One mechanism that has been hypothesized to contribute to older adults’ changes in cognitive performance is goal neglect or impairment in maintaining task set across time. Mind-wandering and task-unrelated thought may underlie these potential age-related changes. The present study investigated age-related changes in mind-wandering in three different versions of the Sustained Attention to Response task (SART), along with self-reported mind-wandering during a reading for comprehension task. In the SART, both younger and older adults produced similar levels of faster reaction times before No-Go errors of commission, whereas, older adults produced disproportionate post-error slowing. Subjective self-reports of mind-wandering recorded during the SART and the reading task indicated that older adults were less likely to report mind-wandering than younger adults. Discussion focuses on cognitive and motivational mechanisms that may account for older adults’ relatively low levels of reported mind-wandering.

Objectives: Amyloid-beta (Aβ) and tau pathologies are commonly observed among clinically normal older individuals at postmortem and can now be detected with in vivo neuroimaging. The association and interaction of these proteinopathies with prospective cognitive decline in normal aging and preclinical Alzheimer's disease (AD) remains to be fully elucidated. Methods: One hundred thirty-seven older individuals (age = 76.3 AE 6.22 years) participating in the Harvard Aging Brain Study underwent Aβ ( 11 C-Pittsburgh compound B) and tau ( 18 F-flortaucipir) positron emission tomography (PET) with prospective neuropsychological assessments following PET imaging (mean number of cognitive visits = 2.8 AE 1.1). Tau and Aβ PET measures were assessed in regions of interest (ROIs) as well as vertex-wise map analyses. Cognitive change was evaluated with Memory and Executive Function composites. Results: Higher levels of Aβ and tau were both associated with greater memory decline, but not with change in executive function. Higher cortical Aβ was associated with higher tau levels in all ROIs, independent of age, and very elevated levels of tau were observed primarily in clinically normal with elevated Aβ. A significant interaction between tau and Aβ was observed in both ROI and map-level analyses, such that rapid prospective memory decline was observed in participants who had high levels of both pathologies. Interpretation: Our results are consistent with the supposition that both Aβ and tau are necessary for memory decline in the preclinical stages of AD. These findings may be relevant for disambiguating aging and early cognitive manifestations of AD, and to inform secondary prevention trials in preclinical AD.

Introduction Sensitive detection of cognitive decline over the course of preclinical Alzheimer’s disease is critical as the field moves toward secondary prevention trials. Methods We examined Aβ-related change in several variations of the preclinical Alzheimer cognitive composite (PACC) and each individual PACC component in clinically normal (CN) older participants in the Harvard Aging Brain Study. We then examined the PACC variations in the Alzheimer’s Disease Cooperative Study Prevention Instrument Study as a replication cohort. Results Aβ+ CN individuals demonstrated longitudinal decline on all individual PACC components and all PACC variations. Aβ group differences emerged earlier when Free and Cued Selective Reminding Test Free Recall was included in the PACC. PACC decline was associated with Clinical Dementia Rating progression. Discussion This independent data set and a replication cohort confirm the ability of the PACC to capture both early and late cognitive decline during the preclinical stages of Alzheimer’s disease, which may prove advantageous in the prevention trial design.