Antidepresivi nemaju učinak u svih bolesnika na simptome depresije, uključujući i kognitivne simptome. Za sada ne postoje pouzdani predskazatelji učinka antidepresiva, a jedan od kandidata je moždani neurotrofni čimbenik (BDNF). Njegova je koncentracija snižena u depresivnih bolesnika, dok neki antidepresivi povisuju koncentraciju BDNF-a. Ovo prospektivno, randomizirano, longitudinalno istraživanje uključilo je 121 depresivnog bolesnika, među kojima je 61 bolesnik liječen vortioksetinom, a 60 escitalopramom. Nakon 4 tjedna terapije, unatoč podjednakom poboljšanju simptoma depresije, vortioksetin je izazvao porast koncentracije BDNF-a u plazmi, dok uz terapiju escitalopramom nije zapažena promjena. Oba antidepresiva podjednako su ublažila kognitivnu disfunkciju, osim što escitalopram nije pokazao učinak na testu pažnje. Nadalje, escitalopram je izazvao veći pad koncentracije trombocitnog serotonina u usporedbi s vortioksetinom, pri čemu je veći pad koncentracije serotonina predvidio dobar odgovor na escitalopram. Oba lijeka nisu značajno utjecala na aktivnost trombocitne MAO-B. Rezultati istraživanja upućuju na razlike u biološkom učinku escitaloprama i vortioksetina, koje mogu biti povezane i s kliničkim učinkom. Istraživanje predstavlja doprinos razumijevanju mehanizma djelovanja antidepresiva i naglašava potrebu individualnog pristupa u liječenju.
Antidepressants are not effective in all patients in treating depressive symptoms, as well as cognitive dysfunction. So far, there are no established predictors of treatment response, and brain derived neurotrophic factor (BDNF) is potential biomarker candidate. While its concentration has been decreased in depressed patients, some antidepressants increase BDNF levels. This prospective, randomized, longitudinal study included 121 patients with depression: 61 patients were treated with vortioxetine and 60 with escitalopram. After 4 weeks of treatment, despite similar improvement in depressive symptoms, vortioxetine increased plasma BDNF concentration, while escitalopram had no effects. Escitalopram induced larger reduction in platelet serotonin concentration than vortioxetine, whereas greater decrease in serotonin concentration predicted better response to escitalopram. Both antidepressants produced similar improvement of cognitive symptoms, although escitalopram has not affected attention. Both antidepressants have not changed platelet MAO-B activity. Our findings suggest different biological effects of escitalopram and vortioxetine, which may be associated with clinical outcome. This research contributes to better understanding of antidepressant mechanism of action and emphasizes the need for personalized treatment approach.