Abstract
RationaleN−3 polyunsaturated fatty acids (n−3 PUFA) influence multiple biochemical mechanisms postulated in the pathogenesis of schizophrenia that may influence BDNF synthesis.ObjectivesA randomized placebo-controlled study was designed to compare the efficacy of a 26-week intervention composed of either 2.2 g/day of n−3 PUFA or olive oil placebo, with regard to symptom severity in first-episode schizophrenia patients. The secondary outcome measure of the study was to describe the association between n−3 PUFA clinical effect and changes in peripheral BDNF levels.MethodsSeventy-one patients aged 16–35 were enrolled in the study and randomly assigned to the following study arms: 36 to the EPA + DHA group and 35 to the placebo group. Plasma BDNF levels were assessed three times, at baseline and at weeks 8 and 26 of the intervention. BDNF levels were determined in plasma samples using Quantikine Human BDNF ELISA kit. Plasma BDNF level changes were further correlated with changes in the severity of symptoms in different clinical domains.ResultsA significantly greater increase in plasma BDNF levels was observed in the intervention compared to the placebo group (Cohen’s d = 1.54). Changes of BDNF levels inversely correlated with change in depressive symptoms assessed using the Calgary Depression Rating Scale in Schizophrenia (Pearson’s r = − 0.195; p = 0.018).ConclusionsThe efficacy of a six-month intervention with n−3 PUFA observed in first-episode schizophrenia may be related to an increase in BDNF levels, which may be triggered by the activation of intracellular signaling pathways including transcription factors such as cAMP-reactive element binding protein.
Highlights
Neurodegenerative and neurodevelopmental hypotheses have been proposed to explain the pathogenesis of schizophrenia (SCZ)
Postmortem studies have revealed that the mRNA levels of Brain-derived neurotrophic factor (BDNF), those of its receptor tyrosine kinase B (TrkB), and those of BDNF protein levels are decreased in the brains of patients with schizophrenia in specific regions like the prefrontal cortex and hippocampus, which are crucial for disease pathophysiology (Sugai et al 2004; Thompson Ray 2011; Mohammadi et al 2018b)
Reduced peripheral levels of other neurotrophins, including nerve growth factor (NGF) and vascular growth factor (VEGF), have been described in SCZ patients. These observations have led to the formulation of the neurotrophin hypothesis of schizophrenia (SCZ), which postulates that the changes observed in the brains of SCZ patients occur as a result of disturbances in developmental processes involving neurotrophic factors (Lang et al 2004)
Summary
Neurodegenerative and neurodevelopmental hypotheses have been proposed to explain the pathogenesis of schizophrenia (SCZ) The latter proposes that SCZ develops due to disrupted developmental processes occurring in the brain, including the maturation and differentiation of neural cells, synaptic plasticity, and synaptogenesis. Brain-derived neurotrophic factor (BDNF) is one of the best studied and the most abundant members of the neurotrophin family in the adult brain It plays a crucial role in processes known to be disrupted in SCZ, including neuronal migration, differentiation, and cell survival. Reduced peripheral levels of other neurotrophins, including nerve growth factor (NGF) and vascular growth factor (VEGF), have been described in SCZ patients These observations have led to the formulation of the neurotrophin hypothesis of schizophrenia (SCZ), which postulates that the changes observed in the brains of SCZ patients occur as a result of disturbances in developmental processes involving neurotrophic factors (Lang et al 2004)
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