Genomics and behavior - Toward behavioral genomics
ABSTRACT The genetic influences on behavior are even more difficult to tease out than the genetic bases of complex diseases. But
discuss how the ultimate availability of the complete genome sequences of many individuals will offer a solution to this problem.
The sequencing of the human genome has opened the door to obtaining extensive maps of markers for single nucleotide variations
among people. This information will allow the use of allelic association, a method for identifying the genes that contribute
to variations in behavior among people and to complex behavioral disorders.
- SourceAvailable from: Doron Shultziner
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- "Interestingly, reports of heritability measures in twin studies are often higher for personal characteristics and political preferences than for medical disorders and other physiological traits. For example, happiness (self-reported well-being, 0.8), general intelligence and IQ (0.52 and 0.65$), divorce (0.52), extraversion (0.51), neuroticism (0.46), vocational interests in adolescence (0.42), and scholastic achievements in adolescence (0.38) have higher heritability estimates than memory (0.22) and processing speed (0.22) in twin studies (McGue and Lykken 1992; Plomin, Owen, and McGuffin 1994, 1734–5; Lykken and Tellegen 1996; McGuffin, Riley, and Plomin 2001, 1232). "
ABSTRACT: This article offers a new explanation for the results of twin studies in political science that supposedly disclose a genetic basis for political traits. I argue that identical twins tend to be more alike than nonidentical twins because the former are more similarly affected by the same environmental conditions, but the content of those greater trait similarities is nevertheless completely malleable and determined by particular environments. The twin studies method thus can neither prove nor refute the argument for a genetic basis of political traits such as liberal and conservative preferences or voting turnout. The meaning of heritability estimates results in twin studies are discussed, as well as the definition and function of the environment in the political science twin studies. The premature attempts to associate political traits with specific genes despite countertrends in genetics are also examined. I conclude by proposing that the alternative explanation of this article may explain certain puzzles in behavioral genetics, particularly why social and political traits have higher heritability estimates than common physical and medical traits. I map the main point of disagreements with the methodology and the interpretation of its results, and delineate the main operative implications for future research.Political Analysis 07/2013; 21(3):350-367. DOI:10.1093/pan/mps035 · 2.19 Impact Factor
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- "Integration of experiential and cultural influences into the day-to-day research practices of behavioral genetics , neuroscience , and cognitive neuroscience  requires that interactive processes and mechanisms implementing biocultural co-construction of brain, mind, and behavior at different levels be further specified. The lack of such specifications has been one of the reasons why the nature -nurture and mind -brain debates have continued  . "
ABSTRACT: This article deals with some fundamental epistemological problems in psychology; especially connected to how the relationship between biology, psychology and culture may be described and explained. Theories explaining human development have to reflect the biological, psychological and cultural reality and specify the functional relationships between the various aspects during lifespan. The relationships between person and environment and between mind and brain have been recurrent questions in psychological epistemology. In recent years different proposals have been introduced to overcome the epistemological problems concerning these relationships and there are more models that integrate the contradictory positions. Some of the alternatives are presented in the article. Keywords:Mind; Brain; Culture; Systems Theory; Emergence
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- "Schizophrenia recognizes a strong genetic liability (McGuffin et al. 2001). Genetic risk for schizophrenia is also associated with behavioural and physiological correlates of brain processing of different environmental stimuli (Egan et al. 2001 a ; Callicott et al. 2003b). "
ABSTRACT: BACKGROUND: Emotion dysregulation is a key feature of schizophrenia, a brain disorder strongly associated with genetic risk and aberrant dopamine signalling. Dopamine is inactivated by catechol-O-methyltransferase (COMT), whose gene contains a functional polymorphism (COMT Val158Met) associated with differential activity of the enzyme and with brain physiology of emotion processing. The aim of the present study was to investigate whether genetic risk for schizophrenia and COMT Val158Met genotype interact on brain activity during implicit and explicit emotion processing.MethodA total of 25 patients with schizophrenia, 23 healthy siblings of patients and 24 comparison subjects genotyped for COMT Val158Met underwent functional magnetic resonance imaging during implicit and explicit processing of facial stimuli with negative emotional valence. RESULTS: We found a main effect of diagnosis in the right amygdala, with decreased activity in patients and siblings compared with control subjects. Furthermore, a genotype×diagnosis interaction was found in the left middle frontal gyrus, such that the effect of genetic risk for schizophrenia was evident in the context of the Val/Val genotype only, i.e. the phenotype of reduced activity was present especially in Val/Val patients and siblings. Finally, a complete inversion of the COMT effect between patients and healthy subjects was found in the left striatum during explicit processing. CONCLUSIONS: Overall, these results suggest complex interactions between genetically determined dopamine signalling and risk for schizophrenia on brain activity in the prefrontal cortex during emotion processing. On the other hand, the effects in the striatum may represent state-related epiphenomena of the disorder itself.Psychological Medicine 05/2012; 43(2):1-14. DOI:10.1017/S0033291712001134 · 5.43 Impact Factor