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BOLD variability, which measures moment-to-moment fluctuations in brain signal, is sensitive to age differences in cognitive performance. However, the effect of aging on BOLD variability in the context of different cognitive demands is still unclear. The current study examined how aging affects brain variability across cognitive loads and the contribution of BOLD variability to working memory abilities. Participants (N = 149, ages 20‒86) completed an fMRI n-back paradigm with 3 loads and 10-minute resting state scan. We found that BOLD variability was greater during rest compared to task and decreased even further as n-back load increased. Older age was associated with smaller load-related modulations of BOLD variability in default mode and fronto-parietal control networks. Increased variability in default mode, fronto-parietal control, and limbic regions and decreased variability in sensori-motor regions during the n-back task was associated with better working memory performance, regardless of age. Our findings suggest that working memory reductions in older ages are related to failure of core cognitive control and default mode regions to modulate dynamic range of activity in the face of increased demands., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Healthy aging is accompanied by reduced cognitive control and widespread alterations in the underlying brain networks; but the extent to which large-scale functional networks in older age show reduced specificity across different domains of cognitive control is unclear. Here we use cov-STATIS (a multi-table multivariate technique) to examine similarity of functional connectivity during different domains of cognitive control-inhibition, initiation, shifting, and working memory-across the adult lifespan. We report two major findings: (1) Functional connectivity patterns during initiation, inhibition, and shifting were more similar in older ages, particularly for control and default networks, a pattern consistent with dedifferentiation of the neural correlates associated with cognitive control; and (2) Networks exhibited age-related reconfiguration such that frontal, default, and dorsal attention networks were more integrated whereas sub-networks of somato-motor system were more segregated in older age. Together these findings offer new evidence for dedifferentiation and reconfiguration of functional connectivity underlying different aspects of cognitive control in normal aging., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Both younger and older adults prioritize reward-associated stimuli in memory, but there has been little research on possible age differences in the neural mechanisms mediating this effect. In the present study, we examine neural activation and functional connectivity in healthy younger and older adults to test the hypothesis that older adults would engage prefrontal regions to a greater extent in the service of reward-enhanced memory. While undergoing MRI, target stimuli were presented after high- or low-reward cues. The cues indicated the reward value for successfully recognizing the stimulus on a memory test 24 hours later. We replicated prior findings that both older and younger adults had better memory for high- compared to low-reward stimuli. Critically, in older but not younger adults, this enhanced subsequent memory for high-reward items was supported by greater connectivity between the caudate and bilateral inferior frontal gyrus. The findings add to the growing literature on motivation-cognition interactions in healthy aging and provide novel findings of the neural underpinnings of reward-motivated encoding., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Recent evidence has shown that older adults fail to show adaptation in the right fusiform gyrus (FG) to the same face presented repeatedly, despite accurate detection of the previously presented face. We used functional magnetic resonance imaging to investigate whether this phenomenon is associated with age-related reductions in face specificity in brain activity and whether older adults compensate for these face-processing deficiencies by increasing activity in other areas within the face-processing network, or outside this network. A comparison of brain activity across multiple stimulus categories showed that, unlike young adults who engaged a number of brain regions specific to face processing, older adults generalized these patterns of activity to objects and houses. Also, young adults showed functional connectivity between the right FG and its homologous region during face processing, whereas older adults did not engage the left FG but showed a functional connection between the right FG and left orbitofrontal cortex. Finally, this frontotemporal functional connection was activated more strongly in older adults who performed better on a face-matching task (done outside of the scanner), suggesting increased involvement of this functional link for successful face recognition with increasing age. These findings suggest that 2 neural mechanisms, dedifferentiation and compensatory neural recruitment, underlie age differences in face processing., (Copyright © 2013 Elsevier Inc. All rights reserved.)

A PET study of patients with Alzheimer's disease (AD) engaged in a delayed match-to-sample face recognition task revealed that performance declines as a function of increasing delay, a pattern accompanied by reduced functional connectivity of prefrontal cortex but increased connectivity of the left amygdala. Here, we characterize the changes in interactions within this amygdalar circuit across the memory delays using structural equation modeling. The magnitude of effective connections was found to be much greater in the patients than in the controls, notably from the left amygdala to left inferior prefrontal cortex, which, in turn, influenced its right homologue. The influence from the amygdala to the left hippocampus, in contrast, was not strong in either group. We interpret this pattern of interactions as possibly reflecting the compensatory recruitment of a dynamic neural network, perhaps involved in implicit emotional processing, in the context of a faulty executive maintenance and retrieval system., ((c) 2008 Elsevier Inc. All rights reserved.)

Behaviour and fMRI brain activation patterns were compared during encoding and recognition tasks in mild cognitive impairment (MCI) (n=14) and normal controls (NC) (n=14). Deep (natural vs. man-made) and shallow (color vs. black and white) decisions were made at encoding and pictures from each condition were presented for yes/no recognition 20 min later. MCI showed less inferior frontal activation during deep (left only) and superficial encoding (bilaterally) and in both medial temporal lobes (MTL). When performance was equivalent (recognition of words encoded superficially), MTL activation was similar for the two groups, but during recognition testing of deeply encoded items NC showed more activation in both prefrontal and left MTL region. In a region of interest analysis, the extent of activation during deep encoding in the parahippocampi bilaterally and in left hippocampus correlated with subsequent recognition accuracy for those items in controls but not in MCI, which may reflect the heterogeneity of activation responses in conjunction with different degrees of pathology burden and progression status in the MCI group.

The goal of the current study was to determine whether Alzheimer's disease (AD) pathology affects the limbic system of men and women differently as measured by in vivo neuroimaging. Magnetic resonance imaging (MRI) and coregistered single photon emission computed tomography (SPECT) were used to examine the limbic system in 20 men and 20 women with probable AD compared to 40 age- and education-matched normal controls (20 men, 20 women). Limbic volumes and relative perfusion values were obtained from the MR images and coregistered SPECT scans, respectively. No significant differences were found between sexes in limbic volumes or relative perfusion values in the normal controls. Many limbic regions were significantly affected in both men and women with AD compared to normal controls. However, only the men with AD displayed atrophy in the orbitofrontal cortex, middle and posterior cingulate cortices, hypothalamus, and mamillary bodies, and relative hypoperfusion in the anterior and middle cingulate cortices. Women with AD exclusively showed anterior thalamic atrophy. Separating men and women did not substantially improve diagnostic classification.

Changes in regional cerebral blood flow (rCBF) associated with a face-matching task were examined using positron emission tomography (PET) and H2(15)O in 7 patients with mild-moderate dementia of the Alzheimer type (DAT) and in 8 healthy age-matched controls. rCBF was normalized to whole brain flow and pixel-by-pixel difference images were computed by contrasting flow during a control task to flow during face matching. Both patients and controls showed bilateral rCBF increases in occipitotemporal extrastriate cortex during face matching. The magnitude of these increases was not significantly different between the groups. In addition, the patients showed greater rCBF activation in regions of occipital and frontal cortex. These results show that early in the course of DAT, patients utilize extrastriate cortex to perform a visuoperceptual task, as do control subjects but also show rCBF increases in additional cortical areas. Activation of these additional areas of cortex in the patients may reflect an increased attentional load during face matching due to their reduced cognitive capacity.

Recent evidence suggests that Alzheimer's disease is an etiologically heterogeneous disorder. A human model of Alzheimer's disease exists that avoids such problems of etiologic heterogeneity. Down syndrome (DS), trisomy 21, is a genetic disorder in which an extra portion of chromosome 21 leads to mental retardation, short stature, and phenotypic abnormalities. Prior investigations by others have shown that DS subjects over 40 years of age demonstrate neuropathologic and neurochemical defects postmortem that are virtually indistinguishable from those found in brains of Alzheimer's disease patients and a universal cognitive deterioration more severe in demented than nondemented older DS subjects. In our study, these nondemented older DS subjects show a distinctive pattern of age-related deficits, while a more global pattern is seen in demented older DS subjects. Dementia occurs in 40% of older DS subjects. We find that in older demented DS subjects positron emission tomography (PET) shows identical patterns of abnormal glucose metabolism as those described previously in Alzheimer's disease patients, selectively involving the phylogenetically newer association areas of parietal and temporal neocortices but sparing primary sensory and motor regions. Further, we find in older demented DS patients quantitative computer-assisted tomography (CT) indicates accelerated neuronal loss and brain atrophy, similar to that previously shown in Alzheimer's disease patients. As a potential use of the DS model, we observed a case of DS with dementia but without mental retardation. This case suggests that expression of dementia in DS may involve genes on chromosome 21 other than in the "obligatory" distal segment of the q arm. Alternatively, differential expression of genes on the q arm of chromosome 21 might cause dementia without phenotypic features and mental retardation.