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Trinucleotide repeat abnormalities are the cause of monogenic diseases, such as Huntington’s disease and fragile X syndrome. A group of illnesses that mostly affect the nervous system and are caused by the aberrant growth of repeating sequences are known as trinucleotide repeat disorders. Genetic illnesses like Huntington’s disease and fragile X syndrome have attracted a lot of scientific interest because of their significant effects on both people and families. Their molecular characteristics are comparable, despite their differences in many other areas. The goal of this study is to comprehend how these two illnesses are comparable genetically.
The underlying causes of Huntington’s disease and fragile X syndrome are aberrant repetitions of particular gene sequences. An unstable CGG repeat on the X chromosome’s FMR1 gene is linked to fragile X syndrome. Fragile X syndrome patients have alleles with more than 200 CGG repeats, whereas normal people normally have alleles with 6 to 40 repetitions. Conversely, Huntington’s disease is associated with an enlarged CAG repeat in the chromosome 4 HTT gene. While alleles in HD patients have more than 40 repetitions, up to 121, normal alleles have between 9 and 26 repeats. Furthermore, both conditions are linked to
having dominant inheritance, meaning that one copy of the gene mutation comes from either
Huntington’s disease, fragile X syndrome, and other neurological diseases are caused by expansions of trinucleotide repeats. Although the two disorders have similar mental health issues, their distinct features are highlighted by the variations in symptoms. Movement and cognitive function issues are hallmarks of Huntington’s disease. Chorea, for instance, causes “involuntary, jerky movements, resembling a dance-like motion” and slows down information processing, which influences judgment and reaction times. On the other hand, Fragile X syndrome causes distinct cognitive impacts, especially in intellectual and linguistic development. such is trouble with grammar and syntax and delayed speech beginning.
In conclusion, research on Huntington’s disease and fragile X syndrome has shown both unique and shared genetic traits. Although they are both caused by gene repeats, the molecular results are different, resulting in distinct symptoms. The significance of understanding these genetic complexity is highlighted by the fact that neurogenetic abnormalities are present in both illnesses. In addition to improving our knowledge of trinucleotide repeat diseases and the neurogenetic disorders associated with them, this gives us hope for guiding future studies and targeted therapies.
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