Bipolar disorder patients do not have accelerated prefrontal gyrification index (GI) loss, but having at least one brain-derived neurotrophic factor (BDNF) gene variant may increase loss, UK scientists have found.

Brain structural abnormalities, including temporal lobe and prefrontal cortex volume reductions, have been identified in bipolar disorder patients. However, it is not clear whether the abnormalities are present at disease onset or whether they develop over time.

Noting that the BDNF valine (val)⁶⁶methionine (met) variant has been linked to such brain changes, Ajay Mirakur and colleagues from the University of Edinburgh performed magnetic resonance imaging (MRI) at baseline and after 4 years in 18 bipolar I disorder patients and 18 healthy controls.

The GI was calculated as the ratio of folded inner contour to exposed outer contour. In addition, the participants underwent clinical assessment and were genotyped for BDNF val⁶⁶met.

Both bipolar disorder patients and healthy controls were found to have a significant decrease in GI over 4 years in all prefrontal quadrants, and there was no significant difference in the rate of change of GI between patients and controls.

Comparing bipolar disorder patients with and without at least one BDNF val⁶⁶met met allele, the team discovered that having at least one met allele was associated with a significantly increased change in GI over 4 years in all four prefrontal quadrants, but particularly in the right dorsal prefrontal cortex.

Carriers of a met allele were significantly older than val/val homozygotes, at 43.9 years versus 35.1 years. When taking age into account, there was a trend toward a significant difference in change in GI between met carriers and val/val homozygotes in the ventral quadrants, and a significant difference in dorsal quadrants.

The researchers conclude in the journal Biological Psychiatry: “We show that GI decreases significantly over time and that the rate of change in GI is not different in bipolar patients compared with control subjects but is accelerated in bipolar participants possessing at least one BDNF allele.

“These findings suggest that GI is not purely a neurodevelopmental measure and raise the possibility that GI may be a sensitive measure of morphological change with time.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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Study results suggest that abnormalities in perigenual anterior cingulate cortex (pACC) “amygdala functional connectivity occur during emotional processing in bipolar disorder (BD).

The pACC and amygdala are critical components of emotional processing circuitry and share extensive interconnections.

“Taken together, these data provide some of the first evidence that abnormalities in the structural integrity of white matter may contribute to disruptions in the coordinated response of the pACC and amygdale to emotional stimuli in BD,” say Fei Wang (Yale University, New Haven, Connecticut, USA) and co-authors.

The researchers performed functional magnetic resonance imaging (fMRI) during processing of an event-related emotional face task and diffusion tensor imaging (DTI) on 33 patients with BD and 31 healthy controls.

When comparing the strength of the pACC “amygdala functional connections between the groups, the authors found that functional connectivity was significantly decreased in the BD during the processing of fearful and happy faces. No significant group differences were seen during neutral face processing.

Wang et al also found a significant positive association between the pACC “amygdala functional coupling during fearful and happy face processing and fractional anisotropy (FA) values in the region of the uncinate fasciculus and neighboring ventrofrontal white matter, regions of fronto-thalamo-striatal projections, as well as frontotemporal projections to the posterior association cortex.

Furthermore, FA values were significantly decreased in the BD group compared with the control group.

“The decrease in pACC “amygdala functional connectivity in BD could reflect a reduction in the pACC’s inhibitory control over the amygdala,” writes the team in the journal Biological Psychiatry.

However no group differences in amygdala activation were seen between the groups despite the significant decreases in pACC “amygdala connectivity, which the authors say is unclear.

The researchers call for further study of gray-white matter relationships and their associations to pACC “amygdala functional connectivity disruptions. They suggest that since the ACC receives a progressive and extensive growth of fibers originating from the amygdale during adolescence, further studies during this period could help elucidate a neurodevelopmental mechanism contributing to the disorder.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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