Pilot Assessment of Salivary Cortisol Levels as a Marker for Depression in Patients with Parkinson Disease (P3.060)

Objective: To assess the utility of salivary cortisol measurements as a biomarker for depression in patients with Parkinson disease. Background: Parkinson disease (PD) causes several non-motor symptoms that negatively impact quality of life including depression. Due to symptom overlap, diagnosis may be delayed or missed and treatment is often ineffective. A useful biomarker for depression in PD could be of great utility. Salivary cortisol (SC) has been explored as a biomarker for depression in the general population but not in PD. Design/Methods: Over a period of one year, 3 subject groups were recruited: PD patients with depression (PDD), PD patients without depression (PDND), and healthy age-matched controls (C). Depression was identified by a score ≥1 on UPDRS part 1 and Beck Depression Inventory (BDI) ≥14. An State Trait Anxiety Inventory (STAI-T) score above the mean for our subject population identified positive anxiety symptoms. Subjects collected a morning and evening SC sample on three non-consecutive days. Subjects recorded their exercise, medications, and caffeine intake on days samples were taken. Results: 47 subjects participated: for the PDD group (n=20), mean SC levels were AM=0.533 mg/dL (±0.089 mg/dL), PM= .154 mg/dL (±0.042 mg/dL). PDND group (n=16), mean AM SC levels =0.511 mg/dL (±0.044 mg/dL), PM =0.086 mg/dL (±0.009 mg/dL). C group (n=11), mean AM SC levels=0.337 mg/dL (±0.054 mg/dL), PM =0.076 mg/dL (±0.015 mg/dL). No statistically significant group difference was found (F(2,44)=1.270, p=0.290). Similarly, treatment with antidepressants had no significant effect on AM or PM SC levels. Mean STAI-T scores were significantly higher in PDD=42.526 (±2.534) vs PDND=26.933 (±1.485), (t(32)=4.952, p=0.008), but presence of anxiety did not influence AM or PM SC levels. Conclusions: In this pilot study, SC samples collected by subjects at home did not correlate with depression or depression medication in a PD population. This is contrary to what has been reported regarding depression in a general population and may be due to the small sample size. Disclosure: Dr. Sweeney has nothing to disclose. Dr. Prusik has received research support from Jazz Pharmaceuticals. Dr. Molho has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Nerocrine Biosciences, Acadia Pharmaceuticals. Dr. Molho has received research support from Biotie, Civitas Therapeutics, Biogen, Kyowa Hakko Kirin.