 Cognitive reserve against Alzheimer’s pathology is linked to brain activity during memory formationNiklas Vockert (),
Judith Machts,
Luca Kleineidam,
Aditya Nemali,
Enise I. Incesoy,
Jose Bernal,
Hartmut Schütze,
Renat Yakupov,
Oliver Peters,
Daria Gref,
Luisa Sophie Schneider,
Lukas Preis,
Josef Priller,
Eike Jakob Spruth,
Slawek Altenstein,
Anja Schneider,
Klaus Fliessbach,
Jens Wiltfang,
Ayda Rostamzadeh,
Wenzel Glanz,
Stefan Teipel,
Ingo Kilimann,
Doreen Goerss,
Christoph Laske,
Matthias H. Munk,
Annika Spottke,
Nina Roy,
Michael T. Heneka,
Frederic Brosseron,
Michael Wagner,
Steffen Wolfsgruber,
Laura Dobisch,
Peter Dechent,
Stefan Hetzer,
Klaus Scheffler,
Peter Zeidman,
Yaakov Stern,
Björn H. Schott,
Frank Jessen,
Emrah Düzel,
Anne Maass () and
Gabriel Ziegler ()
Nature Communications, 2024, vol. 15, issue 1, 1-16 Abstract: Abstract The cognitive reserve (CR) hypothesis posits that individuals can differ in how their brain function is disrupted by pathology associated with aging and neurodegeneration. Here, we test this hypothesis in the continuum from cognitively normal to at-risk stages for Alzheimer’s Disease (AD) to AD dementia using longitudinal data from 490 participants of the DELCODE multicentric observational study. Brain function is measured using task fMRI of visual memory encoding. Using a multivariate moderation analysis, we identify a CR-related activity pattern underlying successful memory encoding that moderates the detrimental effect of AD pathological load on cognitive performance. CR is mainly represented by a more pronounced expression of the task-active network encompassing deactivation of the default mode network (DMN) and activation of inferior temporal regions including the fusiform gyrus. We devise personalized fMRI-based CR scores that moderate the impact of AD pathology on cognitive performance and are positively associated with years of education. Furthermore, higher CR scores attenuate the effect of AD pathology on cognitive decline over time. Our findings primarily provide evidence for the maintenance of core cognitive circuits including the DMN as the neural basis of CR. Individual brain activity levels of these areas during memory encoding have prognostic value for future cognitive decline. Date: 2024 Downloads: (external link) Related works: Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-53360-9 Ordering information: This journal article can be ordered from DOI: 10.1038/s41467-024-53360-9 Access Statistics for this article Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie More articles in Nature Communications from Nature |
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