Epigenetic regulation refers to genetic-like effects that are not related to changes in the DNA sequence. These effects may be inherited, or they may be spontaneous and arise in the genome after conception.
Epigenetic mechanisms include changes in the histone proteins that package DNA into chromosomes and in the methylation of promoter-inhibitor regions in genes. For genes to be effectively transcribed, their promoters must be unmethylated and histones need to be appropriately unraveled so that the transcriptional machinery has access to the DNA molecule.
One example of epigenetic regulation is the modification of a chromosome inherited from one parent that effects gene transcription in the offspring. This is called imprinting.
Neuropsychological genetics is the discipline of characterizing the genetic contribution to variation in human cognition and emotion. This involves characterizing human behavior as a phenotype that will show variation based on genetic variation, that is, genotype.
From the zodiac signs to the four humors, we have attempted to derive systems to better define personality types. While most ancient forms used a categorical method, modern personality research has also focused on dimensional traits. For example, Hans Eysenck and his associates enumerated a set of independent personality characteristics based on a factorial analysis of personality measures.
In the field of personality dimensional research, the most widely used of such factor-based inventories is the “Big Five,” or NEÖAC (also called NEO). This instrument consists of five factors, dubbed Neuroticism, Extro-version, Openness to Experience, Agreeableness, and Conscientiousness.
From a genetic perspective, however, categorical descriptions of human neuropsychological and temperamental characteristics are problematic, because they attempt to represent a complex and likely quantitative trait as a binary state. Either you have it or you do not. However, the genes associated with these complex traits are not about the behaviors, per se, but reflect the underlying neurobiology.
Familial aggregation studies compare rates of disease between the relatives of individuals with a disease versus rates observed in relatives of individuals who do not have the disease. If a trait is under genetic influence, the rate of disease among relatives of affected individuals would be expected to be higher than among relatives of disease-free individuals. Indeed, the degree of relationship (e.g., full siblings, first cousins) should be predictive of disease rates if a trait is under strong genetic control because, on average, full siblings share 50% of their genomes, whereas more distantly related relatives such as first cousins share 25%.
Twin and migrant studies are used to untangle the correlation between genes and environment. Because monozygotic (MZ) twins share 100% of their genomes, we expect any trait greatly determined by genetics to show more similar phenotypes in MZ twins than in dizygotic (DZ) twins or full siblings, both of whom share, on average, 50% of their genomes.
Migrant studies assess differences between, for example, the rate of disease in individuals who have migrated to a new environment-lifestyle versus that observed in the migrants’ source population, with differences in rates often interpreted to be reflective of environmental factors if the migrants are representative of the source population. A related paradigm is the adoption study, in which the rate of illness in individuals adopted at birth who have biological relatives with illness is compared with that of control adoptees that have illness-free relatives.
Decision making is a high-level cognitive process that relates to everyday choices according to long-term and short-term outcomes inter-relationships. It depends on systems responsible for memory as well as those for emotion and affect. With some limitations, different components of human decision-making tasks can be modeled using tasks designed for rodents.
“Delay discounting” tasks are used as a measure of impulsive decision making where “response costs” are varied by imposing a delay before delivery of larger reward versus obtaining an immediate, smaller reward.
Source : The Genetics of Cognitive Neuroscience by Terry E. Goldberg (Editor), Daniel R. Weinberger (Editor)
Goodreads : https://www.goodreads.com/book/show/6902204-the-genetics-of-cognitive-neuroscience
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