Mikko Joensuu

Reduced midbrain serotonin transporter availability in drug-naïve patients with depression measured by SERT-specific [123I] nor-β-CIT SPECT imaging

Earlier results have indicated that serotonin transporter (SERT) availability is altered in major depression. We examined SERT density with a more serotonin-specific ligand and with a larger number of patients than in previous studies. Twenty-nine antidepressant-naïve patients with major depressive disorder (MDD) and 19 healthy age- and sex-matched controls were studied with SPECT using [(123)I] nor-beta-CIT as a ligand. The patients had a significantly lower (-10%) binding potential in the midbrain region than controls. No correlation with depression severity was found. These findings indicate that SERT availability in the midbrain area is reduced in depression, and that interindividual variation is considerable in both patients and controls.

Midbrain serotonin and striatum dopamine transporter binding in double depression: A one-year follow-up study

Data on neurobiological differences between major depression (MD) and double depression (DD) are scarce. We examined the striatum dopamine (DAT) and midbrain serotonin transporter (SERT) binding of [123I] nor-beta-CIT in DD patients (n=8) and compared it to that in MD patients (n=11) and healthy controls (n=19). Drug-naïve patients and controls were imaged by single-photon emission computed tomography at baseline, and the patients also after one year of psychodynamic psychotherapy. Both DD and MD groups had lower midbrain [123I] nor-beta-CIT binding compared with the controls. Baseline 17-item Hamilton Depression Rating Scale (HAM-D-17) scores significantly decreased in both groups after one year of psychotherapy (DD: t=3.55, p=0.009; MD: t=5.86, p<0.001). No differences between the DD and MD groups were observed in age-adjusted baseline striatum or midbrain [123I] nor-beta-CIT binding or its change during psychotherapy. Age-adjusted baseline striatum [123I] nor-beta-CIT binding correlated inversely with the duration of both dysthymia (rho=-0.76, p=0.03) and MD (rho=-0.83, p=0.01) in the DD group. No such finding was observed in the MD group (rho=0.26, p=0.44). Baseline HAM-D-17 did not correlate with the change in striatum or midbrain [123I] nor-beta-CIT binding in either group. In conclusion, our findings suggest that when using midbrain [123I] nor-beta-CIT binding as a marker of SERT binding, no differences are detectable between patients with DD and MD. However, low striatum [123I] nor-beta-CIT binding, a marker of DAT binding, may be associated with a longer illness duration in dysthymia.

Elevated midbrain serotonin transporter availability in mixed mania: a case report

BackgroundResults obtained from brain imaging studies indicate that serotonin transporter (SERT) and dopamine transporter (DAT) densities are altered in major depression. However, no such studies have been published on current mania or hypomania.Case presentationIn this single photon emission computed tomography (SPECT) study with [123I]nor-β-CIT we present a case with simultaneous symptoms of major depression and hypomania. She had an elevated serotonin transporter availability (SERT) in the midbrain and elevated dopamine transporter availability (DAT) in the striatum, which normalised in a one-year follow-up period during which she received eight months of psychodynamic psychotherapy.ConclusionsTo our knowledge, this is the first report on SERT and DAT associated with mania. In our case the availability of both SERT in the midbrain and DAT in the striatum were elevated at baseline and declined during psychotherapy, while the SERT and DAT of the depressed controls increased during psychotherapy. Symptoms of hypomania in the case were alleviated during psychotherapy. Clinical recovery was also reflected in the Hamilton Depression Rating Scale (HDRS) scores.

Serotonin‐transporter‐linked promoter region polymorphism and serotonin transporter binding in drug‐naïve patients with major depression

Aims:  Both the serotonin transporter and its genetic regulation by the serotonin‐transporter‐linked polymorphic region have a role in the pathophysiology of depression. Most of the previous studies have found no influence of serotonin‐transporter‐linked polymorphic region allelic variation on serotonin transporter binding in healthy controls or patients with major depression. Due to the inconsistency of the previous findings, we compared single photon emission computed tomography imaging with the serotonin‐transporter‐linked polymorphic region genotype in patients with major depressive disorder.

Baseline symptom severity predicts serotonin transporter change during psychotherapy in patients with major depression

The role of the serotonin transporter (SERT) in the pathophysiology of depression is unclear and only a few follow‐up studies exist. Our aim was to measure changes in SERT availability during psychodynamic psychotherapy in patients with major depression over a follow‐up time of 12 or 18 months.

Effects of Scheduled Waiting for Psychotherapy in Patients With Major Depression

Abstract The role of nonspecific factors in the outcome of psychotherapy is poorly understood. To study the effects of pretreatment expectancy of scheduled psychotherapy, we examined the effects of an agreed waiting time on the outcome of psychodynamic psychotherapy. Thirty-three treatment-naive outpatients with major depressive disorder were randomly selected to start psychotherapy either directly (DG; n = 17) or after waiting for 6 months (WG; n = 16). In WG, 18% to 60% of the total decline in symptoms took place during the waiting time. After 1 year of active psychotherapy, the anxiety score declined significantly only in WG, and the total length of treatment needed was shorter in WG. No other outcome differences between WG and DG were found. We conclude that scheduled waiting associates with a significant decline in depressive symptoms. Scheduled waiting should be regarded as a preparatory treatment and not as an inert nontreatment control.

Toward Molecular Psychotherapy of Depression

The 30–40% share of genetic factors in the disposition to unipolar major depression (MD) leaves an important role for psychosocial and developmental factors in the etiology and treatment of depression [1–3]. Moreover, it is likely that the biological and psychosocial factors are not independent. Their interaction in depression has been suggested in numerous studies, although the relevant mechanisms are not well understood [4–7]. Especially in the psychodynamic picture of depression, the role of somatic factors has been little illuminated due to the lack of a viable theory that would connect somatic signs with the psychodynamic profile of depression [8, 9].