This study investigated the leukocyte T helper and T suppressor‐cytotoxic cell (sub)set profile of minor, simple major and melancholic depressives versus normal controls. Using both monoclonal antibody staining and flow cytometry, we determined the absolute numbers and percentages of the following T cell immune subsets: T helper (CD4 + ), T virgin (CD4 + CD45 + ), T memory (CD4 + CD45 ‐ ), T suppressor/cytotoxic (CD8 + ), CD8 + T suppressor (CD8 + CD57 ‐ ) and CD8 + T cytotoxic (CD8 + CD57 + ) cells. After computing the CD4 + /CD8 + ratio, we detected a significantly increased ratio in depressed patients as compared with healthy controls. Depression per se is characterized by a higher percentage of CD4 + and a lower percentage of CD8 + CD57 ‐ cells. Melancholic depressed subjects exhibit a significantly increased number of CD4 + and CD4 + CD45 ‐ cells. The combined use of various percentages of CD4 + and CD8 + (sub)sets yields a high degree of marker positivity for melancholia: through cumulative evaluation of those percentages, the marker positivity increases to 68% (sensitivity) and the specificity is 95%. These results together with our previous reports may refer to a depression‐related state of T cell activation.
Recent schizophrenia (SCZ) research aims to establish biomarkers with high predictive value for the diagnosis, severity of illness or treatment resistance. SCZ is accompanied by activated immune-inflammatory pathways, including increased levels of cytokines and chemokines, but few studies tried to identify predictive properties of such measures.We included 54 medicated SCZ patients and 118 healthy controls and examined 15 cytokines and chemokines. Possible associations between these immune-inflammatory biomarkers and the diagnosis of SCZ, severity of illness and treatment resistance were investigated.SCZ is associated with a specific cytokine - chemokine profile, i.e., increased CCL11, MIP-1α, sTNF-R1 and sTNF-R2 levels, and decreased levels of IP-10, TNF-α, IL-2 and IL-4. The combination of five biomarkers (sTNF-R1, sTNF-R2, CCL11, IP-10, IL-4) may predict the diagnosis of SCZ with a sensitivity of 70.0% and a specificity of 89.4%. There was a weak association between the negative symptoms and biomarkers, i.e., IL-2 (inversely) and CCL11 (positively). Patients with treatment resistance showed increased levels of sTNF-R1, sTNF-R2 and MCP-1.The findings of this study reinforce that SCZ is associated with a pro-inflammatory profile and suggest that some immune mediators may be used as reliable biomarkers for the diagnosis of SCZ and treatment resistance.
No precision medicine models of temporal lobe epilepsy (TLE) and associated mental comorbidities have been developed to date. This observational study aimed to develop a precision nomothetic, data-driven comorbid TLE model with endophenotype classes and pathway phenotypes that may have prognostic and therapeutical implications. We recruited forty healthy controls and 108 TLE patients for this research and assessed TLE and psychopathology (PP) features as well as oxidative stress (OSTOX, e.g., malondialdehyde or MDA, lipid hydroperoxides, and advanced oxidation protein products) and antioxidant (paraoxonase 1 or PON1 status, -SH groups, and total radical trapping potential or TRAP) biomarkers. A large part (57.2%) of the variance in a latent vector (LV) extracted from the above TLE and PP features was explained by these OSTOX and antioxidant biomarkers. The PON1 Q192R genetic variant showed indirect effects on this LV, which were completely mediated by PON1 activity and MDA. Factor analysis showed that a common core could be extracted from TLE, PP, OSTOX and antioxidant scores, indicating that these features are manifestations of a common underlying construct, i.e., a novel pathway phenotype of TLE. Based on the latter, we constructed a new phenotype class that is characterized by increased severity of TLE, PP and OSTOX features and lowered antioxidant defenses. A large part of the variance in episode frequency was explained by increased MDA, lowered antioxidant, and nitric oxide metabolite levels. In conclusion, (a) PP symptoms belong to the TLE phenome, and the signal increased severity; and (b) cumulative effects of aldehyde formation and lowered antioxidants determine epileptogenic kindling.
Purpose of review Efavirenz is currently regarded as an effective first-line treatment for HIV infection. It is therefore important that possible side effects are well investigated. Recent findings The most frequent adverse events of efavirenz are central nervous system symptoms, such as depressive symptoms, insomnia, vivid nightmares, headache, dizziness, fatigue and impaired concentration. Summary Future research should focus on the neuropsychiatric side effects of efavirenz and on the mechanisms by which efavirenz induces side effects.
Depression is prevalent in about 30% during the first 18 months post myocardial infarction (MI). Depression increases the risk of developing cardiac disease, in particular coronary artery disease and cardiac death. It is an independent risk factor for increased post MI cardiac morbidity and mortality, comparable with well-known risk factors such as hypercholesterolaemia. Both coronary artery disease and depressive disorder are highly prevalent and co-morbid, resulting in poor overall prognosis. Therefore understanding the relationship of both disorders, as well as the effects of treatment of depressive and cardiac functioning, is important, not only from the physical health and quality of life perspectives, but also from an economic perspective. In this paper we review the evidence indicating a pivotal role of inflammatory mediators as a common factor in the pathophysiology of MI, depression and cardiac mortality. The effects of antidepressant treatment on these inflammatory mediators in MI-related depression are reviewed.
