Wiesław Jerzy Cubała1, Jerzy Landowski2. 1. Department of Psychiatry, Medical University of Gdańsk, Gdańsk 80-952, Poland. Electronic address: cubala@gumed.edu.pl. 2. Department of Psychiatry, Medical University of Gdańsk, Gdańsk 80-952, Poland.
Abstract
BACKGROUND: Altered monoamine neurotransmission accompanied by hypothalamic-pituitary-adrenal axis dysfunction and autonomic nervous system hyperactivity have been associated with major depressive disorder (MDD). Salivary α-amylase (sAA) is indicative of autonomic activation and reflects central noradrenergic activity. Scarce studies on sAA in MDD produce confounded results and no data is available regarding baseline sAA activity. METHODS: The basal, non-stimulated sAA activity was studied in this cross-sectional case-control study on 20 non-late-life adult, short-illness-duration first-episode, treatment-naïve MDD patients and in 20 age- and sex-matched healthy controls. Depressed patients showed a basal score in the Hamilton Rating Scale for Depression (HAMD-17) higher than 20. RESULTS: The sAA was significantly lower in depressed individuals as compared to controls (p=0.011). In post hoc analysis significantly lower sAA was present in melancholic MDD (p=0.016) as related to controls whereas no difference was seen between non-melancholic MDD patients and controls. The sAA activity was not significantly correlated neither with duration nor the severity of depressive symptoms as measured by the total HAMD-17 score. LIMITATIONS: The current study is limited by its cross-sectional design, small sample size, and factors related to saliva sampling methodology. CONCLUSION: Low baseline sAA levels were found in MDD in basal, non-stimulated conditions. The study provides no support for elevated sAA in drug-naïve patients with short-illness-duration first episode MDD. The results support the evidence for decreased central noradrenergic transmission in MDD when sAA activity is considered indicative of central noradrenergic function.
BACKGROUND: Altered monoamine neurotransmission accompanied by hypothalamic-pituitary-adrenal axis dysfunction and autonomic nervous system hyperactivity have been associated with major depressive disorder (MDD). Salivary α-amylase (sAA) is indicative of autonomic activation and reflects central noradrenergic activity. Scarce studies on sAA in MDD produce confounded results and no data is available regarding baseline sAA activity. METHODS: The basal, non-stimulated sAA activity was studied in this cross-sectional case-control study on 20 non-late-life adult, short-illness-duration first-episode, treatment-naïve MDDpatients and in 20 age- and sex-matched healthy controls. Depressedpatients showed a basal score in the Hamilton Rating Scale for Depression (HAMD-17) higher than 20. RESULTS: The sAA was significantly lower in depressed individuals as compared to controls (p=0.011). In post hoc analysis significantly lower sAA was present in melancholic MDD (p=0.016) as related to controls whereas no difference was seen between non-melancholic MDDpatients and controls. The sAA activity was not significantly correlated neither with duration nor the severity of depressive symptoms as measured by the total HAMD-17 score. LIMITATIONS: The current study is limited by its cross-sectional design, small sample size, and factors related to saliva sampling methodology. CONCLUSION: Low baseline sAA levels were found in MDD in basal, non-stimulated conditions. The study provides no support for elevated sAA in drug-naïve patients with short-illness-duration first episode MDD. The results support the evidence for decreased central noradrenergic transmission in MDD when sAA activity is considered indicative of central noradrenergic function.