Cortisol and TNF-soluble receptor levels and 1-year cognitive and functional performance in a community-based sample of the oldest Brazilian elderly: The Pietà Study

Inflammation has a putative involvement in the pathogenesis of several degenerative diseases. There is preliminary clinical evidence pointing to a possible role for both cortisol and TNF signaling pathway in progressive cognitive decline. In this regard, however, data from community-based elderly is still very scarce. We conducted a community based survey of cognitive and neuropsychiatric disorders in Caete, a small town in southeast Brazil. A total of 639 participants gave written informed consent and completed the main evaluations from the study protocol, of which 359 gave blood samples for serum biomarker analysis. Among several routine laboratory tests, we measured BDNF, TFN, TNF soluble receptors (sTNFR) type 1 and 2, and basal cortisol levels. Cognitive status was ascertained through an expert consensus panel. Participants were divided into three groups: dementia, cognitive impairment not dementia (CIND), and those without cognitive impairment (WCI). One year later 199 participants without dementia agreed to be reevaluated according to the same protocol. Multiple regression analysis in the reevaluation sample disclosed no associations between baseline laboratory data and worsening performance in any cognitive tests or functional measurement. In the CIND group, cortisol levels correlated with MMSE (rho= -0,33; p=0,015) and Functional Assessment Questionnaire decline (rho=-0,30; p=0,038). sTNFR1 levels correlated with worsening category fluency test performance (rho=0,31; p=0,029). Even though the magnitude of the associations was generally weak, in the CIND group we did found significant relationships between cortisol and sTNFR1 levels, and prospective cognitive and functional outcomes, which might encourage further research in the field.