scholarly journals Propensity score-based nonparametric test revealing genetic variants underlying bipolar disorder

2011 ◽  
Vol 35 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Yuan Jiang ◽  
Heping Zhang
2014 ◽  
Vol 157 ◽  
pp. 80-86 ◽  
Author(s):  
Wen-Chi Jan ◽  
Shi-Yi Yang ◽  
Li-Chung Chuang ◽  
Ru-Band Lu ◽  
Ming-Kun Lu ◽  
...  

2011 ◽  
Vol 08 (02) ◽  
pp. 82-90
Author(s):  
N. Craddock

Summary“Schizoaffective” refers to a mix of clinical features associated with prototypical schizophrenia and prototypical bipolar disorder. Such cases are common but definitions have varied substantially. Nosological possibilities considered include (a) a form of schizophrenia, (b) a form of mood disorder, (c) a distinct disorder, (d) some mixture of (a)-(c). In current usage “schizoaffective disorder” tends to be used only when cases cannot be fitted to definitions of schizophrenia or bipolar disorder and such cases have been under-represented in cases collections to date. Methodological and practicalissues continue to cause difficulty for accumulating robust knowledge about schizoaffectivedisorder. Here we consider genetic understanding of schizoaffective disorder, particularly recent findings. These show that bipolar disorder andschizophrenia are not completely separate disease entities and confirm that schizoaffectivedisorder is genetically related to both. Some genetic variants influencerisk broadly across the mood-psychosis spectrum (e.g. Variation at CACNA1C). Some studies have implicated common variation at specific genes and gene families as conferring relatively specific phenotypic risk for a schizoaffective-type clinical pattern (e.g. GABAA receptorgenes). Such findings are of great interest and offer promise ofgreat advances in understanding over the next 20 years. It is important that there is a willingnessof researchers to study schizoaffective cases and to use approaches to phenotypic assessmentand classification that go beyond the traditional approaches enshrined within DSM and ICD.


Author(s):  
Mette Rathje ◽  
Hannah Waxman ◽  
Marc Benoit ◽  
Prasad Tammineni ◽  
Costin Leu ◽  
...  

2013 ◽  
Vol 151 (3) ◽  
pp. 967-972 ◽  
Author(s):  
Yun-Hsuan Chang ◽  
Sheng-Yu Lee ◽  
Shiou-Lan Chen ◽  
Nian-Sheng Tzeng ◽  
Tzu-Yun Wang ◽  
...  

2006 ◽  
Vol 16 (5) ◽  
pp. 183-184 ◽  
Author(s):  
Alexander Georgi ◽  
Rami A. Jamra ◽  
Johannes Schumacher ◽  
Tim Becker ◽  
Christine Schmael ◽  
...  

2019 ◽  
Vol 106 (2) ◽  
pp. 131-146 ◽  
Author(s):  
Zhiyong Cui ◽  
Xiangyu Meng ◽  
Siying Zhuang ◽  
Zhaorui Liu ◽  
Fang Zhou ◽  
...  

Abstract Until recently, it remains unclear whether schizophrenia, bipolar disorder (BD), and Alzheimer’s disease (AD) is associated with bone mineral density (BMD). We aimed to investigate the causal effects of schizophrenia, BD and AD on BMD with Mendelian randomization (MR) analysis. Single-nucleotide polymorphisms (SNPs) strongly associated with these three neuropsychiatric diseases as instrumental variables were selected from genome-wide association studies in the MR Base database. We analyzed the effects of these SNPs on the femoral neck BMD (FN-BMD), lumbar spine BMD (LS-BMD) and forearm BMD (FA-BMD), and evaluated the heterogeneities and pleiotropy of these genetic variants. We also evaluated the potential confounding factors in the association between these three neuropsychiatric diseases and the BMD level. It was found that none of these genetic variants were significantly associated with BMD or confounding factors. Using these genetic variants, we did not find statistically significant causal effects of per unit increase in the log-odds of having schizophrenia, BD or AD with FN-BMD, LS-BMD and FA-BMD changes (e.g. schizophrenia and FN-BMD, MR-Egger OR 0.9673, 95% CI 0.8382 to 1.1163, p = 0.6519). The MR results also revealed that directional pleiotropy was unlikely to bias the causality (e.g., schizophrenia and FN-BMD, intercept = 0.0023, p = 0.6887), and no evidence of heterogeneity was found between the genetic variants (e.g., schizophrenia and FN-BMD, MR-Egger Q = 46.1502, I2 = 0.0899, p = 0.3047). Our MR study did not support causal effects of increased risk of schizophrenia, BD and AD status with BMD level.


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