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http://crossmark.crossref.org/dialog/?doi=10.1007/s11682-016-9640-4&domain=pdf
Web End = http://crossmark.crossref.org/dialog/?doi=10.1007/s11682-016-9640-4&domain=pdf
Web End = Brain Imaging and Behavior (2017) 11:383390 DOI 10.1007/s11682-016-9640-4
SI: RESILIENCE/RESERVE IN AD
Cognitive resilience in clinical and preclinical Alzheimers disease: the Association of Amyloid and Tau Burdenon cognitive performance
Dorene M. Rentz1,2 & Elizabeth C. Mormino1 & Kathryn V. Papp1,2 &
Rebecca A. Betensky3 & Reisa A. Sperling1,2,4 & Keith A. Johnson1,2,4,5
Published online: 13 October 2016# Springer Science+Business Media New York 2016
Abstract We explored the cross-sectional relationships between -amyloid (A) and inferior temporal tau deposition (IFT Tau) on cognitive performance and whether cognitive reserve (CR) modifies these associations. We studied 156 participants classified into groups of clinically normal (CN = 133), mild cognitive impairment (MCI = 17) and Alzheimer disease (AD = 6) dementia. AMNART IQ served as a proxy of CR and cognitive performance was assessed using the MMSE. In separate linear regression models predicting MMSE, we examined the interactions of CR x global A and CR x IFT tau across all participants and within the CN group alone. In the whole sample, the interaction between CR and IFT tau was significant (p < 0.003), such that higher CR participants with elevated IFT tau had better MMSE scores compared with low CR participants with similar levels of IFT tau. The interaction between CR and A status did not reach significance (p = 0.093). In CN only, no cross-sectional interactions among CR, A, and IFT tau were
observed on MMSE. These findings imply that CR may be protective against early AD processes and enable some individuals to remain cognitively stable despite elevated tau and A burden.
Keywords Aging .PreclinicalAlzheimersdisease .Amyloid PET imaging . Tau PET imaging . Resilience
Introduction
Advances in positron emission tomography (PET) using radiotracers that bind to -amyloid (A) has allowed for the in vivo detection of Alzheimers disease (AD) pathology in otherwise clinically normal (CN) older adults (Klunk et al. 2004). Based on this evidence, we now understand that AD includes a long preclinical stage whereby CN exhibit bio-marker abnormalities approximately 15 years prior to the onset of dementia (Bateman et al. 2012; Rowe et al. 2010; Sperling et al. 2011a). As the field moves toward the identification and treatment of individuals with preclinical AD (Sperling and Jack 2011b), the factors...