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1.
“遗传与环境”的争论一直是创造力研究的核心问题, 但目前对于环境以及遗传与环境交互作用对创造力影响的分子生物机制还未有研究涉及。近年来, 随着表观遗传学的兴起, 揭示影响心理行为的表观遗传机制现已成为心理学研究的热点。作为环境与基因组之间的纽带, 表观遗传学研究为揭示环境以及遗传与环境交互作用对创造力影响的分子生物机制提供了机遇。本研究以多巴胺相关基因、家庭环境以及两者对于创造力的交互作用为切入点, 对影响创造力的表观遗传机制进行考察, 并在此基础之上, 对环境以及遗传与环境交互作用对创造力影响的分子生物机制进行探索。具体研究内容包括:(1)通过对多巴胺相关基因甲基化模式与创造力关系的系统考察, 筛选出甲基化模式与创造力有关的基因; (2)对筛选出的基因, 进一步考察其甲基化模式在家庭环境及其遗传多态性与家庭环境交互作用对创造力影响中的中介作用。本研究有助于揭示创造力的表观遗传机制, 深化关于遗传与环境对创造力影响的作用机制的理解。  相似文献   

2.
DRD4基因是亲社会行为的重要候选基因,且与环境交互影响亲社会行为的发生发展。通过梳理既有研究,本文从性别差异、亲社会行为的不同类型及发展动态性等角度探讨了亲社会行为遗传研究存在分歧的原因,并在此基础上探索了DRD4基因作用于亲社会行为的潜在脑机制。未来研究应采用纵向设计探究DRD4基因影响亲社会行为的发展动态性问题,并深入探索其性别差异;采用多质多法分析考察不同类型亲社会行为遗传机制的差异性;采用影像遗传学设计揭示“DRD4基因—脑—亲社会行为”作用机制。  相似文献   

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4.
抑郁症具有中等的遗传度。通过影像遗传学方法探讨抑郁相关基因的多态性对神经活动的影响,发现编码五羟色胺、促肾上腺素释放激素受体、多巴胺等神经递质或受体的基因多态性会影响杏仁核、前扣带等情绪加工脑区的功能或结构,且多数基因与压力生活经历发生交互作用。表明基因与环境的交互作用在抑郁症发病机理中扮演重要角色。未来的研究应拓展遗传和神经影像分析方法,重视环境因素的测量,通过整合遗传、神经影像及环境变量构建抑郁病理模型。  相似文献   

5.
The recently completed sequencing of the human genome heralds a new era in the study of social influences upon health. Because the interactions between genes and the environment are bidirectional, expertise in the areas of psychosocial processes and health behaviors will be necessary for elucidating how genes, behavior, and the environment interact to affect health outcomes. For investigators whose primary background is in social health research, the terminology used by geneticists may seem like a foreign language. To help navigate this foreign territory, the nature of genetic variation and gene action is presented in non‐technical terms using the serotonin transporter gene as an example because it is thought to influence sensitivity to the social environment. In addition, we describe several methodological pitfalls to be avoided when associating genetic variation with psychosocial and behavioral risk factors for poor health outcomes.  相似文献   

6.
ABSTRACT This article deals with the contribution of genetic and environmental factors to individual differences in the three major dimensions of personality (Psychoticism, Extraversion, and Neuroticism) Twin studies indicate, and family studies confirm within limits, the strong genetic determination of these and many other personality factors, additive genetic variance accounting for roughly half the total phenotypic variance On the environmental side, shared family environment plays little or no part, all environmental effects being within-family Assortative mating, important in the formation of social attitudes, has little impact on personality Dominance may be important for Extraversion Epistasis (emergenesis) may account for the comparative low values of dizygotic (DZ) twins' correlations Evidence for differential heritability of traits is present, but not very strong It is concluded that behavioral genetics forms a vital part of the psychological understanding of the causes of individual differences in personality  相似文献   

7.
This article is part of the Twin Mother's Study, a study that examines influences on maternal adjustment. A number of studies have investigated the importance of genetic factors for mental health, but few of these examine how genes and the environment influence resiliency/salutogenic factors. This article investigates the relative importance of genetic and environmental influences on resiliency/salutogenic factors. This study includes 326 twin pairs (150 monozygotic and 176 dizygotic) who are mothers, who are living with their spouse, and who are part of the Swedish twin register. Using self‐report structured questionnaires, we assessed salutogenic factors, depression, and quality of life; however, we analyzed the questionnaires completed by the mothers. Statistical analyses were conducted using structural equation modeling. We conclude that nonshared environmental components were of principal importance in individual resiliency/salutogenic factors in a genetically informative design, but we also noted that genetic influences were important. The shared environment had mainly no effect.  相似文献   

8.
One of the clearest results in previous studies on social trust is the robust positive relationship with educational attainment. The most common interpretation is that education has a causal effect on social trust. The theoretical argument and empirical results in this article suggest a different interpretation. We argue that common preadult factors such as cognitive abilities and personality traits rooted in genes and early‐life family environment may confound the relationship between educational attainment and social trust. We provide new evidence on this question by utilizing the quasi‐experiment of twinning. By looking at the relationship between education and social trust within monozygotic (MZ) twin pairs, we are able to avoid potential confounders rooted in genetic factors and common environmental influences because the monozygotic twins share both. The results suggest that when controlling for such familial factors the estimated effects of education on social trust are close to zero and far from reaching statistical significance. Further analyses show that the relationship between education and social trust largely is driven by common genetic factors.  相似文献   

9.
ABSTRACT— We review association studies that have examined the genetic basis of eating disorders. Overall, findings suggest that serotonin, brain-derived neurotrophic factor, and estrogen genes may be important for the development of the disorders. These neuronal systems influence behavioral and personality characteristics (e.g., anxiety, food intake) that are disrupted in eating disorders. Future studies would benefit from larger sample sizes and inclusion of behavioral and personality covariates in analyses. Consideration of the mechanisms of genetic effects and interactions between genes and environment is also needed to extend conceptualizations of the genetic basis of these disorders.  相似文献   

10.
It is now well established that nature and nurture are both important contributors to variation in human personality. As a result, the field of personality behavior genetics is moving beyond simply estimating the magnitude of genetic and environmental influences on various personality constructs. Recent methodological advances provide for the study of how these different sources of influence interact in the development of personality. Specifically, newer biometrical moderation models allow for group‐specific estimates of heritability and environmental influences on personality (a form of gene–environment interaction). In the current paper, we review selected recent research using these models. Furthermore, we explore how moderation might also be important in understanding links between specific genes and personality. Accounting for the contingencies between genes and environment will be an important catalyst for the molecular genetic study of personality, as unmoderated ‘main effect’ types of gene → personality associations have been elusive.  相似文献   

11.
Personality disorders have a long history in the literature but a short scientific history. The point prevalence of personality disorders is 10%, but the lifetime prevalence is probably 30–40%. Genetic factors contribute to around 40–50% of the variation in the development of personality disorders. The effect of shared environment is very small or non‐existent. Some researchers have tried to promote gene‐environment interaction. However, in reality, the studies investigated gene‐situation interaction, as the “environment” may in reality be partly of a genetic nature. Thus, we are dealing with an unknown part of gene‐gene interaction. Gene‐experience (not gene‐environment) correlations are the rule in human life. Personality disorders co‐occur (are comorbid) with symptom disorders (Axis I) and correlate with common personality dimensions. Possibly, the concept of personality disorder could merge with dysfunctional personality types. But it is likely that the concept will survive on its own.  相似文献   

12.
Although both aggressive (AGG) and deceitful behaviors (DEC) are symptoms of childhood conduct problems, few studies have examined common vs. specific etiological influences. Early intervention is encouraged for conduct problems and findings from genetically informative studies can suggest whether interventions should focus on conduct problems in general or groupings of conduct problems more specifically. Twin model-fitting analyses were conducted on same and different teacher ratings of AGG and DEC for 872 9-year old male twin pairs. Common genetic influences were found to underlie the susceptibility for both AGG and DEC. The same teacher ratings resulted in somewhat higher heritability estimates than different teacher ratings. Results also indicated stronger environmental effects for DEC as compared with AGG, with a significant shared environmental component for same teachers and a substantial non-shared environmental component for different teachers. Our data suggest that AGG and DEC share risk genes and environmental factors may differentiate these two types of conduct problems. Characterizing these specific environmental factors may be useful when developing interventions.  相似文献   

13.
根据攻击行为的意图可以将攻击分为主动性攻击和反应性攻击。近年来, 研究者对遗传和环境在主动性攻击和反应性攻击发展中的作用进行了探讨, 并获得了两类攻击具有不同遗传和环境基础的重要发现。既有研究主要采用定量行为遗传学研究的范式考察两类攻击的遗传基础, 未来研究应从确定与两类攻击相关的候选基因、遗传基因与环境的交互作用机制、遗传基因作用于两类攻击的神经生物机制等方面展开。  相似文献   

14.
风险决策是指个体对不同选项及其概率进行权衡之后做出决定的过程。它是一个复杂的加工过程, 需要平衡奖赏选项的诱惑和损失选项的忧虑。风险决策能力是人脑最重要的高级功能之一。在现实生活中, 风险决策能力具有非常大的个体差异, 而遗传和环境各自都在其中起着关键的作用。在这篇文章中, 我们首先综述近年来风险决策研究领域中探讨遗传影响风险决策加工的研究, 包括双生子研究与分子遗传学研究。在介绍分子遗传学研究时, 按照基因所属神经递质系统, 分别介绍了多巴胺递质系统相关基因(如COMT、DAT等)、五羟色胺递质系统相关基因(如SLC6A4、TPH1等)和其他基因(如BDNF)对风险决策能力个体差异的影响。随后, 我们探讨了环境对风险决策个体差异的影响, 以及基因-环境交互作用对风险决策个体差异的影响。接下来, 我们介绍了将脑的结构与功能作为内表型来考察基因和环境对风险决策个体差异的影响的最新进展。在文章的最后, 我们指出今后对风险决策个体差异的研究应该同时考虑遗传和环境, 并考察脑的结构和功能在其中的中介作用。  相似文献   

15.
Both genetic and environmental factors contribute to the pathogenesis of a wide variety of neurodevelopmental disorders, including autism, mental retardation, and schizophrenia. Some heritable disorders approach 100% penetrance; nonetheless, even in these disorders, subtle aspects of clinical disease expression may be influenced by the environment. In other disorders with genetic influences, exogenous factors, and the timepoint(s) during nervous system development at which they are introduced, modulate expression of disease. Elucidation of the mechanisms guiding this intricate interplay between host response genes, environmental agents, and the neurodevelopmental context within which these interactions occur, is necessary to understand the continuum of clinical outcomes. This chapter will review the evidence that infectious and immune factors may contribute to the pathogenesis of neurodevelopmental disorders, describe an animal model of neurodevelopmental disorders based upon viral infection, identify processes by which neural circuitry may be compromised, and outline areas for future research.  相似文献   

16.
抑郁具有复杂的、非孟德尔式的多基因遗传模式, 但是目前多数抑郁的遗传研究集中于考察单个候选基因, 不能全面揭示遗传因素的作用机制。近年来, 多基因遗传得分研究和基因−基因交互研究分别为抑郁的多基因累加效应和交互效应提供了新的证据。多基因不仅直接影响抑郁, 还通过与环境因素的交互作用影响抑郁的发生发展, 并且这一复杂交互作用存在性别差异。抑郁的内表型研究发现多基因可能通过认知因素、人格、压力荷尔蒙等间接影响个体的抑郁水平。未来研究应更加关注多基因与多种环境因素如何相互作用影响抑郁, 探索多基因遗传机制的性别差异, 考察多基因对抑郁影响随年龄的发展动态变化。  相似文献   

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18.
抑郁的遗传效应存在发展动态性。一方面,在发展过程中,抑郁的遗传率会发生改变,抑郁的风险基因及其与环境的交互作用模式也存在动态变化。另一方面,遗传因素会影响抑郁的发展变化模式。通过梳理既有相关研究,本文从生理成熟因素、表观遗传和发展级联效应三方面分析抑郁遗传效应发展动态性的原因。未来研究应区分重要发展阶段,增加脑功能、性激素、神经生物蛋白以及表观遗传等指标考察抑郁遗传效应的变化模式及其发生机制。  相似文献   

19.
ABSTRACT— Interactions between genes and the environment are a critical feature of development. Insights into the dynamic interplay between these factors have come from laboratory studies exploring experience-dependent changes in gene function, which illustrate the importance of environmental factors in determining activity of the genome. These studies have implications for our understanding of the origins of individual differences in behavior and may provide new ways of thinking about the transmission of traits across generations. Here we will highlight how these new findings illustrate the importance of putting genes in context.  相似文献   

20.
The Presidential Address of the European Association of Developmental Psychology, Goossens (2012, this issue), this year concerned how genes and environments interplay to shape loneliness and other developmental psychological relevant outcomes. This is a very welcome. However, when developmental psychology is now ready to integrate recent genetic and neuroscience knowledge and methods, I think it would be very wise not to go uncritically through the mistakes that have been made in other disciplines and instead to learn from their hard lessons. I discuss some problems (genes vs. environments, identifying genes for a phenotype, environmental causes of developmental outcomes, and gene×environment interaction and epigenetics) and some suggestions for solutions that can be used to avoid throwing the bathwater in with the baby.  相似文献   

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