The human neuropsychiatric disease has a large impact on the life and work of the patients’s life, and brings a huge burden through the family and the society. Doctors, geneticists, neuroimage researchers have done a lot of work in various aspects, aiming to find a new point of view for these diseases. We have studied this problem through the candidate gene exploring and clarifying and image statistical analysis. Our contributions are at bellows: 1. For the association of risk gene with major depression, the published studies have controversial results. To evaluate the controversial, putative associations between the three common polymorphisms (promoter uVNTR，T941G，(CA) repeat) of MAOA and mood disorders (major depressive or bipolar disorders) by systematically meta-analyzing published case-control association studies. Our meta-analysis suggests a significant association of the MAOA gene with major depressive disorder and bipolar disorder within specific groups, indicating that these three polymorphisms of the MAOA gene may be associated with mood disorders by gender and ethnicity. 2. Previous studies have consistently suggested that the ε4 allele of apolipoprotein E (APOE) gene, a major risk factor for Alzheimer’s disease (AD). However, whether the ε2 allele, a possible protective factor for AD, will express its protective effect in terms of cortical thickness in healthy elderly carriers is unclear. The goal of this study is to clarify the effects of APOE genotypes on cortical thickness in nondemented elderly subjects. We used cognitively normal and elderly subjects, who were grouped into ε2 carriers, ε3 homozygotes, and ε4 carriers. We performed comparision for group differences in different genotypes and comparision with longitudinal data. These findings suggest that the different alleles of the APOE gene have distinct neuroanatomic effects in elderly healthy subjects and may play specific roles in the development of AD. 3. The present study aims to examine genetic factors in addition to Apolipoprotein E (APOE) for late onset Alzheimer’s disease (LOAD), and check their functional effects thought cortical thickness. To identify candidate loci associated with AD, we peformed the genome wide association analysis (GWAS). We used genome data for single nucleotide polymorphism and copy number variation data. Subsequently, we examine these genetic effects observed from GWAS on cortical thickness. We concluded that rs439401 might have a so called...
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