Hippocampal volume and serotonin transporter polymorphism in major depressive disorder

2013 ◽  
Vol 25 (4) ◽  
pp. 206-214 ◽  
Author(s):  
Jamila Ahdidan ◽  
Leslie Foldager ◽  
Raben Rosenberg ◽  
Anders Rodell ◽  
Poul Videbech ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Serotonin Transporter ◽  
Brain Volume ◽  
Hippocampal Volume ◽  
Healthy Controls ◽  
Major Depressive ◽  
Total Brain Volume ◽  
Total Brain ◽  
Serotonin Transporter Polymorphism

ObjectiveThe main aim of the present study was to replicate a previous finding in major depressive disorder (MDD) of association between reduced hippocampal volume and the long variant of the di- and triallelic serotonin transporter polymorphism inSLC6A4on chromosome 17q11.2. Secondarily, we also hypothesised that 5-HTTLPR may be a risk factor for MDD.MethodsQuantitative magnetic resonance imaging (MRI) of the hippocampus was studied in 23 inpatients suffering from MDD and in 33 healthy controls. Normalised volumetric MRI data of hippocampus were assessed with adjustment for total brain volume and tensor-based morphometry was used to elucidate structural brain differences. A triallelic genetic marker resulting from twoSLC6A4promoter region polymorphisms, 5-HTTLPR and rs25531, was analysed for association with MDD and quantitative traits.ResultsHealthy controls had a smaller relative hippocampal volume (relative to brain size) but a larger total brain volume compared with patients with MDD. For patients compared with healthy controls, atrophy was found in the right temporal lobe and pons medulla. Allele and genotype frequencies were strikingly different from the previous study that we aimed to replicate, and no significant associations with the serotonin transporter polymorphism were found.ConclusionsThe present quantitative and morphometric MRI study was not able to replicate the previous finding of association between reduced hippocampal volume in depressed patients and the serotonin transporter polymorphism.

Lower availability of midbrain serotonin transporter between healthy subjects with and without a family history of major depressive disorder – a preliminary two-ligand SPECT study

2014 ◽  
Vol 29 (7) ◽  
pp. 414-418 ◽  
Author(s):  
P.C. Hsieh ◽  
K.C. Chen ◽  
T.L. Yeh ◽  
I.H. Lee ◽  
P.S. Chen ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Family History ◽  
Depressive Disorder ◽  
Serotonin Transporter ◽  
Healthy Subjects ◽  
Healthy Controls ◽  
Major Depressive ◽  
Dopaminergic Dysfunction ◽  
History Of ◽  
Family History Of Depression

AbstractPurposeSerotonin transporter (SERT) and dopamine transporter (DAT) levels differ in patients with major depressive disorder (MDD) who are in a depressed state in comparison with healthy controls. In addition, a family history of depression is a potent risk factor for developing depression, and inherited vulnerability to serotonergic and dopaminergic dysfunction is suspected in this. The aim of this study was to examine the availabilities of midbrain SERT and striatal DAT in healthy subjects with and without a first-degree family history of MDD.MethodsEight healthy subjects with first-degree relatives with MDD and 16 sex- and age-matched healthy controls were recruited. The availabilities of SERT and DAT were approximated using SPECT, employing [123I] 2-((2-((dimethylamino)methyl)phenyl)thio)-5-iodophenylamine (ADAM) and [99mTc] TRODAT-1 as the ligands, respectively. There are missing data for one participant with a first-degree family history of MDD from the ADAM study, due to a lack of the radio-ligand at the time of experiment.ResultsSERT availability in the midbrain was significantly lower in subjects with a first-degree family history of MDD than in healthy subjects. However, DAT availability was no different between two groups.ConclusionsThe results with regard to the midbrain SERT level suggest the heritability of MDD.

The power of sample size and homogenous sampling: Association between the 5-HTTLPR serotonin transporter polymorphism and major depressive disorder

2005 ◽  
Vol 57 (3) ◽  
pp. 247-251 ◽  
Author(s):  
Barbara Hoefgen ◽  
Thomas G. Schulze ◽  
Stephanie Ohlraun ◽  
Olrik von Widdern ◽  
Susanne Höfels ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Sample Size ◽  
Serotonin Transporter ◽  
Major Depressive ◽  
Serotonin Transporter Polymorphism

scholarly journals Phosphodiesterase 8A to discriminate in blood samples depressed patients and suicide attempters from healthy controls based on A-to-I RNA editing modifications

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nicolas Salvetat ◽  
Fabrice Chimienti ◽  
Christopher Cayzac ◽  
Benjamin Dubuc ◽  
Francisco Checa-Robles ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Rna Editing ◽  
Whole Blood ◽  
Healthy Controls ◽  
Major Depressive ◽  
Suicide Attempters ◽  
Blood Samples ◽  
Depressed Patients ◽  
The Brain

AbstractMental health issues, including major depressive disorder, which can lead to suicidal behavior, are considered by the World Health Organization as a major threat to global health. Alterations in neurotransmitter signaling, e.g., serotonin and glutamate, or inflammatory response have been linked to both MDD and suicide. Phosphodiesterase 8A (PDE8A) gene expression is significantly decreased in the temporal cortex of major depressive disorder (MDD) patients. PDE8A specifically hydrolyzes adenosine 3′,5′-cyclic monophosphate (cAMP), which is a key second messenger involved in inflammation, cognition, and chronic antidepressant treatment. Moreover, alterations of RNA editing in PDE8A mRNA has been described in the brain of depressed suicide decedents. Here, we investigated PDE8A A-to-I RNA editing-related modifications in whole blood of depressed patients and suicide attempters compared to age-matched and sex-matched healthy controls. We report significant alterations of RNA editing of PDE8A in the blood of depressed patients and suicide attempters with major depression, for which the suicide attempt took place during the last month before sample collection. The reported RNA editing modifications in whole blood were similar to the changes observed in the brain of suicide decedents. Furthermore, analysis and combinations of different edited isoforms allowed us to discriminate between suicide attempters and control groups. Altogether, our results identify PDE8A as an immune response-related marker whose RNA editing modifications translate from brain to blood, suggesting that monitoring RNA editing in PDE8A in blood samples could help to evaluate depressive state and suicide risk.

scholarly journals Hot and cold cognitive disturbances in antidepressant-free patients with major depressive disorder: a NeuroPharm study

2020 ◽  
pp. 1-10
Author(s):  
V. H. Dam ◽  
D. S. Stenbæk ◽  
K. Köhler-Forsberg ◽  
C. Ip ◽  
B. Ozenne ◽  
...  
Keyword(s):  
Working Memory ◽  
Major Depressive Disorder ◽  
Reaction Time ◽  
Depressive Disorder ◽  
Healthy Controls ◽  
Cognitive Profiles ◽  
Depression Severity ◽  
Major Depressive ◽  
Depressed Patients ◽  
Cognitive Disturbances

Abstract Background Cognitive disturbances are common and disabling features of major depressive disorder (MDD). Previous studies provide limited insight into the co-occurrence of hot (emotion-dependent) and cold (emotion-independent) cognitive disturbances in MDD. Therefore, we here map both hot and cold cognition in depressed patients compared to healthy individuals. Methods We collected neuropsychological data from 92 antidepressant-free MDD patients and 103 healthy controls. All participants completed a comprehensive neuropsychological test battery assessing hot cognition including emotion processing, affective verbal memory and social cognition as well as cold cognition including verbal and working memory and reaction time. Results The depressed patients showed small to moderate negative affective biases on emotion processing outcomes, moderate increases in ratings of guilt and shame and moderate deficits in verbal and working memory as well as moderately slowed reaction time compared to healthy controls. We observed no correlations between individual cognitive tasks and depression severity in the depressed patients. Lastly, an exploratory cluster analysis suggested the presence of three cognitive profiles in MDD: one characterised predominantly by disturbed hot cognitive functions, one characterised predominantly by disturbed cold cognitive functions and one characterised by global impairment across all cognitive domains. Notably, the three cognitive profiles differed in depression severity. Conclusion We identified a pattern of small to moderate disturbances in both hot and cold cognition in MDD. While none of the individual cognitive outcomes mapped onto depression severity, cognitive profile clusters did. Overall cognition-based stratification tools may be useful in precision medicine approaches to MDD.

Sign in / Sign up

Export Citation Format

Share Document