Salivary interleukins are associated with cognitive function

Introduction: There is a need to accurately identify mild cognitive impairment (MCI) and diagnose dementia-causing diseases such as Alzheimer’s at an early stage. Saliva is an accessible and non-invasive biomarker. Studies have linked inflammatory salivary markers such as cortisol and cytokines to cognition in the context of neurodegenerative diseases. However, there are discrepancies in the literature, differences in methodology and study sample sizes are small. Aim: We aimed to test the feasibility of a simple saliva collection procedure amongst an older population and determine whether salivary cortisol, interleukin-6 (IL-6) and interleukin-1-beta (IL-1β) are associated with cognitive function. Method: The passive-drool method was used to collect saliva from 50 participants (age = 73 (70,77), which was analysed with cortisol, IL-6 and IL-1β ELISA kits (Salimetrics, State College, PA). The cognitive function of participants was assessed using the Montreal Cognitive Assessment (MoCA), adjusted for years in education. The data was analysed using the Mann-Whitney U test and multiple regression. Results: The median MoCA score was 73 (70,77). Median salivary levels were: cortisol 0.4 (0.3,0.6) µg/dL, IL-6 8.6 (3.9,23.1) pg/mL and IL-1β 997.4 (376.9,1929.8) pg/mL. There was no significant difference between participants classified as cognitively normal (n = 30) and MCI (n = 20) in levels of salivary cortisol (U = 299, p = 0.922), IL-6 (U = 261, p = 0.919) or IL-1β (U = 261, p = 0.634). However, multiple regression with all salivary biomarkers and age as covariates showed that adjusted MoCA scores had a significant negative association with salivary IL-6 levels (b = -0.009, t = -2.630, p = 0.019). Conclusion: The results from this feasibility and pilot study indicate that salivary IL-6 levels increase with decreasing cognitive function. This finding needs to be confirmed using a larger sample, but this may help to develop alternative diagnostic and therapeutic pathways for dementia-causing diseases.