Neural basis of depression found
By ANIWednesday, September 1, 2010
WASHINGTON - Using functional Magnetic Resonance Imaging (fMRI), researchers have shown that depressed patients had an abnormal activation of the medial prefrontal cortex.
During the study, subjects had to judge whether personality traits described them or not (i.e. ‘Am I selfish?’), or whether it described a generally desirable trait or not (i.e. ‘Is it good or bad to be greedy?’).
The dysfunction of the medial prefrontal region may explain specific complaints of depressed patients such as self-blame, rumination and feeling of guilt.
It was observed that this activation pattern was maintained over the course of depression after 8 weeks of antidepressant treatment.
These results are difficult to interpret but suggest that, after remission of depression, some patients show persistent abnormalities of specific brain regions.
Such abnormalities may indicate the need for complementary treatment such as cognitive behavioural therapy in order to reduce the risk of depressive recurrence.
Overall, these findings suggest that brain-imaging studies could provide biomarkers of diagnosis and improve patients� chances to responding to specific treatment modalities.
Such neurobiological markers of depression may help psychiatrists to tailor antidepressant treatment to the brain and the biological needs of the patients.
In the general population, depression is still frequently associated with bad life style, impairment of volition and ‘psychological weakness’.
However, the results of brain imaging studies clearly have confirmed that depression is a true brain disease associated with dysfunction of specific brain regions involved in cognitive control and emotional response.
Depression needs to be defined at the neurobiological level in order to improve the efficiency of treatment and reduce the burden of depressive disorders.
Neurobiological markers of depression may help psychiatrists to target specific neural processes and regions involved in affective regulation and to tailor antidepressant treatment according to the biological needs of the patients.
This could improve patients� chances to responding to specific treatment modalities.
The results were presented at a press conference on the occasion of the 23rd ECNP Congress, Amsterdam. (ANI)