Zapater-Fajari, Mariola, Diaz-Galvan, Patricia, Cedres, Nira, Sterner, Therese Rydberg, Ryden, Lina, Sacuiu, Simona, Waern, Margda, Zettergren, Anna, Zetterberg, Henrik, Blennow, Kaj, Kern, Silke, Hidalgo, Vanesa, Salvador, Alicia, Westman, Eric, Skoog, Ingmar, Ferreira, Daniel, Zapater-Fajari, Mariola, Diaz-Galvan, Patricia, Cedres, Nira, Sterner, Therese Rydberg, Ryden, Lina, Sacuiu, Simona, Waern, Margda, Zettergren, Anna, Zetterberg, Henrik, Blennow, Kaj, Kern, Silke, Hidalgo, Vanesa, Salvador, Alicia, Westman, Eric, Skoog, Ingmar, and Ferreira, Daniel
Background Subjective cognitive decline (SCD) has gained recent interest as a potential harbinger of neurodegenerative diseases such as Alzheimer's disease (AD) and cerebrovascular disease (CVD). In addition, SCD can be related to depressive symptomatology. However, the association between AD and CVD biomarkers, depressive symptomatology, and SCD is still unclear. We investigated the association of AD and CVD biomarkers and depressive symptomatology with SCD in individuals with subjective memory complaints (SCD-memory group) and individuals with subjective concentration complaints (SCD-concentration group). Methods We recruited a population-based cohort of 217 individuals (all aged 70 years, 53% female participants, 119 SCD-memory individuals, 23 SCD-concentration individuals, and 89 controls). AD and CVD were assessed through cerebrospinal fluid levels of the A beta 42/40 ratio and phosphorylated tau, and white matter signal abnormalities on magnetic resonance imaging, respectively. Associations between biomarkers, depressive symptomatology, and SCD were tested via logistic regression and correlation analyses. Results We found a significant association between depressive symptomatology with SCD-memory and SCD-concentration. Depressive symptomatology was not associated with AD and CVD biomarkers. Both the phosphorylated tau biomarker and depressive symptomatology predicted SCD-memory, and the A beta 42/40 ratio and depressive symptomatology predicted SCD-concentration. Conclusions The role of depressive symptomatology in SCD may differ depending on the stage within the spectrum of preclinical AD (as determined by amyloid-beta and tau positivity), and does not seem to reflect AD pathology. Our findings contribute to the emerging field of subclinical depressive symptomatology in SCD and clarify the association of different types of subjective complaints with distinct syndromic and biomarker profiles.