High S100B Levels Predict Antidepressant Response in Patients With Major Depression Even When Considering Inflammatory and Metabolic Markers

Abstract

Background The relationship between antidepressant response and glial, inflammatory, and metabolic markers is poorly understood in depression. This study assessed the ability of biological markers to predict antidepressant response in major depressive disorder (MDD). Methods We included 31 MDD outpatients treated with escitalopram or sertraline for 8 consecutive weeks. The Montgomery-Asberg Depression Rating Scale (MADRS) was administered at baseline and at week 4 and 8 of treatment. Concomitantly, blood samples were collected for the determination of serum S100B, CRP, and HDL-C levels. Treatment response was defined as ≥50% improvement in the MADRS score from baseline to either week 4 or 8. Variables associated with treatment response were included in a linear regression model as predictors of treatment response. Results Twenty-seven patients (87%) completed 8 weeks of treatment; 74% and 63% were responders at week 4 and 8, respectively. High S100B and low HDL-C levels at baseline were associated with better treatment response at both time-points. Low CRP levels were correlated with better response at week 4. Multivariate analysis showed that high baseline S100B levels and low baseline HDL-C levels were good predictors of treatment response at week 4 (R 2=0.457, p=0.001), while S100B was at week 8 (R 2=0.239, p=0.011). Importantly, baseline S100B and HDL-C levels were not associated with depression severity and did not change over time with clinical improvement. Conclusions Serum S100B levels appear to be a useful biomarker of antidepressant response in MDD even when considering inflammatory and metabolic markers.

Peripheral S100B Protein Levels in Five Major Psychiatric Disorders: A Systematic Review

“…In the study by Navines et al (2022), patients with high baseline S100B levels significantly improved Montgomery Åsberg Depression Rating Scale scores compared to those with low S100B levels during pharmacotherapy with escitalopram or sertraline [ 79 ]. No correlation of S100B with ketamine treatment of drug-resistant depression was found [ 80 , 81 ], nor correlation with suicidal ideation in ketamine-treated patients [ 81 ].…”

“…Most of the studies reported a lack of correlation of S100B levels with symptoms severity using different clinical scales: Hamilton Depression Rating Scale (HDRS) [ 59 , 60 , 62 , 65 , 72 , 73 , 74 , 77 , 78 ], Clinical Global Impression (CGI), Mini-Mental State Examination (MMSE) [ 72 ]. Quick Inventory of Depressive Symptomatology Self-Report (QIDS-SR) [ 82 ], Beck Depression Inventory (BDI) [ 61 ], Hamilton Anxiety Scale (HAMA) scores [ 59 ], and Montgomery Åsberg Depression Rating Scale (MADRS) [ 79 ].…”

“…We can notice high heterogeneity of the studied groups (with regard to diagnosis, duration of the illness, and drug status: drug-naïve/free or medicated), as well as different pharmacological, non-pharmacological, or adjuvant interventions. In most of the reports, a decrease [ 12 , 19 , 45 , 47 , 48 , 49 ] or no differences [ 13 , 15 , 23 , 32 , 33 , 39 , 41 , 42 , 43 , 44 , 45 , 46 , 58 , 62 , 64 , 65 , 67 , 77 ] in S100B concentration were reported, and some correlations of S100B with treatment response were found [ 73 , 78 , 79 ].…”

Serum Levels of S100B Protein and Myelin Basic Protein as a Potential Biomarkers of Recurrent Depressive Disorders

“…Being a highly organized structure and coordinating adaptive reactions, the brain tries to restore neuroplasticity by increasing S100B levels in persons with DD. However, the compensatory–restorative mechanism and neuroimmune functioning differ in patients with depression; therefore, some researchers report elevated S100B levels in patients with Affective Disorders [ 34 , 35 , 36 ]. Other authors show a decrease or no difference in the content of the S100B protein in the blood serum and in the cerebrospinal fluid of patients with Affective and Anxiety Disorders compared to mentally healthy individuals [ 19 , 37 , 38 , 39 , 40 ].…”

Recent advances in the study of sepsis-induced depression

“… [24] In clinical studies, the S100B level was found to be elevated in the serum and cerebrospinal fluid of patients with major depressive disorder. [25] , [26] Real-time in vivo two-photon microscopy revealed that depression model mice had significant leakage of a 40-kDa fluorophore-conjugated dextran into the perivascular region, implying a loss of BBB integrity. [27] Inflammatory factors were shown to cross the BBB and induce depression in polycystic ovary syndrome.…”