Plasma brain-derived neurotrophic factor levels, learning capacity and cognition in patients with first episode psychosis

45 FEP patients and 45 healthy controls matched by age, gender and educational level were selected from the Basque Country area of Spain. Plasma BDNF levels were assessed in healthy controls and in patients. A battery of cognitive tests was applied to both groups, with the patients being assessed at 6 months after the acute episode and only in those with a clinical response to treatment.Plasma BDNF levels were altered in patients compared with the control group. In FEP patients, we observed a positive association between BDNF levels at six months and five cognitive domains (learning ability, immediate and delayed memory, abstract thinking and processing speed) which persisted after controlling for medications prescribed, drug use, intelligence quotient (IQ) and negative symptoms. In the healthy control group, BDNF levels were not associated with cognitive test scores.Our results suggest that BDNF is associated with the cognitive impairment seen after a FEP. Further investigations of the role of this neurotrophin in the symptoms associated with psychosis onset are warranted.Cognitive deficits have been described in patients with psychotic illnesses. More specifically, studies have found alterations in executive functioning, verbal memory and attention from the onset of psychosis [1,2]. Although the presence of these cognitive deficits is evident during the acute episode, it has also been established that patients diagnosed with chronic schizophrenia or bipolar disorder continue to have cognitive deficits [3].Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin that has been associated with some mental diseases, such as depression [4], Alzheimer’s disease [5] and psychotic disorders [6,7]. BDNF is highly expressed in the cerebral cortex and hippocampus, brain areas known to regulate functions such as memory and emotion [6]. There is a correlation between hippocampal volumes and serum BDNF levels, such that smaller hippocampal volumes in drug-na？ve patients with