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Major depressive disorder (MDD) is a highly prevalent and devastating psychiatric illness with strong individual and societal burdens. However, biomarkers to improve the limited preventive and therapeutic approaches are scarce. Multilevel evidence suggests that the pathophysiological involvement of sphingolipids particularly increases the levels of ceramides and the ceramide hydrolyzing enzyme, acid sphingomyelinase. The activity of secretory acid sphingomyelinase (S-ASM) and routine blood parameters were determined in the serum of patients with current (unmedicated n = 63, medicated n = 66) and remitted (n = 39) MDD and healthy subjects (n = 61). Depression severity and anxiety and their 3-weeks prospective course of treatment were assessed by psychometric inventories. S-ASM activity was not different between the four groups, did not decrease during treatment, and was not lower in individuals taking medication that functionally inhibited ASM. However, S-ASM correlated positively with depression severity only in remitted patients. High enzyme activity at inclusion predicted milder clinician-evaluated and self-rated depression severity (HAM-D, MADRS, BDI-II) and state anxiety at follow-up, and was related to stronger improvement in these scores in medicated patients. S-ASM was strongly and contrariwise associated with serum lipids in unmedicated and medicated females. These findings contribute to a better understanding of the pathomechanisms underlying depression and the development of clinical strategies and biomarkers.

Major depressive disorder (MDD) is a highly prevalent and devastating psychiatric illness with strong individual and societal burdens. However, biomarkers to improve the limited preventive and therapeutic approaches are scarce. Multilevel evidence suggests that the pathophysiological involvement of sphingolipids particularly increases the levels of ceramides and the ceramide hydrolyzing enzyme, acid sphingomyelinase. The activity of secretory acid sphingomyelinase (S-ASM) and routine blood parameters were determined in the serum of patients with current (unmedicated n = 63, medicated n = 66) and remitted (n = 39) MDD and healthy subjects (n = 61). Depression severity and anxiety and their 3-weeks prospective course of treatment were assessed by psychometric inventories. S-ASM activity was not different between the four groups, did not decrease during treatment, and was not lower in individuals taking medication that functionally inhibited ASM. However, S-ASM correlated positively with depression severity only in remitted patients. High enzyme activity at inclusion predicted milder clinician-evaluated and self-rated depression severity (HAM-D, MADRS, BDI-II) and state anxiety at follow-up, and was related to stronger improvement in these scores in medicated patients. S-ASM was strongly and contrariwise associated with serum lipids in unmedicated and medicated females. These findings contribute to a better understanding of the pathomechanisms underlying depression and the development of clinical strategies and biomarkers.

Background Effects of depression on parenting and on cognitive development of newborns are augmented when symptoms continue throughout the first postnatal year. Current classification systems recognize maternal depression as postnatal if symptoms commence within four to six weeks. Traditional cultural rituals in Sudan offer new mothers adequate family support in the first 6–8 weeks postpartum. The course of postnatal depression symptoms beyond that period is not explored in such settings. We therefore aim to investigate the change in screening status and in severity of depression and distress symptoms between three and eight months postpartum among a sample of Sudanese women using the Edinburgh Postnatal Depression Scale (EPDS) and a locally used tool: the 10-items Hopkins Symptoms Checklist (HSCL-10). Methods Three hundred pregnant women in their 2nd or 3rd trimester were recruited from two clinics in Khartoum state. They were followed up and screened for depression symptoms eight months after delivery by EPDS at ≥12, and by HSCL-10 at ≥1.85. The same sample was previously screened for depression at three months after birth. Results Prevalence of postnatal depression symptoms by EPDS was lower at eight months compared to three months after birth (3.6% at eight months (8/223) compared to 9.2% at three months (22/238), p