The serotonin transporter promoter repeat length polymorphism, seasonal affective disorder and seasonality

Johansson, Carolina; Willeit, Matthäus; Levitan, Robert; Partonen, Timo; Smedh, C; Del-Favero, Jurgen; Kacem, Slim; Praschak-Rieder, Nicole; Neumeister, Alexander; Masellis, Mario; Basile, Vincenzo S.; Zill, Peter; Bondy, Brigitta; Paunio, Tiina; Kasper, Siegfried; Broeckhoven, Christine Van; Nilsson, Lars‐Göran; Lam, Raymond W.; Schalling, Martin; Adolfsson, Rolf

doi:10.1017/s0033291703007372

Cited by 36 publications

(22 citation statements)

References 20 publications

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“…In accordance with previous results (Johansson et al, 2003;Willeit et al, 2003), 5-HTTLPR genotype distribution did not differ significantly between patients with SAD and healthy controls (patients: ll: 22; ls: 38; ss: 13; controls: ll: 26; ls: 35; ss: 9; w 2 (2) ¼ 1.121; p ¼ 0.571). An earlier study reported significant seasonal variations in serotonin uptake velocity in 5-HTTLPR ll homozygous subjects only (Greenberg et al, 1999).…”

Section: -Httlpr and 5-htt Functionsupporting

confidence: 92%

Enhanced Serotonin Transporter Function during Depression in Seasonal Affective Disorder

Willeit

Sitte

Thierry

et al. 2007

Neuropsychopharmacol

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Decreased synaptic serotonin during depressive episodes is a central element of the monoamine hypothesis of depression. The serotonin transporter (5-HTT, SERT) is a key molecule for the control of synaptic serotonin levels. Here we aimed to detect state-related alterations in the efficiency of 5-HTT-mediated inward and outward transport in platelets of drug-free depressed patients suffering from seasonal affective disorder (SAD). 5-HTT turnover rate, a measure for the number of inward transport events per minute, and tyramineinduced, 5-HTT-mediated outward transport were assessed at baseline, after 4 weeks of bright light therapy, and in summer using a case-control design in a consecutive sample of 73 drug-free depressed patients with SAD and 70 nonseasonal healthy controls. Patients were drug-naive or medication-free for at least 6 months prior to study inclusion, females patients were studied in the follicular phase of the menstrual cycle. All participants were genotyped for a 5-HTT-promoter polymorphism (5-HTTLPR) to assess the influence of this polymorphism on 5-HTT parameters. Efficiency of 5-HTT-mediated inward (p ¼ 0.014) and outward (p ¼ 0.003) transport was enhanced in depressed patients. Both measures normalized toward control levels after therapy and in natural summer remission. Changes in outward transport showed a clear correlation with treatment response (r ¼ 0.421, p ¼ 0.001). Changes in inward transport were mediated by changes in 5-HTT transport efficiency rather than affinity or density. 5-HTTLPR was not associated with any of the 5-HTT parameters. In sum, we conclude that the 5-HTT is in a hyperfunctional state during depression in SAD and normalizes after light therapy and in natural summer remission.

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Section: -Httlpr and 5-htt Functionsupporting

confidence: 92%

Enhanced Serotonin Transporter Function during Depression in Seasonal Affective Disorder

Willeit

Sitte

Thierry

et al. 2007

Neuropsychopharmacol

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“…However, a recent metaanalysis questioned the finding of a gene-environment interaction of 5-HTTLPR genotype and traumatic life events [120] . Findings in SAD are contradictory as well: while two earlier studies found associations between 5-HTTLPR and SAD/seasonality [121,122] , a large metaanalysis yielded negative results [123] . Another SAD study found evidence for an association of 5-HTTLPR with atypical and melancholic depression subtypes, suggesting that the low-expressing 5-HTTLPR s-allele is associated with atypical symptoms rather than with a diagnosis of SAD [124] .…”

Section: Role Of Monoaminesmentioning

confidence: 99%

Bright-Light Therapy in the Treatment of Mood Disorders

et al. 2011

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Bright-light therapy (BLT) is established as the treatment of choice for seasonal affective disorder/winter type (SAD). In the last two decades, the use of BLT has expanded beyond SAD: there is evidence for efficacy in chronic depression, antepartum depression, premenstrual depression, bipolar depression and disturbances of the sleep-wake cycle. Data on the usefulness of BLT in non-seasonal depression are promising; however, further systematic studies are still warranted. In this review, the authors present a comprehensive overview of the literature on BLT in mood disorders. The first part elucidates the neurobiology of circadian and seasonal adaptive mechanisms focusing on the suprachiasmatic nucleus (SCN), the indolamines melatonin and serotonin, and the chronobiology of mood disorders. The SCN is the primary oscillator in humans. Indolamines are known to transduce light signals into cells and organisms since early in evolution, and their role in signalling change of season is still preserved in humans: melatonin is synthesized primarily in the pineal gland and is the central hormone for internal clock circuitries. The melatonin precursor serotonin is known to modulate many behaviours that vary with season. The second part discusses the pathophysiology and clinical specifiers of SAD, which can be seen as a model disorder for chronobiological disturbances and the mechanism of action of BLT. In the third part, the mode of action, application, efficacy, tolerability and safety of BLT in SAD and other mood disorders are explored.

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“…In addition, an increase in seasonality of mood symptoms in first-degree relatives of SAD patients 10 and the link between polymorphisms in the promoter region of the serotonin transporter gene and seasonal affective symptoms 18 has lent support to a genetic vulnerability, although the latter finding has been debated. 19 The first clock gene (period or per) was discovered 30 years ago in the fly Drosophila melanogaster and since then multiple genes have been identified in humans, which together regulate the activity of the clock cells in the SCN through positive and negative feedback loops. The influence in SAD may arise from defective clock genes affecting the functioning of the clock cells in the SCN, as demonstrated in other chronobiological disorders such as familial advanced sleep phase syndrome and delayed sleep phase syndrome.…”

Section: Genetics Clock Genes and Sadmentioning

confidence: 99%

Pathogenesis and management of seasonal affective disorder

Cotterell¹

2010

Prog Neurol Psychiatry

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The serotonin transporter promoter repeat length polymorphism, seasonal affective disorder and seasonality

Abstract: These results do not suggest a major role of the short variant of 5-HTTLPR in susceptibility to SAD, but provide modest evidence for an effect on seasonality.

Cited by 36 publications

References 20 publications

Enhanced Serotonin Transporter Function during Depression in Seasonal Affective Disorder

Enhanced Serotonin Transporter Function during Depression in Seasonal Affective Disorder

Bright-Light Therapy in the Treatment of Mood Disorders

Pathogenesis and management of seasonal affective disorder

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