Mel Charbonneau - University of Wisconsin-Madison

A new study at the University of Wisconsin-Madison suggests that depressed patients are unable to sustain activity in brain areas related to positive emotion.

The study challenges previous notions that individuals with depression show less brain activity in areas associated with positive emotion. Instead, the new data suggest similar initial levels of activity, but an inability to sustain them over time. The new work was reported in the Proceedings of the National Academy of Sciences.

"Anhedonia, the inability to experience pleasure in things normally rewarding, is a cardinal symptom of depression," explains UW-Madison graduate student Aaron Heller, who led the project. "Scientists have generally thought that anhedonia is associated with a general reduction of activity in brain areas thought to be important for positive emotion and reward. In fact, we found that depressed patients showed normal levels of activity early on in the experiment. However, towards the end of the experiment, those levels of activity dropped off precipitously.

"Those depressed subjects who were better able to sustain activity in brain regions related to positive emotion and reward also reported higher levels of positive emotion in their everyday experience," Heller continues.

"Being able to sustain and even enhance one's own positive emotional experience is a critical component of health and well-being," notes the study's senior author, Richard Davidson, professor of psychology and psychiatry and director of both the UW-Madison Center for Investigating Healthy Minds, and the Waisman Laboratory for Brain Imaging and Behavior. "These findings may lead to therapeutic interventions that enable depressed individuals to better sustain positive emotion in their daily lives."

During the study, 27 depressed patients and 19 control participants were presented with visual images intended to evoke either a positive or a negative emotional response. While viewing these images, participants were instructed to use cognitive strategies to increase, decrease or maintain their emotional responses to the images by imagining themselves in similar scenarios. Heller and colleagues used functional magnetic resonance imaging (fMRI) to measure brain activity in the target areas. The researchers examined the extent to which activation in the brain's reward centers to positive pictures was sustained over time.

The study was funded by grants from the National Institute of Mental Health, Wyeth-Ayerst Pharmaceuticals, Fetzer Institute and Impact Foundation, and by gifts from the John W. Kluge Foundation, Bryant Wangard, Ralph Robinson and Keith and Arlene Bronstein.

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Heller AS, Johnstone T, Shackman AJ, et al. Reduced capacity to sustain positive emotion in major depression reflects diminished maintenance of fronto-striatal brain activation. Proc Natl Acad Sci U S A. 2009 Dec;doi:10.1073/pnas.0910651106 [Abstract | Full text ()]

Lisanby SH.

Professor of Clincal Psychiatry; Director of the Brain Stimulation Division, Columbia University/New York State Psychiatric Institute

Introduction

With the increasing number of new brain stimulation techniques now available and on the horizon, does electroconvulsive therapy (ECT) still have a role? As a clinician and researcher, my reply is a definitive "yes." Some recent and unexpected developments at the FDA concerning the classification of medical devices may, however, affect the availability of ECT to severely depressed patients.

History of ECT Classification

Codified in 1938, the FDA is nearly as old as ECT. The FDA was codified with the Federal Food, Drug, and Cosmetic Act during the same year that Cerletti and Bini introduced ECT in Italy (though Meduna introduced chemoconvulsive therapy two years prior). When the Medical Device Amendments were introduced in 1976, ECT devices were already on the market in the US. They are thus considered "pre-amendment" devices, meaning they did not go through the premarket approval application (PMA) route that devices introduced after 1976 are required to go through today.

Fan M, Liu B, Jiang T, Jiang X, Zhao H, Zhang J.

Objective: To evaluate the controversial, putative associations between the three common polymorphisms [promoter variable number tandem repeat (uVNTR), T941G, (CA) repeat] of monoamine oxidase A (MAOA) and mood disorders (major depressive or bipolar disorders, BPD) by systematically meta-analyzing published case-control association studies.

Methods: We queried PubMed using the keywords 'MAOA', 'association' and 'depression' or 'bipolar'. Nine studies on uVNTR, seven studies on T941G, and eight studies on CA met the inclusion criteria. The meta-analysis was performed by sex and ethnicity.

Main results: Our meta-analysis showed a significant association between uVNTR and MDD for the Asian group [odds ratio (OR) = 1.23 (1.02-1.47), P=0.03] and male Asian group [OR = 1.47 (1.06-2.05), P=0.02]. For the CA polymorphism, we found a significant association with BPD in the Caucasian group [OR = 1.28 (1.01-1.62), P=0.04] and female Caucasian group [OR = 1.36 (1.031-1.81), P=0.03]. For the CA polymorphism, we identified significant associations with BPD in all Caucasians for the overall alleles and for the specific alleles in a6 [OR = 1.35 (1.11-1.64), P=0.002] and in female Caucasians for the overall alleles and for the specific alleles in a2 [OR = 0.65 (0.48-0.90), P=0.009], a5 [OR = 1.44 (1.04-1.99), P=0.03], and a6 [OR = 1.41(1.12-1.78), P=0.004].

Conclusion: Our meta-analysis suggests a significant association of the MAOA gene with major depressive disorder and BPD within specific groups, indicating that these three polymorphisms of the MAOA gene may be associated with mood disorders by sex and ethnicity. Moreover, our systematic meta-analysis has revealed that although MAOA may be a common candidate gene for mood disorders, different polymorphisms and alleles appear to play different roles in major depressive disorder and BPD.

(Information links added; ed.)

Bergemann ER, Boles RG.

Major depressive disorder (MDD) is believed to have a genetic factor in its pathogenesis. On the basis of studies in MDD showing brain energy depletion and maternal inheritance in some families, we hypothesize that some of the genetic factor is likely maternally inherited on the mitochondrial DNA (mtDNA).

Six hundred and seventy-two pedigrees from the Genetics of Recurrent Early-Onset Depression project were analyzed for matrilineal/nonmatrilineal pairs. Pairs were constructed to control for sex, age and autosomal gene contribution (e.g. maternal vs. paternal aunts). Individuals with and without any mood disorder were tallied and compared across five different pairs.

Matrilineal relatives (with the same mtDNA sequence as the proband) were significantly more likely to suffer from a mood disorder than were nonmatrilineal relatives (with another mtDNA sequence; odds ratio 2.0, 95% confidence interval: 1.5-2.6, P = 3×10-6).

Our data show a modest maternal bias in the susceptibility towards the development of depression, suggesting that predisposing genetic factors likely reside on the mtDNA. Thus, our data strengthen the hypothesis that energy metabolism may be involved in the pathogenesis of depression.

(Text has been reformatted for online visual clarity; ed.)

By Joene Hendry

NEW YORK (Reuters Health) - Elderly men and women who sip on several cups of green tea a day may be less likely to have the blues, hint findings of a study from Japan.

Dr Kaijun Niu, at Tohoku University Graduate School of Biomedical Engineering in Sendai, and colleagues found men and women aged 70 and older who drank four or more, versus one or fewer, cups of green tea daily were 44 percent less likely to have symptoms of depression.

By LESLEY ALDERMAN

LET me start by saying I'm a fan of generic drugs. They save Americans billions of dollars each year and give us access to wonderful drugs at affordable prices. I've recommended generics in this column many times and use them myself when possible.

But there is a gnawing concern among some doctors and researchers that certain prescription generic drugs may not work as well as their brand-name counterparts.