Serotonin transporter binding in patients with mood disorders: a PET study with [11C](+)McN5652

Ichimiya, Tetsuya; Suhara, Tetsuya; Sudo, Yasuhiko; Okubo, Yoshiro; Nakayama, Keiichi I.; Nankai, Masahiro; Inoue, Makoto; Yasuno, Fumihiko; Takano, Akihiro; Maeda, Jun; Shibuya, Haruo

doi:10.1016/s0006-3223(01)01351-8

Cited by 141 publications

(83 citation statements)

References 52 publications

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“…We found lower 5-HTT binding (BP P , proportional to the total number of available transporters) in midbrain and amygdala in vivo in major depressive disorder (MDD) using positron emission tomography (PET) with [ 11 C]McN5652 (Parsey et al, 2006b), in agreement with some (Lehto et al, 2006;Malison et al, 1998;Newberg et al, 2005), but not all (Ichimiya et al, 2002;Meyer et al, 2004a), previous reports.…”

Section: Objectives Of the Studysupporting

confidence: 87%

Serotonin transporter binding as a possible predictor of one-year remission in major depressive disorder

Miller

Oquendo

Ogden

et al. 2008

Journal of Psychiatric Research

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Objective-Lower serotonin transporter (5-HTT) binding (BP P = = f P B avail /K D ) is reported during a major depressive episode (MDE) compared to healthy controls. Higher 5-HTT binding in the diencephalon has previously been associated with acute response to antidepressant treatment. We assessed baseline 5-HTT binding as a predictor of one-year remission from a MDE, examining binding in brain regions implicated in the pathophysiology of major depressive disorder (MDD). Results-Significant differences in 5-HTT binding among the three groups (healthy controls, remitters, and non-remitters) were observed in a linear mixed-effects model. Post-hoc, non-remitters had lower 5-HTT binding than controls in midbrain, amygdala, and anterior cingulate. Remitters did not differ significantly from controls or non-remitters in 5-HTT binding. Remitters did not differ from non-remitters in clinical characteristics apart from greater family history of depression among non-remitters. A logistic regression model fit to determine the capacity of baseline 5-HTT binding to predict remission status at one year yielded a coefficient that was suggestive but not significant (p=0.057). Methods-5-HTTLimitations-The small sample size and heterogeneous treatments received reduced statistical power to detect differences in binding based on clinical outcome.Conclusions-Lower pretreatment 5-HTT binding may be predictive of non-remission from major depression following one year of naturalistic antidepressant treatment. Future studies using standardized treatment are warranted.

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Section: Objectives Of the Studysupporting

confidence: 87%

Serotonin transporter binding as a possible predictor of one-year remission in major depressive disorder

Miller

Oquendo

Ogden

et al. 2008

Journal of Psychiatric Research

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“…having relatives with psychiatric diagnoses) or patients (from different source populations) is the most probable explanation for the inconsistent findings. Previous studies recruited patients from general psychiatric outpatient and university clinics [7,8,10,12,18,19,30]. We recruited 65% of our patients from primary care settings.…”

Section: Methodological Explanations For Inconsistent Findingsmentioning

confidence: 99%

“…Other studies have shown increased [19] or decreased [7][8][9][10][11][12][13] SERT availability in MDD patients compared with healthy subjects. However, none of these studies except two [11,13] investigated the effect of gender, and none of the study corrected for season.…”

Section: Comparison With Previous Studiesmentioning

confidence: 99%

“…Studies comparing depressed patients with healthy subjects have shown decreased [7][8][9][10][11][12][13], unchanged [14][15][16][17][18] or increased [19] SERT availability in MDD patients. A negative correlation between SERT availability and the severity of depression, measured in terms of Hamilton depression rating scale (HDRS) scores, has been reported in patients with primary MDD [9] or Wilson's disease [20].…”

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confidence: 99%

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Serotonin transporter binding with [123I]β-CIT SPECT in major depressive disorder versus controls: effect of season and gender

Ruhé

Booij

Reitsma

et al. 2009

Eur J Nucl Med Mol Imaging

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Purpose The serotonin system is undoubtedly involved in the pathogenesis of major depressive disorder (MDD). More specifically the serotonin transporter (SERT) serves as a major target for antidepressant drugs. There are conflicting results about SERT availability in depressed patients versus healthy controls. We aimed to measure SERT availability and study the effects of age, gender and season of scanning in MDD patients in comparison to healthy controls. Methods We included 49 depressed outpatients (mean±SD 42.3±8.3 years) with a Hamilton depression rating scale score above 18, who were drug-naive or drug-free for ≥4 weeks, and 49 healthy controls matched for age (±2 years) and sex. Subjects were scanned with single photon emission computed tomography (SPECT) using [ 123 I]β-CIT. SERT availability was expressed as specific to nonspecific binding ratios (BP ND ) in the midbrain and diencephalon with cerebellar binding as a reference. Results In crude comparisons between patients and controls, we found no significant differences in midbrain or diencephalon SERT availability. In subgroup analyses, depressed males had numerically lower midbrain SERT availability than controls, whereas among women SERT availability was not different (significant diagnosis×gender interaction; p=0.048). In the diencephalon we found a comparable diagnosis×gender interaction (p=0.002) and an additional smoking×gender (p=0.036) interaction. In the midbrain the season of scanning showed a significant main effect (p=0.018) with higher SERT availability in winter. Conclusion Differences in SERT availability in the midbrain and diencephalon in MDD patients compared with healthy subjects are affected by gender. The season of scanning is a covariate in the midbrain. The diagnosis×gender and gender×smoking interactions in SERT availability should be considered in future studies of the pathogenesis of MDD.

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“…Several studies examined dopamine and serotonin density and binding in bipolar disorder. Ichimiya et al 76 found increased serotonin transporter binding in the thalamus in a group of mood-disordered patients, including bipolar patients, in a variety of mood states. However, the increase in specifically bipolar patients was not significant.…”

Section: Subcortical and Medial Temporal Activationmentioning

confidence: 99%

The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings

2004

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The authors review existing structural and functional neuroimaging studies of patients with bipolar disorder and discuss how these investigations enhance our understanding of the neurophysiology of this illness. Findings from structural magnetic resonance imaging (MRI) studies suggest that some abnormalities, such as those in prefrontal cortical areas (SGPFC), striatum and amygdala exist early in the course of illness and, therefore, potentially, predate illness onset. In contrast, other abnormalities, such as those found in the cerebellar vermis, lateral ventricles and other prefrontal regions (eg, left inferior), appear to develop with repeated affective episodes, and may represent the effects of illness progression and associated factors. Magnetic resonance spectroscopy investigations have revealed abnormalities of membrane and second messenger metabolism, as well as bioenergetics, in striatum and prefrontal cortex. Functional imaging studies report activation differences between bipolar and healthy controls in these same anterior limibic regions. Together, these studies support a model of bipolar disorder that involves dysfunction within subcortical (striatalthalamic)-prefrontal networks and the associated limbic modulating regions (amygdala, midline cerebellum). These studies suggest that, in bipolar disorder, there may be diminished prefrontal modulation of subcortical and medial temporal structures within the anterior limbic network (eg, amygdala, anterior striatum and thalamus) that results in dysregulation of mood. Future prospective and longitudinal studies focusing on these specific relationships are necessary to clarify the functional neuroanatomy of bipolar disorder.

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Serotonin transporter binding in patients with mood disorders: a PET study with [11C](+)McN5652

Cited by 141 publications

References 52 publications

Serotonin transporter binding as a possible predictor of one-year remission in major depressive disorder

Serotonin transporter binding as a possible predictor of one-year remission in major depressive disorder

Serotonin transporter binding with [123I]β-CIT SPECT in major depressive disorder versus controls: effect of season and gender

The functional neuroanatomy of bipolar disorder: a review of neuroimaging findings

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