Browsing by Subject "MAJOR DEPRESSION"

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  • Wesolowska, Karolina; Elovainio, Marko; Koponen, Mikael; Tuiskula, Annukka M.; Hintsanen, Mirka; Keltikangas-Jarvinen, Liisa; Maattanen, Ilmari; Swan, Heikki; Hintsa, Taina (2017)
    We examined whether long QT syndrome (LQTS) mutation carrier status or symptomatic LQTS are associated with depression, and whether there are sex differences in these potential relationships. The sample comprised 782 participants (252 men). Of the 369 genetically defined LQTS mutation carriers, 169 were symptomatic and 200 were asymptomatic. The control group consisted of 413 unaffected relatives. Depression was assessed using the Beck Depression Inventory-II (BDI-II). No association was found for LQTS mutation carrier status with depression. The multinomial logistic regression showed that LQTS mutation carrier men with arrhythmic events scored higher on depression compared with the control group, even when adjusting for age, beta-blockers, antidepressants, and social support (OR = 1.09, 95 % CI [1.02, 1.15], p = .007). The binary logistic regression comparing symptomatic and asymptomatic LQTS mutation carriers showed that symptomatic LQTS was associated with depression in men (OR = 1.10, 95 % CI [1.03, 1.19], p = .009). The results were unchanged when additionally adjusted for education. These findings suggest that symptomatic LQTS is associated with depression in men but not in women. Overall, however, depression is more frequent in women than men. Thus, regular screening for depression in LQTS mutation carriers and their unaffected family members can be important.
  • Wesolowska, Karolina; Elovainio, Marko; Hintsa, Taina; Jokela, Markus; Pulkki-Raback, Laura; Lipsanen, Jari; Juonala, Markus; Raitakari, Olli; Keltikangas-Jarvinen, Liisa (2018)
    Objective: Depressive symptoms have been associated with Type 2 diabetes, but the temporal direction of this association and the underlying mechanisms remain unclear. The present study examined a potential bidirectional association between depressive symptoms and glucose levels in women and men, and the factors mediating this association. Method: The participants were from the Cardiovascular Risk in Young Finns Study, a prospective, population-based, cohort study (N = 2,534). Depressive symptoms were assessed using a modified Beck Depression Inventory. Fasting glucose was measured concurrently with depressive symptoms. To analyze the data, a multiple-group cross-lagged analysis and parallel multiple mediation in structural equation modeling were used. Results: Depressive symptoms in 2001 were positively associated with glucose levels in 2012 in women (beta = .07, p = .023) but not in men (beta = -.03, p = .45). This sex difference was statistically significant (p = .042). Glucose levels in 2001 did not predict depressive symptoms in 2012 in either women or men (ps = .96). Changes in body mass index, high-sensitivity C-reactive protein, alcohol consumption, or tobacco or cigarette smoking did not mediate the observed association (ps > .05). Conclusions: The results showed a positive association between depressive symptoms and glucose levels in women but not in men. The direction of this relationship seems to be from depressive symptoms to glucose levels rather than the reverse. Changes in body fat, inflammation, alcohol consumption, or tobacco or cigarette smoking may not play a mediating role in this observed association.
  • Mohammad, H.; Marchisella, F.; Ortega-Martinez, S.; Hollos, P.; Eerola, K.; Komulainen, E.; Kulesskaya, N.; Freemantle, E.; Fagerholm, V.; Savontous, E.; Rauvala, H.; Peterson, B. D.; van Praag, H.; Coffey, E. T. (2018)
    Promoting adult hippocampal neurogenesis is expected to induce neuroplastic changes that improve mood and alleviate anxiety. However, the underlying mechanisms remain largely unknown and the hypothesis itself is controversial. Here we show that mice lacking Jnk1, or c-Jun N-terminal kinase (JNK) inhibitor-treated mice, display increased neurogenesis in adult hippocampus characterized by enhanced cell proliferation and survival, and increased maturation in the ventral region. Correspondingly, anxiety behaviour is reduced in a battery of tests, except when neurogenesis is prevented by AraC treatment. Using engineered retroviruses, we show that exclusive inhibition of JNK in adult-born granule cells alleviates anxiety and reduces depressive-like behaviour. These data validate the neurogenesis hypothesis of anxiety. Moreover, they establish a causal role for JNK in the hippocampal neurogenic niche and anxiety behaviour, and advocate targeting of JNK as an avenue for novel therapies against affective disorders.
  • Madsen, I. E. H.; Nyberg, S. T.; Hanson, L. L. Magnusson; Ferrie, J. E.; Ahola, K.; Alfredsson, L.; Batty, G. D.; Bjorner, J. B.; Borritz, M.; Burr, H.; Chastang, J. -F.; de Graaf, R.; Dragano, N.; Hamer, M.; Jokela, M.; Knutsson, A.; Koskenvuo, M.; Koskinen, A.; Leineweber, C.; Niedhammer, I.; Nielsen, M. L.; Nordin, M.; Oksanen, T.; Pejtersen, J. H.; Pentti, J.; Plaisier, I.; Salo, P.; Singh-Manoux, A.; Suominen, S.; ten Have, M.; Theorell, T.; Toppinen-Tanner, S.; Vahtera, J.; Vaananen, A.; Westerholm, P. J. M.; Westerlund, H.; Fransson, E. I.; Heikkila, K.; Virtanen, M.; Rugulies, R.; Kivimaki, M.; IPD Work Consortium (2017)
    Background. Adverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression. Method. We identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol. Results. We included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47-2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04-1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94-1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81-1.32). Conclusions. Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.
  • Stevanovic, Melisa; Tuhkanen, Samuel; Jarvensivu, Milla; Koskinen, Emmi; Lindholm, Camilla; Paananen, Jenny; Savander, Eniko; Valkeapaa, Taina; Valkiaranta, Kaisa (2022)
    We used a novel interdisciplinary experimental paradigm where two types of dyads-15 dyads with one depressed and one non-depressed participant and 15 dyads with two non-depressed participants-engaged in a series of food-decision-making tasks. We examined how different communicative events during the decision-making process were reflected in the affective responses of the interacting participants, as indicated in their skin conductance (SC) response rates. The participants' SC response rates were found to be higher during the emergence of the final decision, compared to the other segments during the process. Furthermore, relinquishing one's initially expressed preferences was associated with SC response rates higher than the baseline. However, during the relinquishment segments, there was a negative interaction between depression diagnosis and SC response rates, which suggests that, compared to their non-depressed comparisons, it is affectively less arousing for the participants with depression to give up their previously expressed preferences.
  • Toffol, Elena; Kalleinen, Nea; Haukka, Jari; Vakkuri, Olli; Partonen, Timo; Polo-Kantola, Paivi (2014)
  • Lisboa, S. F.; Issy, A. C.; Biojone, C.; Montezuma, K.; Fattori, V.; Del-Bel, E. A.; Guimaraes, F. S.; Cunha, F. Q.; Verri, W. A.; Joca, S. R. L. (2018)
    Preclinical and clinical evidence suggests pro-inflammatory cytokines might play an important role in the neurobiology of schizophrenia and stress-related psychiatric disorders. Interleukin-18 (IL-18) is a member of the IL-1 family of cytokines and it is widely expressed in brain regions involved in emotional regulation. Since IL-18 involvement in the neurobiology of mental illnesses, including schizophrenia, remains unknown, this work aimed at investigating the behavior of IL-18 null mice (KO) in different preclinical models: 1. the prepulse inhibition test (PPI), which provides an operational measure of sensorimotor gating and schizophrenic-like phenotypes; 2. amphetamine-induced hyperlocomotion, a model predictive of antipsychotic activity; 3. resident intruder test, a model predictive of aggressive behavior. Furthermore, the animals were submitted to models used to assess depressive- and anxiety-like behavior. IL-18KO mice showed impaired baseline PPI response, which was attenuated by D-amphetamine at a dose that did not modify PPI response in wild-type (WT) mice, suggesting a hypodopaminergic prefrontal cortex function in those mice. D-Amphetamine, however, induced hyperlocomotion in IL-18KO mice compared to their WT counterparts, suggesting hyperdopaminergic activity in the midbrain. Moreover, IL-18KO mice presented increased basal levels of IL-1 beta levels in the hippocampus and TNF-alpha in the prefrontal cortex, suggesting an overcompensation of IL-18 absence by increased levels of other proinflammatory cytokines. Although no alteration was observed in the forced swimming or in the elevated plus maze tests in naive IL-18KO mice, these mice presented anxiogenic-like behavior after exposure to repeated forced swimming stress. In conclusion, deletion of the IL-18 gene resembled features similar to symptoms observed in schizophrenia (positive and cognitive symptoms, aggressive behavior), in addition to increased susceptibility to stress. The IL-18KO model, therefore, could provide new insights into how changes in brain immunological homeostasis induce behavioral changes related to psychiatric disorders, such as schizophrenia.
  • Sandman, Nils; Valli, Katja; Kronholm, Erkki; Vartiainen, Erkki; Laatikainen, Tiina; Paunio, Tiina (2017)
    Nightmares are intensive dreams with negative emotional tone. Frequent nightmares can pose a serious clinical problem and in 2001, Tanskanen et al. found that nightmares increase the risk of suicide. However, the dataset used by these authors included war veterans in whom nightmare frequency -and possibly also suicide risk -is elevated. Therefore, re-examination of the association between nightmares and suicide in these data is warranted. We investigated the relationship between nightmares and suicide both in the general population and war veterans in Finnish National FINRISK Study from the years 1972 to 2012, a dataset overlapping with the one used in the study by Tanskanen et al. Our data comprise 71,068 participants of whom 3139 are war veterans. Participants were followed from their survey participation until the end of 2014 or death. Suicides (N = 398) were identified from the National Causes of Death Register. Frequent nightmares increase the risk of suicide: The result of Tanskanen et al. holds even when war experiences are controlled for. Actually nightmares are not significantly associated with suicides among war veterans. These results support the role of nightmares as an independent risk factor for suicide instead of just being proxy for history of traumatic experiences.
  • Frank, Philipp; Jokela, Markus; Batty, G. David; Lassale, Camille; Steptoe, Andrew; Kivimaki, Mika (2022)
    Objectives: Obesity is associated with increased risk of depression, but the extent to which this association is symptom-specific is unknown. We examined the associations of overweight and obesity with individual depressive symptoms. Methods: We pooled data from 15 population-based cohorts comprising 57,532 individuals aged 18 to 100 years at study entry. Primary analyses were replicated in an independent cohort, the UK Biobank study (n = 122,341, age range 38 to 72). Height and weight were assessed at baseline and body mass index (BMI) was computed. Using validated self-report measures, 24 depressive symptoms were ascertained once in 16 cross-sectional, and twice in 7 prospective cohort studies (mean follow-up 3.2 years). Results: In the pooled analysis of the primary cohorts, 22,045 (38.3 %) participants were overweight (BMI between 25 and 29.9 kg/m(2)), 12,025 (20.9 %) class I obese (BMI between 30 and 34.9 kg/m(2)), 7,467 (13.0 %) class II-III obese (BMI >= 35 kg/m(2)); and 7,046 (12.3 %) were classified as depressed. After multivariable adjustment, obesity class I was cross-sectionally associated with 1.11-fold (95 % confidence interval 1.01-1.22), and obesity class II-III with 1.31-fold (1.16-1.49) higher odds of overall depression. In symptom-specific analyses, robust associations were apparent for 4 of the 24 depressive symptoms ('could not get going/lack of energy', 'little interest in doing things', 'feeling bad about yourself, and 'feeling depressed'), with confounder-adjusted odds ratios of having 3 or 4 of these symptoms being 1.32 (1.10-1.57) for individuals with obesity class I, and 1.70 (1.34-2.14) for those with obesity class II-III. Elevated C-reactive protein and 21 obesity-related diseases explained 23 %-31 % of these associations. Symptom-specific associations were confirmed in longitudinal analyses where obesity preceded symptom onset, were stronger in women compared with men, and were replicated in UK Biobank. Conclusions: Obesity is associated with a distinct set of depressive symptoms. These associations are partially explained by systemic inflammation and obesity-related morbidity. Awareness of this obesity-related symptom profile and its underlying biological correlates may inform better targeted treatments for comorbid obesity and depression.
  • Neyazi, Alexandra; Theilmann, Wiebke; Brandt, C; Rantamäki, Tomi Pentti Johannes; Matsui, Nobuaki; Rhein, M; Kornhuber, J; Bajbouj, M; Sperling, W; Bleich, S; Frieling, H; Löscher, W (2018)
    Although electroconvulsive therapy (ECT) is among the most effective treatment options for pharmacoresistant major depressive disorder (MDD), some patients still remain refractory to standard ECT practise. Thus, there is a need for markers reliably predicting ECT non/response. In our study, we have taken a novel translational approach for discovering potential biomarkers for the prediction of ECT response. Our hypothesis was that the promoter methylation of p11, a multifunctional protein involved in both depressive-like states and antidepressant treatment responses, is differently regulated in ECT responders vs. nonresponders and thus be a putative biomarker of ECT response. The chronic mild stress model of MDD was adapted with the aim to obtain rats that are resistant to conventional antidepressant drugs (citalopram). Subsequently, electroconvulsive stimulation (ECS) was used to select responders and nonresponders, and compare p11 expression and promoter methylation. In the rat experiments we found that the gene promoter methylation and expression of p11 significantly correlate with the antidepressant effect of ECS. Next, we investigated the predictive properties of p11 promoter methylation in two clinical cohorts of patients with pharmacoresistant MDD. In a proof-of-concept clinical trial in 11 patients with refractory MDD, higher p11 promoter methylation was found in responders to ECT. This finding was replicated in an independent sample of 65 patients with pharmacoresistant MDD. This translational study successfully validated the first biomarker reliably predicting the responsiveness to ECT. Prescreening of this biomarker could help to identify patients eligible for first-line ECT treatment and also help to develop novel antidepressant treatment procedures for depressed patients resistant to all currently approved antidepressant treatments.
  • Liskola, Krista; Raaska, Hanna; Lapinleimu, Helena; Elovainio, Marko (2018)
    Parental depressive symptoms have shown to be associated with offspring depression but much of the research has been focused on maternal depression. The aim of our study was to investigate the extent to which depressive symptoms of both parents associate with offspring depressive symptoms and whether social factors mediate these associations using data from adopted children with no shared genetic background. Data were derived from the Finnish Adoption survey study (a subsample of adopted children aged between 9 and 12years, n=548). Parental depressive symptoms were measured using short version of the General Health Questionnaire and Children's Depression Inventory (CDI) was used to measure depressive symptoms in adoptees. Paternal depressive symptoms were related to the total CDI (B=0.33, p=0.05) and two dimensions of offspring depressive symptoms: negative mood (B=0.10, p=0.03) and interpersonal problems (B=0.06, p=0.009). These associations remained significant even when adjusted for child's age and gender, age at adoption, type of placement before adoption, continent of birth and adoptive family's SES. No associations were found between maternal and any dimensions of offspring depressive symptoms. No information about the mental health of biological parents was available. We interpret the results as demonstrating that intergenerational transmission of depressive symptoms is not solely related to shared genes. Also, the results highlight the association of paternal depression with offspring depressive symptoms.
  • Berg, Noora; Kiviruusu, Olli; Karvonen, Sakari; Rahkonen, Ossi; Huurre, Taina (2017)
    Poor childhood family conditions have a long-term effect on adult mental health, but the mechanisms behind this association are unclear. Our aim was to study the pathways from problematic family relationships in adolescence to midlife psychological distress via disadvantages in early adulthood. Participants of a Finnish cohort study at the age of 16 years old in 1983 were followed up at ages 22, 32 and 42 years old (N = 1334). Problems in family relationships were measured with poor relationship with mother and father, lack of parental support in adolescent's individuation process and poor home atmosphere, and mental health was assessed using Kessler's Psychological Distress Scale (K10). We analyzed the indirect effects of adolescent family relations on mental health at age 42 years old via various disadvantages (somatic and psychological symptoms, relationship/marital status, low education/unemployment and heavy drinking) at ages 22 and 32 years old. Problematic adolescent family relationships were associated with midlife psychological distress in women (0.19; 95% CI 0.11, 0.26) and men (0.13; 95% CI 0.04, 0.21). However, after adjustment for adolescent psychological symptoms, the association was only significant for women (0.12; 95% CI 0.04, 0.20). Poor family relationships were associated with various disadvantages in early adulthood. The association from poor family relationships (16 years old) to psychological distress (42 years old) was in part mediated via psychological symptoms in women (0.03; 95% CI 0.01, 0.04) and men (0.02; 95% CI 0.00, 0.04) and in women also via heavy drinking in early adulthood (0.02; 95% CI 0.00, 0.03). Adolescent family relationships have a role in determining adult mental health. Targeted support addressing psychological well-being and hazardous drinking for adolescents with problematic family relationships might prevent disadvantages in early adulthood, and further prevent poor midlife mental health.
  • Ribeiro, Deidiane Elisa; Casarotto, Plinio C.; Staquini, Laura; Pinto e Silva, Maria Augusta; Biojone, Caroline; Wegener, Gregers; Joca, Samia (2019)
    Purinergic receptors, especially P2RX, are associated to the severity of symptoms in patients suffering from depressive and bipolar disorders, and genetic deletion or pharmacological blockade of P2RX7 induces antidepressant-like effect in preclinical models. However, there is scarce evidence about the alterations in P2RX7 or P2RX4 levels and in behavioral consequences induced by previous exposure to stress, a major risk factor for depression in humans. In the present study, we evaluated the effect of imipramine (IMI) on P2RX7 and P2RX4 levels in dorsal and ventral hippocampus as well as in the frontal cortex of rats submitted to the pretest session of learned helplessness (LH) paradigm. Repeated, but not acute administration of IMI (15 mg/kg ip) reduced the levels of both P2RX7 and P2RX4 in the ventral, but not in dorsal hippocampus or frontal cortex. In addition, we tested the effect of P2RX7/ P2RX4 antagonist brilliant blue G (BBG: 25 or 50 mg/kg ip) on the LH paradigm. We observed that repeated (7 days) but not acute (1 day) treatment with BBG (50 mg) reduced the number of failures to escape the shocks in the test session, a parameter mimicked by the same regimen of IMI treatment. Taken together, our data indicates that pharmacological blockade or decrease in the expression of P2RX7 is associated to the antidepressant-like behavior observed in the LH paradigm after repeated drug administration.
  • Riihimaki, K.; Vuorilehto, M.; Jylhä, P.; Isometsa, E. (2016)
    Background: Response styles theory of depression postulates that rumination is a central factor in occurrence, severity and maintaining of depression. High neuroticism has been associated with tendency to ruminate. We investigated associations of response styles and neuroticism with severity and chronicity of depression in a primary care cohort study. Methods: In the Vantaa Primary Care Depression Study, a stratified random sample of 1119 adult patients was screened for depression using the Prime-MD. Depressive and comorbid psychiatric disorders were diagnosed using SCID-I/P and SCID-II interviews. Of the 137 patients with depressive disorders, 82% completed the prospective five-year follow-up with a graphic life chart enabling evaluation of the longitudinal course of episodes. Neuroticism was measured with the Eysenck Personality Inventory (EPI-Q). Response styles were investigated at five years using the Response Styles Questionnaire (RSQ-43). Results: At five years, rumination correlated significantly with scores of Hamilton Depression Rating Scale (r = 0.54), Beck Depression Inventory (r = 0.61), Beck Anxiety Inventory (r = 0.50), Beck Hopelessness Scale (r = 0.51) and Neuroticism (r = 0.58). Rumination correlated also with proportion of follow-up time spent depressed (r = 0.38). In multivariate regression, high rumination was significantly predicted by current depressive symptoms and neuroticism, but not by anxiety symptoms or preceding duration of depressive episodes. Conclusions: Among primary care patients with depression, rumination correlated with current severity of depressive symptoms, but the association with preceding episode duration remained uncertain. The association between neuroticism and rumination was strong. The findings are consistent with rumination as a state-related phenomenon, which is also strongly intertwined with traits predisposing to depression. (C) 2015 Elsevier Masson SAS. All rights reserved.
  • Pelkonen, Mirjami; Marttunen, Mauri; Aro, Hillevi (2003)
    Background: Few longitudinal studies have attempted to identify risk factors in mid-adolescence for subsequent depression in young adulthood. Mid-adolescence is a critical developmental phase for studying vulnerability to depression due to high incidence and prevalence of depression. Methods: In a longitudinal study, following an urban Finnish community cohort (761 males and 887 females) from age 16, mid-adolescent risk factors for depression at age 22 years were studied. Data were collected by a questionnaire at school at age 16, and by a postal questionnaire at age 22. Results: Of the females 116 (13%) and of the males 69 (9%) had depression (S-BDI) in young adulthood. In multivariate analyses baseline depressive symptoms, low self-esteem, dissatisfaction with academic achievement, problems with the law, poor atmosphere at home and having no close friends predicted subsequent depression. Risk factors for males included more 'externalizing' aspects, for females more 'internalizing' factors. Conclusions: Mid-adolescence is an important age to study risk for depression, and self-reported perceptions of psychosocial well-being have predictive value. Preventive efforts can be selectively targeted at adolescents who have been exposed to identifiable risk factors. (C) 2002 Elsevier B.V. All rights reserved.
  • Fisher, Miranda L.; Loukola, Anu; Kaprio, Jaakko; Turner, Jill R. (ACADEMIC PRESS INC ELSEVIER SCIENCE, 2015)
    International Review of Neurobiology
    Smoking is currently the leading cause of preventable death in the United States and is responsible for over four million deaths annually worldwide. Therefore, there is a vast clinical unmet need with regards to therapeutics targeting smoking cessation. This is even more apparent when examining smokers co-morbid with psychiatric illness, as rates of smoking in this population are similar to 4 x higher than in the general population. Examining common genetic and molecular signaling pathways impinging upon both smoking behavior and psychiatric illness will lead to a better understanding of co-morbid disorders and potential development of novel therapeutics. Studies have implicated the Neuregulin Signaling Pathway in the pathophysiology of a number of psychiatric illnesses. Additionally, recent studies have also shown an association between the Neuregulin Signaling Pathway and smoking behaviors. This review outlines basic mechanisms of the Neuregulin Signaling Pathway and how it may be exploited for precision medicine approaches in treating nicotine dependence and mental illness.
  • Kraus, Christoph; Castrén, Eero; Kasper, Siegfried; Lanzenberger, Rupert (2017)
    Serotonin modulates neuroplasticity, especially during early life, and dysfunctions in both systems likewise contribute to pathophysiology of depression. Recent findings demonstrate that serotonin reuptake inhibitors trigger reactivation of juvenile-like neuroplasticity. How these findings translate to clinical antidepressant treatment in major depressive disorder remains unclear. With this review, we link preclinical with clinical work on serotonin and neuroplasticity to bring two pathophysiologic models in clinical depression closer together. Dysfunctional developmental plasticity impacts on later-life cognitive and emotional functions, changes of synaptic serotonin levels and receptor levels are coupled with altered synaptic plasticity and neurogenesis. Structural magnetic resonance imaging in patients reveals disease-state-specific reductions of gray matter, a marker of neuroplasticity, and reversibility upon selective serotonin reuptake inhibitor treatment. Translational evidence from magnetic resonance imaging in animals support that reduced densities and sizes of neurons and reduced hippocampal volumes in depressive patients could be attributable to changes of serotonergic neuroplasticity. Since ketamine, physical exercise or learning enhance neuroplasticity, combinatory paradigms with selective serotonin reuptake inhibitors could enhance clinical treatment of depression. (C) 2017 Elsevier Ltd. All rights reserved.
  • Santangeli, Olena; Porkka-Heiskanen, Tarja; Virkkala, Jussi; Castaneda, Anu E.; Marttunen, Mauri; Paunio, Tiina; Urrila, Anna S. (2017)
    Objective: Adolescence is a vulnerable period of life that is characterized by increasing incidence of depression. Sleep disturbance is one of the diagnostic symptoms of depressive disorder. Adolescence is also characterized by dramatic maturational changes in sleep and its regulation. The goal of this study was to assess sleep macroarchitecture and slow-wave activity (SWA) in depressed adolescent boys. Methods: Eight non-medicated adolescent boys meeting the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria for depressive disorder and 10 age-matched healthy controls (average age 16.0 years) underwent polysomnography in their home environment for two consecutive nights. Sleep macroarchitecture, SWA, and SWA dissipation were assessed in all subjects. Results: Depressed boys showed a flattened pattern of SWA dissipation through the night. SWA power was lower during the first non-rapid eye movement (NREM) episode in the frontal derivation and higher during the third NREM episode in the central derivation in the group of depressed boys as compared to healthy boys. The SWA dissipation pattern correlated with the severity of depressive symptoms, and the correlation was strongest in the frontal derivation. In addition, total sleep time was shorter in patients as compared to the control group, but no other differences were found in the macroarchitecture of sleep. Conclusion: Depression in adolescent boys is characterized by more evenly distributed SWA through the night as compared to healthy subjects, and we showed for the first time that this pattern of SWA distribution is associated with severity of depressive symptoms. These findings suggest that homeostatic regulation of sleep may be impaired in adolescent depression. (C) 2017 Elsevier B.V. All rights reserved.
  • Urrila, Anna S.; Karlsson, Linnea; Kiviruusu, Olli; Pankakoski, Maiju; Pelkonen, Mirjami; Strandholm, Thea; Marttunen, Mauri; Adolescent Depression Study Grp (2014)