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Jinbei Zhang

Bio: Jinbei Zhang is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Major depressive disorder & Bipolar disorder. The author has an hindex of 9, co-authored 21 publications receiving 1024 citations.

Papers
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Journal ArticleDOI
30 Jul 2015-Nature
TL;DR: Using low-coverage whole-genome sequencing of 5,303 Chinese women with recurrent MDD selected to reduce phenotypic heterogeneity, and 5,337 controls screened to exclude MDD, two loci contributing to risk of MDD on chromosome 10 are identified: one near the SIRT1 gene and the other in an intron of the LHPP gene.
Abstract: Genomic analysis of 5,303 Chinese women with recurrent major depressive disorder (MDD) enables the identification and replication of two genome-wide significant loci contributing to risk of MDD on chromosome 10: one near the SIRT1 gene; the other in an intron of the LHPP gene.

745 citations

Journal ArticleDOI
TL;DR: It is demonstrated that changes in the amount of mtDNA and telomere length are consequences of stress and entering a depressed state and have important implications for understanding how stress causes the disease.

205 citations

Journal ArticleDOI
29 Jan 2014-PLOS ONE
TL;DR: CSA is strongly associated with recurrent MD and this association increases with greater severity of CSA, and among the depressed women, those with CSA had an earlier age of onset, longer depressive episodes.
Abstract: Background Our prior study in Han Chinese women has shown that women with a history of childhood sexual abuse (CSA) are at increased risk for developing major depression (MD). Would this relationship be found in our whole data set? Method Three levels of CSA (non-genital, genital, and intercourse) were assessed by self-report in two groups of Han Chinese women: 6017 clinically ascertained with recurrent MD and 5983 matched controls. Diagnostic and other risk factor information was assessed at personal interview. Odds ratios (ORs) were calculated by logistic regression. Results We confirmed earlier results by replicating prior analyses in 3,950 new recurrent MD cases. There were no significant differences between the two data sets. Any form of CSA was significantly associated with recurrent MD (OR 4.06, 95% confidence interval (CI) [3.19–5.24]). This association strengthened with increasing CSA severity: non-genital (OR 2.21, 95% CI 1.58–3.15), genital (OR 5.24, 95% CI 3.52–8.15) and intercourse (OR 10.65, 95% CI 5.56–23.71). Among the depressed women, those with CSA had an earlier age of onset, longer depressive episodes. Recurrent MD patients those with CSA had an increased risk for dysthymia (OR 1.60, 95%CI 1.11–2.27) and phobia (OR 1.41, 95%CI 1.09–1.80). Any form of CSA was significantly associated with suicidal ideation or attempt (OR 1.50, 95% CI 1.20–1.89) and feelings of worthlessness or guilt (OR 1.41, 95% CI 1.02–2.02). Intercourse (OR 3.47, 95%CI 1.66–8.22), use of force and threats (OR 1.95, 95%CI 1.05–3.82) and how strongly the victims were affected at the time (OR 1.39, 95%CI 1.20–1.64) were significantly associated with recurrent MD. Conclusions In Chinese women CSA is strongly associated with recurrent MD and this association increases with greater severity of CSA. Depressed women with CSA have some specific clinical traits. Some features of CSA were associated with greater likelihood of developing recurrent MD.

41 citations

Journal ArticleDOI
TL;DR: Bipolar disorder patients have a higher suicide risk than major depressive disorder patients, and the factors that were significantly associated with suicide risk may aid in identifying major affective disorder patients who are at risk for future suicidal behavior.

30 citations

Journal ArticleDOI
31 Jan 2014-PLOS ONE
TL;DR: Significantly more episodes of MDD occur among those with lower educational attainment (rather than longer episodes of disease), consistent with the hypothesis that the lower socioeconomic position increases the likelihood of developing MDD.
Abstract: Background The prevalence of major depressive disorder (MDD) is higher in those with low levels of educational attainment, the unemployed and those with low social status. However the extent to which these factors cause MDD is unclear. Most of the available data comes from studies in developed countries, and these findings may not extrapolate to developing countries. Examining the relationship between MDD and socio economic status in China is likely to add to the debate because of the radical economic and social changes occurring in China over the last 30 years. Principal findings We report results from 3,639 Chinese women with recurrent MDD and 3,800 controls. Highly significant odds ratios (ORs) were observed between MDD and full time employment (OR = 0.36, 95% CI = 0.25–0.46, logP = 78), social status (OR = 0.83, 95% CI = 0.77–0.87, logP = 13.3) and education attainment (OR = 0.90, 95% CI = 0.86–0.90, logP = 6.8). We found a monotonic relationship between increasing age and increasing levels of educational attainment. Those with only primary school education have significantly more episodes of MDD (mean 6.5, P-value = 0.009) and have a clinically more severe disorder, while those with higher educational attainment are likely to manifest more comorbid anxiety disorders. Conclusions In China lower socioeconomic position is associated with increased rates of MDD, as it is elsewhere in the world. Significantly more episodes of MDD occur among those with lower educational attainment (rather than longer episodes of disease), consistent with the hypothesis that the lower socioeconomic position increases the likelihood of developing MDD. The phenomenology of MDD varies according to the degree of educational attainment: higher educational attainment not only appears to protect against MDD but alters its presentation, to a more anxious phenotype.

29 citations


Cited by
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Journal ArticleDOI
Shane A. McCarthy1, Sayantan Das2, Warren W. Kretzschmar3, Olivier Delaneau4, Andrew R. Wood5, Alexander Teumer6, Hyun Min Kang2, Christian Fuchsberger2, Petr Danecek1, Kevin Sharp3, Yang Luo1, C Sidore7, Alan Kwong2, Nicholas J. Timpson8, Seppo Koskinen, Scott I. Vrieze9, Laura J. Scott2, He Zhang2, Anubha Mahajan3, Jan H. Veldink, Ulrike Peters10, Ulrike Peters11, Carlos N. Pato12, Cornelia M. van Duijn13, Christopher E. Gillies2, Ilaria Gandin14, Massimo Mezzavilla, Arthur Gilly1, Massimiliano Cocca14, Michela Traglia, Andrea Angius7, Jeffrey C. Barrett1, D.I. Boomsma15, Kari Branham2, Gerome Breen16, Gerome Breen17, Chad M. Brummett2, Fabio Busonero7, Harry Campbell18, Andrew T. Chan19, Sai Chen2, Emily Y. Chew20, Francis S. Collins20, Laura J Corbin8, George Davey Smith8, George Dedoussis21, Marcus Dörr6, Aliki-Eleni Farmaki21, Luigi Ferrucci20, Lukas Forer22, Ross M. Fraser2, Stacey Gabriel23, Shawn Levy, Leif Groop24, Leif Groop25, Tabitha A. Harrison10, Andrew T. Hattersley5, Oddgeir L. Holmen26, Kristian Hveem26, Matthias Kretzler2, James Lee27, Matt McGue28, Thomas Meitinger29, David Melzer5, Josine L. Min8, Karen L. Mohlke30, John B. Vincent31, Matthias Nauck6, Deborah A. Nickerson11, Aarno Palotie23, Aarno Palotie19, Michele T. Pato12, Nicola Pirastu14, Melvin G. McInnis2, J. Brent Richards32, J. Brent Richards16, Cinzia Sala, Veikko Salomaa, David Schlessinger20, Sebastian Schoenherr22, P. Eline Slagboom33, Kerrin S. Small16, Tim D. Spector16, Dwight Stambolian34, Marcus A. Tuke5, Jaakko Tuomilehto, Leonard H. van den Berg, Wouter van Rheenen, Uwe Völker6, Cisca Wijmenga35, Daniela Toniolo, Eleftheria Zeggini1, Paolo Gasparini14, Matthew G. Sampson2, James F. Wilson18, Timothy M. Frayling5, Paul I.W. de Bakker36, Morris A. Swertz35, Steven A. McCarroll19, Charles Kooperberg10, Annelot M. Dekker, David Altshuler, Cristen J. Willer2, William G. Iacono28, Samuli Ripatti25, Nicole Soranzo1, Nicole Soranzo27, Klaudia Walter1, Anand Swaroop20, Francesco Cucca7, Carl A. Anderson1, Richard M. Myers, Michael Boehnke2, Mark I. McCarthy3, Mark I. McCarthy37, Richard Durbin1, Gonçalo R. Abecasis2, Jonathan Marchini3 
TL;DR: A reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies.
Abstract: We describe a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry. Using this resource leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies, and it can help to discover and refine causal loci. We describe remote server resources that allow researchers to carry out imputation and phasing consistently and efficiently.

2,149 citations

Journal ArticleDOI
Naomi R. Wray1, Stephan Ripke2, Stephan Ripke3, Stephan Ripke4  +259 moreInstitutions (79)
TL;DR: A genome-wide association meta-analysis of individuals with clinically assessed or self-reported depression identifies 44 independent and significant loci and finds important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia.
Abstract: Major depressive disorder (MDD) is a common illness accompanied by considerable morbidity, mortality, costs, and heightened risk of suicide. We conducted a genome-wide association meta-analysis based in 135,458 cases and 344,901 controls and identified 44 independent and significant loci. The genetic findings were associated with clinical features of major depression and implicated brain regions exhibiting anatomical differences in cases. Targets of antidepressant medications and genes involved in gene splicing were enriched for smaller association signal. We found important relationships of genetic risk for major depression with educational attainment, body mass, and schizophrenia: lower educational attainment and higher body mass were putatively causal, whereas major depression and schizophrenia reflected a partly shared biological etiology. All humans carry lesser or greater numbers of genetic risk factors for major depression. These findings help refine the basis of major depression and imply that a continuous measure of risk underlies the clinical phenotype.

1,898 citations

Journal ArticleDOI
15 Sep 2016
TL;DR: An overview of the current evidence of major depressive disorder, including its epidemiology, aetiology, pathophysiology, diagnosis and treatment, is provided.
Abstract: 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.

1,728 citations

Journal ArticleDOI
TL;DR: A genetic meta-analysis of depression found 269 associated genes that highlight several potential drug repositioning opportunities, and relationships with depression were found for neuroticism and smoking.
Abstract: Major depression is a debilitating psychiatric illness that is typically associated with low mood and anhedonia. Depression has a heritable component that has remained difficult to elucidate with current sample sizes due to the polygenic nature of the disorder. To maximize sample size, we meta-analyzed data on 807,553 individuals (246,363 cases and 561,190 controls) from the three largest genome-wide association studies of depression. We identified 102 independent variants, 269 genes, and 15 genesets associated with depression, including both genes and gene pathways associated with synaptic structure and neurotransmission. An enrichment analysis provided further evidence of the importance of prefrontal brain regions. In an independent replication sample of 1,306,354 individuals (414,055 cases and 892,299 controls), 87 of the 102 associated variants were significant after multiple testing correction. These findings advance our understanding of the complex genetic architecture of depression and provide several future avenues for understanding etiology and developing new treatment approaches.

1,312 citations

Shane A. McCarthy, Sayantan Das, Warren W. Kretzschmar, Olivier Delaneau, Andrew R. Wood, Alexander Teumer, Hyun Min Kang, Christian Fuchsberger, Petr Danecek, Kevin Sharp, Yang Luo, Carlo Sidorel, Alan Kwong, Nicholas J. Timpson, Seppo Koskinen, Scott I. Vrieze, Laura J. Scott, He Zhang, Anubha Mahajan, Jan H. Veldink, Ulrike Peters, Carlos N. Pato, Cornelia M. van Duijn, Christopher E. Gillies, Ilaria Gandin, Massimo Mezzavilla, Arthur Gilly, Massimiliano Cocca, Michela Traglia, Andrea Angius, Jeffrey C. Barrett, D.I. Boomsma, Kari Branham, Gerome Breen, Chad M. Brummett, Fabio Busonero, Harry Campbell, Andrew T. Chan, Sai Che, Emily Y. Chew, Francis S. Collins, Laura J Corbin, George Davey Smith, George Dedoussis, Marcus Dörr, Aliki-Eleni Farmaki, Luigi Ferrucci, Lukas Forer, Ross M. Fraser, Stacey Gabriel, Shawn Levy, Leif Groop, Tabitha A. Harrison, Andrew T. Hattersley, Oddgeir L. Holmen, Kristian Hveem, Matthias Kretzler, James Lee, Matt McGue, Thomas Meitinger, David Melzer, Josine L. Min, Karen L. Mohlke, John B. Vincent, Matthias Nauck, Deborah A. Nickerson, Aarno Palotie, Michele T. Pato, Nicola Pirastu, Melvin G. McInnis, J. Brent Richards, Cinzia Sala, Veikko Salomaa, David Schlessinger, Sebastian Schoenherr, P. Eline Slagboom, Kerrin S. Small, Tim D. Spector, Dwight Stambolian, Marcus A. Tuke, Jaakko Tuomilehto, Leonard H. van den Berg, Wouter van Rheenen, Uwe Völker, Cisca Wijmenga, Daniela Toniolo, Eleftheria Zeggini, Paolo Gasparini, Matthew G. Sampson, James F. Wilson, Timothy M. Frayling, Paul I.W. de Bakker, Morris A. Swertz, Steven A. McCarroll, Charles Kooperberg, Annelot M. Dekker, David Altshuler, Cristen J. Willer, William G. Iacono, Samuli Ripatti, Nicole Soranzo, Klaudia Walter, Anand Swaroop, Francesco Cucca, Carl A. Anderson, Richard M. Myers, Michael Boehnke, Mark I. McCarthy, Richard Durbin, Gonçalo R. Abecasis, Jonathan Marchini 
01 Jan 2016
TL;DR: In this article, a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry is presented.
Abstract: We describe a reference panel of 64,976 human haplotypes at 39,235,157 SNPs constructed using whole-genome sequence data from 20 studies of predominantly European ancestry. Using this resource leads to accurate genotype imputation at minor allele frequencies as low as 0.1% and a large increase in the number of SNPs tested in association studies, and it can help to discover and refine causal loci. We describe remote server resources that allow researchers to carry out imputation and phasing consistently and efficiently.

1,261 citations