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Brenda W J H Penninx - One of the best experts on this subject based on the ideXlab platform.
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major Depressive Disorder
Nature Reviews Disease Primers, 2016Co-Authors: Christian Otte, Brenda W J H Penninx, Stefan M Gold, Carmine M Pariante, Amit Etkin, Maurizio Fava, David C Mohr, Alan F SchatzbergAbstract:Major Depressive Disorder (MDD) is a debilitating disease that is characterized by depressed mood, diminished interests, impaired cognitive function and vegetative symptoms, such as disturbed sleep or appetite. MDD occurs about twice as often in women than it does in men and affects one in six adults in their lifetime. The aetiology of MDD is multifactorial and its heritability is estimated to be approximately 35%. In addition, environmental factors, such as sexual, physical or emotional abuse during childhood, are strongly associated with the risk of developing MDD. No established mechanism can explain all aspects of the disease. However, MDD is associated with alterations in regional brain volumes, particularly the hippocampus, and with functional changes in brain circuits, such as the cognitive control network and the affective-salience network. Furthermore, disturbances in the main neurobiological stress-responsive systems, including the hypothalamic-pituitary-adrenal axis and the immune system, occur in MDD. Management primarily comprises psychotherapy and pharmacological treatment. For treatment-resistant patients who have not responded to several augmentation or combination treatment attempts, electroconvulsive therapy is the treatment with the best empirical evidence. In this Primer, we provide an overview of the current evidence of MDD, including its epidemiology, aetiology, pathophysiology, diagnosis and treatment.
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bipolar polygenic loading and bipolar spectrum features in major Depressive Disorder
Bipolar Disorders, 2014Co-Authors: Anna Wiste, Brenda W J H Penninx, Elise B Robinson, Yuri Milaneschi, Sandra Meier, Stephan Ripke, Caitlin C Clements, Garrett M Fitzmaurice, Marcella RietschelAbstract:Objectives Family and genetic studies indicate overlapping liability for major Depressive Disorder and bipolar Disorder. The purpose of the present study was to determine whether this shared genetic liability influences clinical presentation. Methods A polygenic risk score for bipolar Disorder, derived from a large genome-wide association meta-analysis, was generated for each subject of European-American ancestry (n=1,274) in the Sequential Treatment Alternatives to Relieve Depression study (STAR*D) outpatient major Depressive Disorder cohort. A hypothesis-driven approach was used to test for association between bipolar Disorder risk score and features of depression associated with bipolar Disorder in the literature. Follow-up analyses were performed in two additional cohorts. Results A generalized linear mixed model including seven features hypothesized to be associated with bipolar spectrum illness was significantly associated with bipolar polygenic risk score [F=2.07, degrees of freedom (df)=7, p=0.04]. Features included early onset, suicide attempt, recurrent depression, atypical depression, subclinical mania, subclinical psychosis, and severity. Post-hoc univariate analyses demonstrated that the major contributors to this omnibus association were onset of illness at age 18years [odds ratio (OR)=1.2, p=0.003], history of suicide attempt (OR=1.21, p=0.03), and presence of at least one manic symptom (OR=1.16, p=0.02). The maximal variance in these traits explained by polygenic score ranged from 0.8% to 1.1%. However, analyses in two replication cohorts testing a five-feature model did not support this association. Conclusions Bipolar genetic loading appeared to be associated with bipolar-like presentation in major Depressive Disorder in the primary analysis. However, the results were at most inconclusive because of lack of replication. Replication efforts were challenged by different ascertainment and assessment strategies in the different cohorts. The methodological approach described here may prove useful in applying genetic data to clarify psychiatric nosology in future studies.
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major Depressive Disorder and accelerated cellular aging results from a large psychiatric cohort study
Molecular Psychiatry, 2014Co-Authors: Josine E Verhoeven, Dora Revesz, Elissa S Epel, Jue Lin, Owen M Wolkowitz, Brenda W J H PenninxAbstract:Major Depressive Disorder and accelerated cellular aging: results from a large psychiatric cohort study
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Disorder-specific cognitive profiles in major Depressive Disorder and generalized anxiety Disorder
BMC Psychiatry, 2014Co-Authors: Sanne M. Hendriks, Carmilla M.m. Licht, Jan Spijker, Aartjan T. F. Beekman, Florian Hardeveld, Ron De Graaf, Brenda W J H PenninxAbstract:Background This investigation examines differences in cognitive profiles in subjects with major Depressive Disorder (MDD) and generalized anxiety Disorder (GAD).
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estimating the genetic variance of major Depressive Disorder due to all single nucleotide polymorphisms
Biological Psychiatry, 2012Co-Authors: Gitta H Lubke, Joukejan Hottenga, Raymond K Walters, Charles Laurin, Eco J C De Geus, Gonneke Willemsen, Jan Smit, Christel M Middeldorp, Brenda W J H PenninxAbstract:Genome-wide association studies of psychiatric Disorders have been criticized for their lack of explaining a considerable proportion of the heritability established in twin and family studies. Genome-wide association studies of major Depressive Disorder in particular have so far been unsuccessful in detecting genome-wide significant single nucleotide polymorphisms (SNPs). Using two recently proposed methods designed to estimate the heritability of a phenotype that is attributable to genome-wide SNPs, we show that SNPs on current platforms contain substantial information concerning the additive genetic variance of major Depressive Disorder. To assess the consistency of these two methods, we analyzed four other complex phenotypes from different domains. The pattern of results is consistent with estimates of heritability obtained in twin studies carried out in the same population.
William W Eaton - One of the best experts on this subject based on the ideXlab platform.
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population based study of first onset and chronicity in major Depressive Disorder
Archives of General Psychiatry, 2008Co-Authors: William W Eaton, Huibo Shao, Gerald Nestadt, Ben Hochang Lee, Joseph O Bienvenu, Peter P ZandiAbstract:Context There are no studies of the natural history of major Depressive Disorder that lack prevalence and clinic biases. Objectives To estimate risk factors for first lifetime onset and parameters of chronicity following the first episode, including duration, recovery, and recurrence, and to search for predictors of each parameter. Design Prospective population-based cohort study with 23 years of follow-up. Setting East Baltimore, Maryland, an urban setting. Participants Probability sample of 3481 adult household residents in 1981, including 92 with first lifetime onset of major Depressive Disorder during the course of the follow-up, and 1739 other participants followed up for at least 13 years. Outcome Measures Diagnostic Interview Schedule and Life Chart Interview. Results Female participants showed higher risk of onset of Disorder, longer duration of episodes, and a nonsignificant tendency for higher risk of recurrence. Sex was not related to recovery. The median episode length was 12 weeks. About 15% of 92 individuals with first episodes did not have a year free of episodes, even after 23 years. About 50% of first episode participants recovered and had no future episodes. The evolution of the course was relatively stable from first to later episodes. Individuals with 1 or 2 short alleles of the serotonin transporter gene were at higher risk for an initial episode, but experienced episodes of shorter duration. There were few strong predictors of recovery or recurrence. Conclusions Major Depressive Disorder is unremitting in 15% of cases and recurrent in 35%. About half of those with a first-onset episode recover and have no furtherepisodes.
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restless legs syndrome is associated with dsm iv major Depressive Disorder and panic Disorder in the community
Journal of Neuropsychiatry and Clinical Neurosciences, 2008Co-Authors: Hochang B Lee, William W Eaton, M Wayne D A Hening, Richard P Allen, Amanda Kalaydjian, M Ch Christopher B B J Earley, M Constantine H S G LyketsosAbstract:The authors examined the association between restless legs syndrome (RLS) and DSM-IV major Depressive Disorder and panic Disorder based on Wave III and IV of the Baltimore ECA follow-up study. Of 1071 participants, 1024 completed the RLS Questionnaire and Diagnostic Interview Schedule. Adjusted odds ratio for diagnosis of major Depressive Disorder (4.7, 95% confidence interval [1.6, 14.5]) and panic Disorder (12.9 [3.6, 46.0]) and comorbidity of major Depressive Disorder and panic Disorder (9.7 [1.4, 69.0]) in the past 12 months suggested a strong association between restless legs syndrome and major Depressive Disorder and/or panic Disorder.
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Depressive Disorder dysthymia and risk of stroke thirteen year follow up from the baltimore epidemiologic catchment area study
Stroke, 2001Co-Authors: Sharon Larson, Pamela L Owens, Daniel E Ford, William W EatonAbstract:Background and Purpose— This study examined Depressive Disorder as a risk factor for incident stroke in a prospective, population-based design. Methods— The Baltimore Epidemiologic Catchment Area Study is a prospective 13-year follow-up of a probability sample of household residents from Baltimore, Md. Depressive Disorder was measured with the diagnostic interview schedule, and stroke was assessed by questions from the health interview survey or by documentation on a death certificate. Results— During the 13-year follow-up of 1703 individuals, 66 strokes were reported and 29 strokes were identified by death certificate search. Individuals with a history of Depressive Disorder were 2.6 times more likely to report stroke than those without this Disorder after controlling for heart disease, hypertension, diabetes, and current and previous use of tobacco. Medications used in the treatment of Depressive Disorder at baseline did not alter this finding. A history of dysthymia demonstrated a similar relationship ...
Jue Ji - One of the best experts on this subject based on the ideXlab platform.
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no association of the ywhae gene with schizophrenia major Depressive Disorder or bipolar Disorder in the han chinese population
Behavior Genetics, 2011Co-Authors: Guoquan Zhou, Weidong Ji, Junyan Li, Linqing Zheng, Zhen Zeng, Zhiwei Hu, You Li, Ti Wang, Tao Li, Jue JiAbstract:YWHAE is a gene encoding 14-3-3epsilon, which is highly conserved across species, from bacteria to humans, and binds to phosphoserine/phosphothreonine motifs in a sequence-specific manner. YWHAE has been reported to be associated with schizophrenia in a study based on the Japanese population. Here, we conducted a genetic association analysis between common SNPs in the YWHAE gene and psychiatric diseases including schizophrenia, major Depressive Disorder and bipolar Disorder in Han Chinese samples (1140 schizophrenia cases, 1140 major Depressive Disorder cases, 1140 bipolar Disorder cases and 1140 normal controls). We studied 11 SNPs, seven of which had previously been reported as significant, in YWHAE. No association was found with schizophrenia, major Depressive Disorder or bipolar Disorder. Considering the size of our sample sets (power > 90%), our results suggest that the YWHAE does not play a major role in schizophrenia, major Depressive Disorder or bipolar Disorder in the Han Chinese population.
Janusz Szemraj - One of the best experts on this subject based on the ideXlab platform.
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Regular paper Association of the DIO2 gene single nucleotide polymorphisms with recurrent Depressive Disorder*
2016Co-Authors: Elżbieta Gałecka, Monika Talarowska, Agata Orzechowska, Malgorzata Bienkiewicz, Paweł Górski, Janusz SzemrajAbstract:Genetic factors may play a role in the etiology of depres-sive Disorder. The type 2 iodothyronine deiodinase gene (DIO2) encoding the enzyme catalyzing the conversion of T4 to T3 is suggested to play a role in the recurrent Depressive Disorder (rDD). The current study investigates whether a specific single nucleotide polymorphism (SNP) of the DIO2 gene, Thr92Ala (T/C); rs 225014 or ORFa-Gly3Asp (C/T); rs 12885300, correlate with the risk for recurrent depression. Genotypes for these two single nu-cleotide polymorphisms (SNPs) were determined in 179 patients meeting the ICD-10 criteria for rDD group and in 152 healthy individuals (control group) using a poly-merase chain reaction (PCR) based method. The specific variant of the DIO2 gene, namely the CC genotype of the Thr92Ala polymorphism, was more frequently found in healthy subjects than in patients with depression, what suggests that it could potentially serve as a marker of a lower risk for recurrent Depressive Disorder. The distri-bution of four haplotypes was also significantly differ-ent between the two study groups with the TC (Thr-Gly) haplotype more frequently detected in patients with de-pression. In conclusion, data generated from this study suggest for the first time that DIO2 gene may play a role in the etiology of the disease, and thus should be further investigated. Key words: Depressive Disorder, iodothyronine deiodinase type II, polymorphism, haplotyp
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association of the dio2 gene single nucleotide polymorphisms with recurrent Depressive Disorder
Acta Biochimica Polonica, 2015Co-Authors: Elzbieta Galecka, Monika Talarowska, Agata Orzechowska, Pawel Gorski, Malgorzata Bienkiewicz, Janusz SzemrajAbstract:Genetic factors may play a role in the etiology of Depressive Disorder. The type 2 iodothyronine deiodinase gene (DIO2) encoding the enzyme catalyzing the conversion of T4 to T3 is suggested to play a role in the recurrent Depressive Disorder (rDD). The current study investigates whether a specific single nucleotide polymorphism (SNP) of the DIO2 gene, Thr92Ala (T/C); rs 225014 or ORFa-Gly3Asp (C/T); rs 12885300, correlate with the risk for recurrent depression. Genotypes for these two single nucleotide polymorphisms (SNPs) were determined in 179 patients meeting the ICD-10 criteria for rDD group and in 152 healthy individuals (control group) using a polymerase chain reaction (PCR) based method. The specific variant of the DIO2 gene, namely the CC genotype of the Thr92Ala polymorphism, was more frequently found in healthy subjects than in patients with depression, what suggests that it could potentially serve as a marker of a lower risk for recurrent Depressive Disorder. The distribution of four haplotypes was also significantly different between the two study groups with the TC (Thr-Gly) haplotype more frequently detected in patients with depression. In conclusion, data generated from this study suggest for the first time that DIO2 gene may play a role in the etiology of the disease, and thus should be further investigated.
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single nucleotide polymorphisms of nr3c1 gene and recurrent Depressive Disorder in population of poland
Molecular Biology Reports, 2013Co-Authors: Elzbieta Galecka, Malgorzata Bienkiewicz, Janusz Szemraj, Ireneusz Majsterek, Karolina Przybylowskasygut, Piotr Galecki, Andrzej LewinskiAbstract:Depressive Disorder is a disease characterized by disturbances in the hypothalamo–pituitary–adrenal axis. Abnormalities include the increased level of glucocorticoids (GC) and changes in sensitivity to these hormones. The changes are related to glucocorticoid receptors gene (NR3C1) variants. The NR3C1 gene is suggested to be a candidate gene affecting Depressive Disorder risk and management. The aim of this study was to investigate polymorphisms within the NR3C1 gene and their role in the susceptibility to recurrent Depressive Disorder (rDD). 181 Depressive patients and 149 healthy ethnically matched controls were included in the study. Single nucleotide polymorphisms were assessed using polymerase chain reaction/restriction fragment length polymorphism method. Statistical significance between rDD patients and controls was observed for the allele and genotype frequencies at three loci: BclI, N363S, and ER22/23EK. The presence of C allele, CC, and GC genotype of BclI polymorphism, G allele and GA genotype for N363S and ER22/23EK variants respectively were associated with increased rDD risk. Two haplotypes indicated higher susceptibility for rDD, while haplotype GAG played a protective role with ORdis 0.29 [95 % confidence interval (CI) = 0.13–0.64]. Data generated from this study support the earlier results that genetic variants of the NR3C1 gene are associated with rDD and suggest further consideration on the possible involvement of these variants in etiology of the disease.
Junyan Li - One of the best experts on this subject based on the ideXlab platform.
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the ywhae gene confers risk to major Depressive Disorder in the male group of chinese han population
Progress in Neuro-psychopharmacology & Biological Psychiatry, 2017Co-Authors: Hongxin Zhang, Junyan Li, You Li, Ti Wang, Tao Li, Zhiqiang Li, Guoyin Feng, Lin HeAbstract:Abstract Schizophrenia and major Depressive Disorder are two major psychiatric illnesses that may share specific genetic risk factors to a certain extent. Increasing evidence suggests that the two Disorders might be more closely related than previously considered. To investigate whether YWHAE gene plays a significant role in major Depressive Disorder in Han Chinese population, we recruited 1135 unrelated major Depressive Disorder patients (485 males, 650 females) and 989 unrelated controls (296 males, 693 females) of Chinese Han origin. Eleven common SNPs were genotyped using TaqMan® technology. In male-group, the allele and genotype frequencies of rs34041110 differed significantly between patients and control (Pallele = 0.036486, OR[95%CI]: 1.249442(1.013988–1.539571); Pgenotype = 0.045301). Also in this group, allele and genotype frequencies of rs1532976 differed significantly (Pallele = 0.013242, OR[95%CI]: 1.302007(1.056501–1.604563); genotype: P = 0.039152). Haplotype-analyses showed that, in male-group, positive association with major Depressive Disorder was found for the A-A-C-G haplotype of rs3752826-rs2131431-rs1873827-rs12452627 (χ2 = 20.397, P = 6.38E-06, OR[95%CI]: 7.442 [2.691–20.583]), its C-A-C-G haplotype (χ2 = 19.122, P = 1.24E-05, OR and 95%CI: 0.402 [0.264–0.612]), its C-C-T-G haplotype (χ2 = 9.766, P = 0.001785, OR[95%CI]: 5.654 [1.664–19.211]). In female-group, positive association was found for the A-A-C-G haplotype of rs3752826-rs2131431-rs1873827-rs12452627 (χ2 = 78.628, P = 7.94E-19, OR[95%CI]: 50.043 [11.087–225.876]), its A-C-T-G haplotype (χ2 = 38.806, P = 4.83E-10, OR[95%CI]: 0.053 [0.015–0.192]), the C-A-C-G haplotype (χ2 = 18.930, P = 1.37E-05, OR[95%CI]: 0.526 [0.392–0.705]), and the C-C-T-G haplotype (χ2 = 38.668, P = 5.18E-10, OR[95%CI]: 6.130 [3.207–11.716]). Our findings support YWHAE being a risk gene for Major Depressive Disorder in the Han Chinese population.
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no association of the ywhae gene with schizophrenia major Depressive Disorder or bipolar Disorder in the han chinese population
Behavior Genetics, 2011Co-Authors: Guoquan Zhou, Weidong Ji, Junyan Li, Linqing Zheng, Zhen Zeng, Zhiwei Hu, You Li, Ti Wang, Tao Li, Jue JiAbstract:YWHAE is a gene encoding 14-3-3epsilon, which is highly conserved across species, from bacteria to humans, and binds to phosphoserine/phosphothreonine motifs in a sequence-specific manner. YWHAE has been reported to be associated with schizophrenia in a study based on the Japanese population. Here, we conducted a genetic association analysis between common SNPs in the YWHAE gene and psychiatric diseases including schizophrenia, major Depressive Disorder and bipolar Disorder in Han Chinese samples (1140 schizophrenia cases, 1140 major Depressive Disorder cases, 1140 bipolar Disorder cases and 1140 normal controls). We studied 11 SNPs, seven of which had previously been reported as significant, in YWHAE. No association was found with schizophrenia, major Depressive Disorder or bipolar Disorder. Considering the size of our sample sets (power > 90%), our results suggest that the YWHAE does not play a major role in schizophrenia, major Depressive Disorder or bipolar Disorder in the Han Chinese population.