Andrew J. Aschenbrenner

TL;DR: The results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection, and support models of Alzheimer disease staging that suggest that elevated β-amyloid alone may be insufficient to produce cognitive change in individuals at risk for AD.

TL;DR: A randomized, placebo-controlled, multi-arm trial of gantenerumab or solanezumab in participants with DIAD across asymptomatic and symptomatic disease stages was conducted in this paper.

TL;DR: It is demonstrated that tau PET binding is elevated in symptomatic individuals with dominantly inherited Alzheimer's disease, and amyloid-β was increased in both asymptomatic and symptomatic groups relative to non-carriers and was correlated to other biomarkers, particularly markers of neurodegeneration.

TL;DR: Overall cognitive and personality deficits in very mild ADAD are similar to those seen in sporadic AD and differences in the relation between 3 measures indicate that cognitive deficits on some measures can be detected in mutation carriers prior to symptomatic AD, and hence should be useful markers in subsequent longitudinal follow-up.

TL;DR: This work reanalyzed data from 3 published studies to determine if previous trial history moderated the additive pattern when semantic priming was not also manipulated, and showed how a common transformation used in linear mixed effects analyses to normalize the residuals can systematically alter the way in which two variables combine to influence performance.