Huntingtin

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  • Huntington's Disease Research Paper

    The HTT gene was known as the IT15 (interesting transcript 15) which codes for a protein called the huntingtin protein (Htt) (Interesting Transcript 15). This gene has a repeated section called a trinucleotide repeat which is combined to make a codon (Huntington Disease). A codon has three bases on an mRNA molecule that code for a particular amino acid. While a normal person has less than 26 repeated codons, a person with this disease has more (Interesting Transcript 15). When the length of this repeated section reaches more than 36 consecutive series, it produces an altered form of the protein, mutant Huntingtin protein (mHtt). This type of mutation changes the decay rate for certain neurons (Interesting Transcript 15). The gene only affects some neurons and hence not all of the parts of the brain. Depending on how many repeated codons the person has it will determine the severity of the disease. A person with 40 or more repeated codons for this gene will have a severe Huntington disease (Huntington Disease). While the primary purpose for the Huntingtin protein (Htt) is unclear, it certainly interacts with proteins found in cell signaling, intracellular transporting and transcription (Interesting Transcript 15). There are multiple cellular changes through which the wrong function of mHtt may manifest and produce the…

    Words: 1572 - Pages: 7
  • Huntingtin: A Genetic Analysis

    Pathophysiology Huntingtin is a protein whose exact function is unknown. What is understood about it though is how important of a part it serves for the nerve cells in the brain (HTT, 2016). When the gene HTT that codes for this protein becomes mutated (mHTT), it causes what is known as Huntington disease (HD). This is an autosomal dominant disorder meaning only a single gene needs to be altered in order to cause this disease (Huntington disease, 2016). If there is one parent affected, each…

    Words: 815 - Pages: 4
  • Huntington's Disease Summary

    In 2001, Auerbach et al. studied the effect of mutation in HD when the protein huntingtin was limiting. Generally, the study showed that there were lethal neurological effects observed in the heterozygous Hdh knock-in mice with low levels of mutant huntingtin containing 111 glutamines (Q111) and 20 glutamines (Q20). They also found out that there were brain deficits and abnormal development with the mice having low level of Q20 huntingtin in the absence of Q111. Together, the study showed a…

    Words: 1854 - Pages: 8
  • Huntington's Chorea Case Study

    egg. The cause of these spontaneous mutations is still unknown (Payne, 2016). Huntington’s disease is traced back to the fourth chromosome where the Huntington’s disease gene is located. This gene codes for the protein huntingtin (National Human Genome Research Institute, 2011). Symptoms displayed in Huntington’s disease patients are caused by a repeat expansion of the DNA building blocks cytosine, adenine, and guanine (CAG) (United States National Library of Medicine, 2016). In an effective…

    Words: 1906 - Pages: 8
  • Advantages And Disadvantages Of Gene Silencing

    locate and enter the neurons in order to silence huntingtin expression (Dessy and Gorman 2011). Another drawback observed is the fact that high dosages of silencing molecules could have a toxic effect on the cells. This shows how imperative it is to find an ideal dosage that is both safe and effective. As mentioned above, researchers still face challenges with specificity and off target effects for neurodegenerative diseases such as Huntington’s disease (HD). When applying gene silencing as…

    Words: 2167 - Pages: 9
  • Causes Of Huntington's Disease

    Some researchers have specialized in the CAG repeats. Others have focused on the protein, huntingtin, and how it ties into our functioning body. Others take a look at the deconstruction of certain parts of the brain and try to work backwards. For many Huntington’s disease patients it is just a trial and error to try and find a set of drugs that can help manage some of the symptoms without making any of the other ones worse. Usually medicine will consistently be adjusting over the course of the…

    Words: 1729 - Pages: 7
  • Neurodegenerative Disease Essay

    be replaced. Neurodegenerative diseases are debilitating conditions that result in progressive degeneration and/or the death of nerve cells. This creates problems with movement, and mental functioning- known as Dementia. These diseases are said to be incurable (JPND Research, 2014). One example of a dominantly inherited severe autosomal neurodegenerative disease is Huntington’s disease. It is an inherited neurodegenerative disorder, resulting from an expanded poly-glutamine repeat region in the…

    Words: 1597 - Pages: 6
  • Genetic Testing Essay

    counselors are there to aid them. They provide patients with information about the results and advise them about possible choices to make. Patients that know they have a likelihood of having a certain disease, have choices to make. These choices can be to proceed treatment, undergo surgery, or do nothing. For example, people that take a genetic test to determine if they will be diagnosed with Huntington’s disease (HD), a neurological illness that causes emotional disturbance or involuntary…

    Words: 705 - Pages: 3
  • Genetic Testing Advantages And Disadvantages

    Huntington disease (HD) is a neurodegenerative disorder affecting 1 in every 10,000 individuals (Halpin, 2011). Genetic predictive testing is a good option for at-risk individuals to know if they will develop the disease. Therefore in this paper, I will discuss HD genetic testing advancements, as well as the advantages and disadvantages of the test. HD is an inherited neurological disorder that results in involuntary movements as well as cognitive and psychiatric disturbances (Warby et al.,…

    Words: 1001 - Pages: 5
  • Heat Shock Proteins In Poly Glutamine Model

    The disease is caused by the expansion of a polyQ segment located within the first exon of the gene encoding huntingtin, an 350-kDa protein. The neuronal inclusions in HD have fibrillar morphology and contain aggregated amino-terminal fragments of huntingtin . Similar inclusions containing aggregated polyQ proteins were reported in other polyQ diseases.(1,2)Previous studies have shown that two process namely the autophagy and the proteasomal system were mainly involved in the removal of these…

    Words: 918 - Pages: 4
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