Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism contributes to the development of depression (major depressive disorder, MDD), but it is unclear whether neural effects observed in healthy individuals are sustained in MDD.

To investigate BDNF Val66Met effects on key regions in MDD neurocircuitry: amygdala, anterior cingulate, middle frontal and orbitofrontal regions.

Magnetic resonance imaging scans were acquired in 79 persons with MDD (mean age 49 years) and 74 healthy volunteers (mean age 50 years). Effects on surface area and cortical thickness were examined with multiple comparison correction.

People who were Met allele carriers showed reduced caudal middle frontal thickness in both study groups. Significant interaction effects were found in the anterior cingulate and rostral middle frontal regions, in which participants in the MDD group who were Met carriers showed the greatest reduction in surface area.

Modulatory effects of the BDNF Val66Met polymorphism on distinct subregions in the prefrontal cortex in MDD support the neurotrophin model of depression.

White matter abnormalities have been implicated in the aetiology of major depressive disorder; however, the relationship between the severity of symptoms and white matter integrity is currently unclear.

To investigate white matter integrity in people with major depression and healthy controls, and to assess its relationship with depressive symptom severity.

Diffusion tensor imaging data were acquired from 66 patients with recurrent major depression and a control group of 66 healthy individuals matched for age, gender and IQ score, and analysed with tract-based spatial statistics. The relationship between white matter integrity and severity of depression as measured by the Beck Depression Inventory was examined.

Depressive illness was associated with widespread regions of decreased white matter integrity, including regions in the corpus callosum, superior longitudinal fasciculus and anterior corona radiata, compared with the control group. Increasing symptom severity was negatively correlated with white matter integrity, predominantly in the corpus callosum.

Widespread alterations in white matter integrity are evident in major depressive disorder. These abnormalities are heightened with increasing severity of depressive symptoms.

The neurocognitive basis of auditory verbal hallucinations is unclear.

To investigate whether people with a history of such hallucinations would misattribute their own speech as external and show differential activation in brain areas implicated in hallucinations compared with people without such hallucinations.

Participants underwent functional magnetic resonance imaging (fMRI) while listening to pre-recorded words. The source (self/non-self) and acoustic quality (undistorted/distorted) were varied across trials. Participants indicated whether the speech they heard was their own or that of another person. Twenty people with schizophrenia (auditory verbal hallucinations n=10, no hallucinations n=10) and healthy controls (n=11) were tested.

The hallucinator group made more external misattributions and showed altered activation in the superior temporal gyrus and anterior cingulate compared with both other groups.

The misidentification of self-generated speech in patients with auditory verbal hallucinations is associated with functional abnormalities in the anterior cingulate and left temporal cortex. This may be related to impairment in the explicit evaluation of ambiguous auditory verbal stimuli.