Introduction: Alzheimers Disease (AD) is a multifactorial disease. The hypothalamo-pituitaryadrenal (HPA)-axis shows extensive changes in AD. It is observed a hyperactivation of corticotropin-releasing hormone (CRH) neurons with age, which is significantly present in men. The aim of this study is to compare serum levels of cortisol in patients with Alzheimers disease and normal controls.
Material and Methods: Ninety patients with AD and 95 normal controls matched for age and gender were included. The diagnosis of Alzheimer dementia was based on standard criteria provided by the DSM-IV TR system and the NINDS-ADRDA. Blood samples were frozen at −80°C until analysis. Cortisol levels were measured using a commercial routine immunoassay (electrochemiluminescent assay, ECLIA). Differences in cortisol levels were assessed between the two groups using the MannWhitney method. Linear regression analysis was also used to adjust for characteristics shown to be associated with cortisol and cognitive decline. These characteristics were sex, age, weight and smoking. The significant level was set at P<0.05.
Results: From the patients with AD, 74 were women and 16 were men (mean age 80.53±6.03, mean body weight 71.49±8.33) and from the control group 78 were women and 17 men (mean age 79.27±6.86, mean body weight 70.23±6.73).
Serum cortisol levels were significantly higher in patients with AD compared to normal controls (16.95±9.53 in AD patients vs 9.90±5.49 in normal controls, P<0.001, MannWhitney U).
Conclusions: The study showed that patients with AD have high serum cortisol levels. Because of the inhibitory control of the hippocampus on the HPA-axis, damage to this structure was expected to disinhibit the HPA-axis, and to cause a positive feedforward cascade of increasing glucocorticoid levels over time. This glucocorticoid cascade hypothesis of stress and hippocampal damage was proposed to be causally involved in age-related accumulation of hippocampal damage in disorders like Alzheimers disease.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology