is highly speculative. However, there are some suspects; Superoxide Dismutase (SOD1)- overexpression may cause premature aging and decreased function of the immune system; its role in Senile Dementia of the Alzheimer's type or decreased cognition is still speculative., COL6A1- overexpression may be the cause of heart defects. ETS2 -overexpression may be the cause of skeletal abnormalities and/or leukemia. CAF1A-overexpression may be detrimental to DNA synthesis. Cystathione Beta Synthase (CBS)-- overexpression may disrupt metabolism and DNA repair. DYRK-overexpression may be the cause of mental retardation. CRYA1- overexpression may be the cause of cataracts. GART- overexpression may disrupt DNA synthesis and repair. INFAR- the gene for expression of Interferon, (Leshin) overexpression may interfere with the immune system as well as other organ systems. Other genes that are also suspects include APP, GLUR5, S100B, TAM, PFKL, and a few others. (Vosatka, 185) Again, it is important to note that no gene has yet been fully linked to any feature associated with DS. One of the more notable aspects of Down syndrome is the wide variety of features and characteristics of people with trisomy 21: there is a wide range of mental retardation and developmental delay noted among children with DS. Some babies are born with heart defects and others aren't. Some children have associated illnesses such as epilepsy, hypothyroidism or celiac disease, and others don't. The first possible reason is the difference in the genes that are triplicated. As I mentioned above, genes can come in different alternate forms, called "alleles." The effect of overexpression of genes may depend on which allele is present in the person with trisomy 21. The second reason that might be involved is called "penetrance." If one allele causes a condition to be present in some people but not others, that is called "variable penetrance," and that appears to be what happens with tris...
