Low baseline salivary alpha-amylase in drug-naïve patients with short-illness-duration first episode major depressive disorder

AbstractBackground d 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. s sal, 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. s A 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. tions rrent study is limited by its cross-sectional design, small sample size, and factors related to saliva sampling methodology. sion seline 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.