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Genetics term paper

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"Individual differences in cognitive performance stem from variability in the functions of genes and environments. Identifying these genetic and non-genetic influences and how they interact with each other requires molecular (e. g., DNA linkage and association) and quantitative (e. g., twin and adoption studies) genetic designs. Molecular genetic techniques permit identification of genes or regions of chromosomes that are implicated in an outcome of interest-a level of specificity not afforded by quantitative genetic techniques. Nonetheless, quantitative genetic techniques are very useful. They do not require DNA and can be used to estimate heritability (i. e., genetic influences accounting for family member similarity), shared environment (i. e., non-genetic influences that create family member similarity), and non-shared environment (i. e., non-genetic influences that create family member differences, including error variance [Plomin, DeFries, McClearn, & McGuffin, 2000]). Heritability can be estimated in a narrow sense (to include only additive genetic effects) or in a broad sense (to include additive as well as non-additive effects, i. e., dominance, epistasis). The growing quantitative genetics literature shows that genetic influences on cognitive skills increase in magnitude over childhood, level out in adulthood, and then may decrease late in life. Over the entire life span, most of the environmental effects on cognitive performance are non-shared. with shared environmental influences limited to early childhood and perhaps old age (Finkel & Pedersen, 2001; McCartney, Harris, & Bernieri, 1990). Furthermore, individual differences in the degree of change in performance appear to be driven more by non-shared environmental than genetic influences. Unfortunately, there are no data regarding genetic and non-genetic influences on executive control in aging, a noteworthy gap that we turn to in some detail later in this paper."
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"The term "gene-environment interaction" has at least four meanings depending on the context in which it is used. In the context of studying evolution, the presence of gene-environment interaction attests to variance in fitness. Evolutionary, the presence of significant gene-environment interactions indicates the presence of some "uncertainty," an inability to accurately predict the behaviour (i. e., fitness) of a particular combination of genes (referred to as a genotype) in a given environment from the main effects of genotype and environment. Multiple types of gene-environment interactions have been investigated in this context. As most of this work is done with plants, worms, flies, and animals, the genotypes are typically known, and the central idea is to rank-order the genotypes with respect to the trait of interest in a variety of different environments. Clearly, this ordering of genotypes and environments can produce a number of different outcomes, but the following situations are of greatest interest (Remold & Lenski, 2001): (a) A single genotype is advantageous across all environments and thus demonstrates the greatest fitness; (b) no single genotype is advantageous across all environments; (c) genotypes can be rank-ordered and their ranks preserved across various environments, although the extent of variation in phenotypes associated with each genotype is much greater in one environment than another; and (d) both rank orders of genotypes' fitness and the extent of phenotypic variation vary across environments. A great deal of work has been carried out in hopes of understanding the architecture of gene-environment interaction with regard to variance in fitness, and a review of this substantial literature is outside the scope of this article. However, of special interest here is one of many remarkable observations generated in the literature, specifically that a strong gene-environment interaction can arise randomly. For example, in Escherichia coli (a common bacterium intensively studied by geneticists because of its limited number of genes and ease of growth and maintenance in laboratory settings), a single new random mutation (i. e., a mutation that had not experienced any pressure of biological selection forces in any of the environments tested in the laboratory) is sufficient to produce a strong gene-environment interaction. Moreover, contributions of new random mutations to the presence and magnitude of gene-environment interaction can vary for different environmental factors (Remold & Lenski, 2001). These observations have a number of implications, one of which is that gene-environment interaction is an important mechanism underlying phenotypic plasticity, an ability to adapt to new environmental conditions, and that "phenotypic plasticity must often depend on many different genes rather than a handful of 'plasticity' genes" (Remold & Lenski, 2001, p. 11392)."
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"Initially, the genetic discovery with the greatest importance was that point mutations in any of three genes could cause autosomal dominant inherited forms of Alzheimer's disease that were clinically and pathologically identical to non-genetic forms of the disease except that the age at onset was younger. The first mutations were found in the APP gene on chromosome 21. These mutations tend to cluster near sites where the A? peptide is cleaved from amyloid precursor protein (?-and ?-secretase sites) or where the A? peptide itself is cleaved (the a-secretase site). The next group of mutations was found in the genes encoding two proteins called presenilin 1 and 2. Subsequently, it was discovered that these two proteins play a role in the ?-secretase cleavage of A? from amyloid precursor protein. Thus, it became clear that the primary consequence of these mutations was an increase in the deposition of the pathogenic form of A?, A?(1-42), in the brain. These findings, combined with the understanding that Alzheimer's disease in patients with trisomy 21 probably resulted from a lifelong, mild but consistent excess of A?, provided the most important evidence supporting the amyloid-cascade hypothesis for the pathogenesis of the disease."
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