 Abstract background Alzheimer's disease, AD, pathology impairs cognitive function, yet some individuals with high amounts of AD pathology show little impairment. Why is this? One proposed explanation is cognitive reserve, factors that confer resilience against or compensation for the effects of AD pathology. Deep non-rapid eye movement, NIM, slow wave sleep, SWS, is recognized to enhance functions of learning and memory in healthy older adults. However, whether the quality of NIM SWS, NIM slow wave activity, SWA, represents a novel cognitive reserve factor in older adults with AD pathology, thereby providing compensation against memory dysfunction otherwise caused by high AD pathology burden, remains unknown. Methods here, we tested this hypothesis in cognitively normal older adults, N equals 62, by combining 11C, PIB, Pittsburgh Compound B, positron emission tomography, PET, scanning for the quantification of beta amyloid, A, with sleep electroencephalography, EEG, recordings to quantifying RAM SWA and a hippocampal dependent. This article was authored by Zofia Zavec, Vioma Tisha, Olivia G. Morello and others. We are article.tv, links in the description below.