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Implication of BDNF in treatment and pathophysiology of depression

Subject Area Biological Psychiatry
Term from 2009 to 2013
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 146763369
 
The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression and its restoration may underlie the therapeutic efficacy of antidepressant treatments. In humans BDNF protein concentration in serum is decreased in depressive patients and increased by antidepressant treatment. We previously found that BDNF serum concentration was associated to the concentration of N-acetylaspartate (NAA) in the anterior cingulate cortex in healthy volunteers, indicating neuronal vitality of the anterior cingulate cortex, as reflected by a high concentration of NAA, might be related to high concentrations of BDNF in serum. In line with this, decreased levels of NAA in the anterior cingulate cortex and hippocampus have been observed in major depression and bipolar disorder. Moreover, our recent finding that BDNF Val66Met genotype appears to predict the BDNF serum level in healthy human volunteers suggests the Met allele to be connected to higher concentrations of BDNF in serum. Moreover we found NAA in the anterior cingulate cortex to be significantly increased In healthy Met carriers. We hypothesize that higher NAA levels in the anterior cingulate cortex and BDNF in serum might contribute to the protection of Met allele carriers against major psychiatric disorders as major depression and bipolar disorder.This hypothesis prompts us to examine the question whether BDNF genotype is related to antidepressant response in patients and whether changes of NAA In the anterior cingulate cortex and BDNF in semm occur during antidepressive treatment. Moreover the question will be answered, if therapeutic response is connected or predicted by changes of these parameters. Therefore we want to examine BDNF in serum and NAA In the anterior cingulate cortex in 81 depressive patients during the course of an antidepressive treatment.
DFG Programme Research Grants
 
 

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