However, studying the biochemical and genetic structure involved in reading neuromechanics is particularly difficult because of the limitations of animal models. Animals simply do not read or manipulate language in the same way as humans. Even in humans there is variable expressivity and reduced penetrance in the disorder hindering the ability of researchers to identify a specific gene that definitively causes DD.(6) The mechanisms that let language, reading and writing evolve in humans are more than likely to be fundamentally similar to the mechanisms that may have helped other organisms adapt to other tasks. Thus, an understanding of the neurobiological mechanisms of DD will not only tell us something about cognition, the developmental processes of the brain, but also the specific evolution of the human brain. In other words it will help us see how the brains evolved to overcome problems like those with symptoms of DD have to deal with. .
Many genes are involved in manipulating language; however four genes have been linked to an identified specific mutation leading to a change in gene expression or gene function.(3,4,5) In this paper, I will summarize current knowledge on the molecular genetics of one of the genes that undergo a known mutation that have been linked to DD. One of the four genes, DYX1C1 mutation was first discovered by Finnish doctor in the late 1990's. This mutation has also been replicated in many studies since then (although it has also not been found in other papers). Whereas the other mutations (not mentioned in this paper) occur on genes with unknown functions or known functions but an unknown mutation, these four genes have known functions, which have been scientifically validated in multiple experiments although not as thoroughly as the DYX1C1 gene. The first candidate genes for DD were found on chromosomal translocations on the loci of chromosome 15 (DYX1C1) and chromosome 3 (ROBO1).
