https://www.selleckchem.com/products/brd0539.html 0001) were significantly higher to the patient group compared to controls. Leptin levels were significantly decreased in the patient group six weeks after the initiation of antipsychotic treatment (mean change=-0.40, 95% CI=-0.59 to -0.21, W=666; p<0.0001) while those of adiponectin and resistin levels did not change significantly. In our study we found higher levels of adiponectin, leptin and resistin in drug-naïve, first-episode patients with normal Body Mass Index (BMI) compared to controls. After six weeks of antipsychotic treatment, there was no change in adiponectin and resistin levels, while leptin levels were reduced compared to baseline. In our study we found higher levels of adiponectin, leptin and resistin in drug-naïve, first-episode patients with normal Body Mass Index (BMI) compared to controls. After six weeks of antipsychotic treatment, there was no change in adiponectin and resistin levels, while leptin levels were reduced compared to baseline. Traumatic Brain Injury (TBI) has long-term devastating effects for which there is no accurate and effective treatment for inflammation and chronic oxidative stress. As a disease that affects multiple signalling pathways, the search for a drug with a broader spectrum of pharmacological action is of clinical interest. The fact that endocrine disruption (e.g hypogonadism) has been observed in TBI patients suggests that endogenous therapy with testosterone, or its more androgenic derivative, dihydrotestosterone (DHT), may attenuate, at least in part, the TBI-induced inflammation, but the underlying molecular mechanisms by which this occurs are still not completely clear. In this study, the main aim was to investigate proteins that may be related to the pathophysiological mechanism of TBI and also be pharmacological targets of DHT in order to explore a possible therapy with this androgen using network pharmacology. We identified 2.700 proteins related to TBI and 1.