention interval; whether probes of memory involve magnification/minification or change in physical distance), and observer (e.g., allocation of attention; age; planned fixation, gaze direction, and eye movements; monocular or binocular viewing; prior exposure; neurological correlates) that influence boundary extension are reviewed. Proposed mechanisms of boundary extension (perceptual, memory, or motion schema; extension-normalization; attentional selection; errors in source monitoring) are discussed, and possible relationships of boundary extension to other cognitive processes (e.g., representational momentum; remembered distance and remembered size; amodal completion; transsaccadic memory) are briefly addressed.

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Age-related performance declines in visual tasks have been attributed to reductions in processing efficiency. The neural basis of these declines has been explored by comparing the blood-oxygen-level-dependent (BOLD) index of neural activity in older and younger adults during visual task performance. However, neural activity is one of many factors that change with age and lead to BOLD signal differences. We investigated the origin of age-related BOLD changes by comparing blood flow and oxygen metabolic constituents of BOLD signal. Subjects periodically viewed flickering annuli and pressed a button when detecting luminance changes in a central fixation cross. Using magnetic resonance dualecho arterial spin labeling and CO 2 ingestion, we observed age-equivalent (i.e., similar in older and younger groups) fractional cerebral blood flow (∆CBF) in the presence of agerelated increases in fractional cerebral metabolic rate of oxygen (∆CMRO 2 ). Reductions in ∆CBF responsiveness to increased ∆CMRO 2 in elderly led to paradoxical age-related BOLD decreases. Age-related ∆CBF/∆CMRO 2 ratio decreases were associated with reaction times, suggesting that age-related slowing resulted from less efficient neural activity. We hypothesized that reduced vascular responsiveness to neural metabolic demand would lead to a reduction in ∆CBF/∆CMRO 2 . A simulation of BOLD relative to ∆CMRO 2 for lower and higher neurometabolic-flow coupling ratios (approximating those for old and young, respectively) indicated less BOLD signal change in old than young in relatively lower CMRO 2 ranges, as well as greater BOLD signal change in young compared to old in relatively higher CMRO 2 ranges. These results suggest that age-comparative studies relying on BOLD signal might be misinterpreted, as age-related BOLD changes do not merely reflect neural activity changes. Age-related declines in neurometabolic-flow coupling might lead to neural efficiency reductions that can adversely affect visual task performance.

Gulf War Illness is associated with toxic exposure to cholinergic disruptive chemicals. The cholinergic system has been shown to mediate the central executive of working memory (WM). The current work proposes that impairment of the cholinergic system in Gulf War Illness patients (GWIPs) leads to behavioral and neural deficits of the central executive of WM. A large sample of GWIPs and matched controls (MCs) underwent functional magnetic resonance imaging during a varied-load working memory task. Compared to MCs, GWIPs showed a greater decline in performance as WM-demand increased. Functional imaging suggested that GWIPs evinced separate processing strategies, deferring prefrontal cortex activity from encoding to retrieval for high demand conditions. Greater activity during high-demand encoding predicted greater WM performance. Behavioral data suggest that WM executive strategies are impaired in GWIPs. Functional data further support this hypothesis and suggest that GWIPs utilize less effective strategies during high-demand WM.