The structural and social determinants of Alzheimer's disease related dementias.

INTRODUCTION: The projected growth of Alzheimer's disease (AD) and AD-related dementia (ADRD) cases by midcentury has expanded the research field and impelled new lines of inquiry into structural and social determinants of health (S/SDOH) as fundamental drivers of disparities in AD/ADRD. METHODS: In this review, we employ Bronfenbrenner's ecological systems theory as a framework to posit how S/SDOH impact AD/ADRD risk and outcomes. RESULTS: Bronfenbrenner defined the "macrosystem" as the realm of power (structural) systems that drive S/SDOH and that are the root cause of health disparities. These root causes have been discussed little to date in relation to AD/ADRD, and thus, macrosystem influences, such as racism, classism, sexism, and homophobia, are the emphasis in this paper. DISCUSSION: Under Bronfenbrenner's macrosystem framework, we highlight key quantitative and qualitative studies linking S/SDOH with AD/ADRD, identify scientific gaps in the literature, and propose guidance for future research. HIGHLIGHTS: Ecological systems theory links structural/social determinants to AD/ADRD. Structural/social determinants accrue and interact over the life course to impact AD/ADRD. Macrosystem is made up of societal norms, beliefs, values, and practices (e.g., laws). Most macro-level determinants have been understudied in the AD/ADRD literature.

The inter-trial effect of prepared but not executed antisaccades.

A preceding antisaccade increases the latency of the saccade in the next trial. Whether this inter-trial effect is generated by the preparation or the execution of the antisaccade is not certain. Our goal was to examine the inter-trial effects from trials on which subjects prepared an antisaccade but did not make one. We tested 15 subjects on blocks of randomly ordered prosaccades and antisaccades. An instructional cue at fixation indicated whether a prosaccade or antisaccade was required, with the target appearing 2 s later. On 20 % of antisaccade trials, the target did not appear (prepared-only antisaccade trials). We analyzed the latencies of all correct prosaccades or antisaccades preceded by correctly executed trials. The latencies of prosaccade trials were 15 ms shorter if they were preceded by prosaccades than if the prior trial was an antisaccade. Prosaccades preceded by trials on which antisaccades were cued but not executed also showed prolonged latencies that were equivalent to those preceded by executed antisaccades. We conclude that the inter-trial effects from a prior antisaccade are generated by its preparation rather than its execution. This may reflect persistence of pre-target preparatory activity from the prior trial to affect that of the next trial in structures like the superior colliculus and frontal eye field.