학술논문
Association of latent factors of neuroinflammation with Alzheimer's disease pathology and longitudinal cognitive decline
Document Type
article
Author
Stefan J. Teipel; Martin Dyrba; Luca Kleineidam; Frederic Brosseron; Fedor Levin; Davide Bruno; Katharina Buerger; Nicoleta Cosma; Luisa‐Sophie Schneider; Emrah Düzel; Wenzel Glanz; Klaus Fliessbach; Daniel Janowitz; Ingo Kilimann; Christoph Laske; Matthias H. Munk; Franziska Maier; Oliver Peters; Nunzio Pomara; Robert Perneczky; Boris‐Stephan Rauchmann; Josef Priller; Alfredo Ramirez; Nina Roy; Anja Schneider; Annika Spottke; Eike J. Spruth; Sandra Roeske; Michael Wagner; Jens Wiltfang; Steffen Wolfsgruber; Claudia Bartels; Frank Jessen; Michael T. Heneka; for the DELCODE study group and the Alzheimer´s Disease Neuroimaging Initiative
Source
Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring, Vol 16, Iss 1, Pp n/a-n/a (2024)
Subject
Language
English
ISSN
2352-8729
Abstract
Abstract INTRODUCTION We investigated the association of inflammatory mechanisms with markers of Alzheimer's disease (AD) pathology and rates of cognitive decline in the AD spectrum. METHODS We studied 296 cases from the Deutsches Zentrum für Neurodegenerative Erkrankungen Longitudinal Cognitive Impairment and Dementia Study (DELCODE) cohort, and an extension cohort of 276 cases of the Alzheimer's Disease Neuroimaging Initiative study. Using Bayesian confirmatory factor analysis, we constructed latent factors for synaptic integrity, microglia, cerebrovascular endothelial function, cytokine/chemokine, and complement components of the inflammatory response using a set of inflammatory markers in cerebrospinal fluid. RESULTS We found strong evidence for an association of synaptic integrity, microglia response, and cerebrovascular endothelial function with a latent factor of AD pathology and with rates of cognitive decline. We found evidence against an association of complement and cytokine/chemokine factors with AD pathology and rates of cognitive decline. DISCUSSION Latent factors provided access to directly unobservable components of the neuroinflammatory response and their association with AD pathology and cognitive decline.