Hearing impairment in older adults is independently associated in longitudinal studies with accelerated cognitive decline and incident dementia, and in cross-sectional studies, with reduced volumes in the auditory cortex. Whether peripheral hearing impairment is associated with accelerated rates of brain atrophy is unclear. We analyzed brain volume measurements from magnetic resonance brain scans of individuals with normal hearing versus hearing impairment (speech-frequency pure tone average > 25 dB) followed in the neuroimaging substudy of the Baltimore Longitudinal Study of Aging for a mean of 6.4 years after the baseline scan (n = 126, age 56–86 years). Brain volume measurements were performed with semi-automated region-of-interest (ROI) algorithms, and brain volume trajectories were analyzed with mixed-effects regression models adjusted for demographic and cardiovascular factors. We found that individuals with hearing impairment (n = 51) compared to those with normal hearing (n = 75) had accelerated volume declines in whole brain and regional volumes in the right temporal lobe (superior, middle, and inferior temporal gyri, parahippocampus, p < .05). These results were robust to adjustment for multiple confounders and were consistent with voxel-based analyses, which also implicated right greater than left temporal regions. These findings demonstrate that peripheral hearing impairment is independently associated with accelerated brain atrophy in whole brain and regional volumes concentrated in the right temporal lobe. Further studies investigating the mechanistic basis of the observed associations are needed.

In the first part of the reported research, 12 instrument-rated pilots flew a high-fidelity simulation, in which air traffic control presentation of auditory (voice) information regarding traffic and flight parameters was compared with advanced display technology presentation of equivalent information regarding traffic (cockpit display of traffic information) and flight parameters (data link display). Redundant combinations were also examined while pilots flew the aircraft simulation, monitored for outside traffic, and read back communications messages. The data suggested a modest cost for visual presentation over auditory presentation, a cost mediated by head-down visual scanning, and no benefit for redundant presentation. The effects in Part 1 were modeled by multiple-resource and preemption models of divided attention. In the second part of the research, visual scanning in all conditions was fit by an expected value model of selective attention derived from a previous experiment. This model accounted for 94% of the variance in the scanning data and 90% of the variance in a second validation experiment. Actual or potential applications of this research include guidance on choosing the appropriate modality for presenting in-cockpit information and understanding task strategies induced by introducing new aviation technology.

To develop targeted intervention strategies for the treatment of Alzheimer's disease, we first need to identify early markers of brain changes that occur before the onset of cognitive impairment. Here, we examine changes in resting-state brain function in humans from the Baltimore Longitudinal Study of Aging. We compared longitudinal changes in regional cerebral blood flow (rCBF), assessed by 15 O-water PET, over a mean 7 year period between participants who eventually developed cognitive impairment (n ϭ 22) and those who remained cognitively normal (n ϭ 99). Annual PET assessments began an average of 11 years before the onset of cognitive impairment in the subsequently impaired group, so all participants were cognitively normal during the scanning interval. A voxel-based mixed model analysis was used to compare groups with and without subsequent impairment. Participants with subsequent impairment showed significantly greater longitudinal rCBF increases in orbitofrontal, medial frontal, and anterior cingulate regions, and greater longitudinal decreases in parietal, temporal, and thalamic regions compared with those who maintained cognitive health. These changes were linear in nature and were not influenced by longitudinal changes in regional tissue volume. Although all participants were cognitively normal during the scanning interval, most of the accelerated rCBF changes seen in the subsequently impaired group occurred within regions thought to be critical for the maintenance of cognitive function. These changes also occurred within regions that show early accumulation of pathology in Alzheimer's disease, suggesting that there may be a connection between early pathologic change and early changes in brain function.