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研究生： 邱佳慧
Chiu, Chia-Hui
論文名稱： 利用整合性基因體方法的富集分析和多基因風險評分於雙極症的臨床效用
Leverage the enrichment analysis and polygenic risk score of integrative genomic approaches in the clinical utility of bipolar disorder
指導教授： 張惠華
Chang, Hui-Hua
學位類別： 碩士
Master
系所名稱： 醫學院 - 臨床藥學與藥物科技研究所
Institute of Clinical Pharmacy and Pharmaceutical sciences
論文出版年： 2022
畢業學年度： 110
語文別： 英文
論文頁數： 402
中文關鍵詞： 雙極症 、路徑富集分析 、多基因風險評分 、基因體藥物富集評分 、成纖維細胞生長因子-2 、澱粉樣蛋白-β
外文關鍵詞： bipolar disorder, pathway enrichment analysis,, polygenic risk score, pharmagenic enrichment score, fibroblast growth factor-2, amyloid-β
相關次數： 點閱：96  下載：0 
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    • 摘要 I Abstract III Abbreviation VI Contents 1 List of Tables 5 List of Figures 11 List of Supplementary Appendix Tables 15 List of Supplementary Appendix Figures 16 Chapter 1 Introduction 17 1.1 Bipolar disorder (BD) 17 1.1.1 Clinical feature and epidemiology of BD 17 1.1.2 Pharmacotherapy for BD 17 1.2 Challenge in BD and its treatment 19 1.2.1 Neurocognitive function impairment of BD 19 1.2.2 Metabolic disturbance of BD 19 1.2.3 Variation in pharmacotherapy of BD 20 1.3 Genome-wide association study (GWAS) of BD 21 1.3.1 Genetic attribution of BD 21 1.3.2 GWAS to reveal biological insights into complex disorder 21 1.3.3 GWAS and BD disease 21 1.4 Post GWAS analysis 23 1.4.1 Enrichment analysis 23 1.4.2 Mendelian randomization 23 1.5 Polygenic risk score (PRS) 24 1.5.1 Introduction of PRS 24 1.5.2 PRS and disease risk 24 1.5.3 PRS and environmental factors toward the disease risk 24 1.6 Pharmagenic enrichment scores (PES) 25 Chapter 2 Objective of current study 26 Chapter 3 Material and Methods 27 3.1 Study design 27 3.2 Taiwan Biobank (TWBB) 27 3.3 Genome-wide association study (GWAS) and enrichment analysis 29 3.3.1 Subjects selection 29 3.3.2 GWAS 29 3.3.3 SNPs annotation 30 3.3.4 MAGMA gene-based analysis 30 3.3.5 Post GWAS analysis 31 3.4 Clinical measurement collection from the NCKUH cohort 32 3.4.1 Subject recruitment from NCKUH 32 3.4.2 Mood status and disease severity assessment 33 3.4.3 Blood sample collection 33 3.4.4 DNA extraction and genotyping 33 3.4.5 Physical and hematological parameters 34 3.4.6 Metabolic syndrome assessment 36 3.4.7 Treatment response assessment 36 3.4.8 Neurocognitive function assessment 36 3.4.9 SPECT with [99mTc] TRODAT-1 37 3.4.10 Questionnaire 37 3.5 Genotype for apolipoprotein E (APOE) carrier 38 3.6 Statistics 39 3.7 Mendelian randomization 40 3.8 Polygenic risk scores (PRS) 42 3.8.1 The PRS analysis process 42 3.8.2 Software and cohort data for PRS calculation 42 3.8.3 Quality control of base and target data 42 3.8.4 Process of PRS calculation 43 3.9 Pharmagenic enrichment score (PES) 45 Chapter 4 Results 47 4.1 GWAS in BD from the TWBB cohort 48 4.1.1 Characteristic of BD patients and non-BD subjects in TWBB 48 4.1.2 Principal component analysis for comorbidities in TWBB 49 4.1.3 Model selection for GWAS 50 4.1.4 GWAS in TWBB 51 4.2 Post GWAS analysis 55 4.2.1 Enrichment analysis for SNP overlapped genes 55 4.2.2 MAGMA gene-based analysis 56 4.2.3 Enrichment analysis for MAGMA genes 57 4.3 Clinical characteristics of BD and controls from the NCKUH cohort 59 4.3.1 Study population of the NCKUH cohort 59 4.3.2 Clinical characteristic of the BD patients and controls 59 4.3.3 GWAS replication study of BD in the NCKUH cohort 62 4.4 Fibroblast growth factor-2 (FGF2) in BD 62 4.4.1 Characteristics of BD and controls with FGF2 measurements 62 4.4.2 Causal relationship between FGF2 and BD risk using MR 63 4.4.3 Correlation between FGF2 and clinical indices in BD and controls 63 4.4.4 Characteristics of BD VPA users, non-VPA users and controls with FGF2 measurements 64 4.4.5 Correlation between FGF2 and clinical indices in BD VPA users, non-VPA users and controls 65 4.5 Amyloid-β (Aβ) in BD 66 4.5.1 Characteristics of BD and controls with Aβ measurements 66 4.5.2 Causal relationship between Aβ and BD risk using MR 67 4.5.3 Correlation between Aβ and clinical indices 67 4.6 Polygenic risk score (PRS) 70 4.6.1 PRS model construction for BD risk estimation 70 4.6.2 Association of PRS with BD disease risk in NCKUH cohort 71 4.6.3 Association of environmental factors and PRS with BD risk 72 4.6.4 Correlation between PRS and clinical outcomes 74 4.6.5 Enrichment analysis for gene sets within PRS 75 4.7 Pharmacological enrichment and pharmagenic enrichment score 77 4.7.1 Pharmacological enrichment 77 4.7.2 Gene-drug interaction within the pharmacological enrichment 78 4.7.3 Pharmagenic enrichment score (PES) 79 Chapter 5 Discussion 274 5.1 Characteristics of BD in Taiwanese population 274 5.1.1 Characteristics of BD and controls in the TWBB cohort 274 5.1.2 Characteristics of BD and controls in the NCKUH cohort 276 5.2 GWAS in Taiwanese BD population 277 5.2.1 Significant BD-associated loci 277 5.2.2 Significant BD-associated loci within the gene-based analysis 279 5.3 Explore the functional and pathway enrichment in BD 279 5.3.1 Brain tissue expression and network interaction of gene products 280 5.3.2 The functional and pathway enrichment in BD-related gene sets 281 5.3.3 Inflammation, metabolism, and neurological disturbance of BD 284 5.3.4 Suggesting molecular targets of BD 285 5.4 Investigate the role of fibroblast growth factor-2 in BD illness 285 5.4.1 Decreased FGF2 in BD patients 285 5.4.2 Correlation between FGF2 and clinical indices 285 5.4.3 Increased FGF2 levels in BD VPA users 286 5.4.4 Clinical utility of FGF2 in BD patients 286 5.5 Investigate the role of Aβ in BD illness 287 5.5.1 Decreased Aβ in BD illness 287 5.5.2 Cognitive deficits appeared before plaque deposition 290 5.5.3 Aβ morphology and neurological profile 290 5.5.4 Causal relationship between Aβ and BD risk 291 5.5.5 Correlation between Aβ and clinical indices in BD 291 5.6 Implication of polygenic score in BD for precise medication strategy 294 5.6.1 Polygenic risk score (PRS) 294 5.6.2 Pharmacological enrichment and pharmagenic enrichment score (PES) 295 5.7 Clinical utility of the study 300 5.8 Limitation 301 Chapter 6 Conclusion 302 Chapter 7 Reference 303

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