Huntington’s Disease Huntington’s Disease (HD) is a fatal genetic disease which causes nerve cells in the basal ganglia and other regions of the brain to deteriorate and die. Symptoms of HD begin to appear around 30 to 50 years of age and continue to intensify over the next 10 to 25 years after they first surface. Symptoms of HD include changes in personality, mood swings, depression, forgetfulness, impaired judgement, unsteady walking, chorea, slurred speech, difficulty swallowing, and severe weight loss. The cause of death in patients with HD is not Huntington’s Disease itself, but the complications that the symptoms of HD cause in patients (most notably pneumonia and heart disease) that end up killing the patient. Treatments for Huntington’s disease includes both talk therapy and physical therapy. While there is no cure for HD right now, there is research currently being done on a possible cure to the genetic disease due to a breakthrough in 1993. Researchers and scientists nationwide could not pin the cause of HD on any specific genetic factor up until 1993; researchers discovered via intense research and technological advancements that when the cytoplasmic protein huntingtin (mHtt), which is located in the short arm of chromosome four, had more than thirty-six glutamine residues (abnormal) rather than less (normal), the patient would have Huntington’s Disease. Huntingtin proteins are found in every cell in the body. The genetic code for the huntingtin protein can be found in the nucleus of the cell where genetic information is stored. DNA which contains hereditary information and genetic instructions can be found in the Nucleus, which serves as storage for the DNA and the majority of genetic material within the cell. The nucleus also directs the cell’s activities, growth, reproduction, metabolism, and protein synthesis. In a nerve cell, the type of cell that is affected by HD, the nucleus is responsible for storing the DNA and directing the cell’s activities. The function of neurons is to communicate messages to and from the cranial and spinal cavities via electrochemical processes, which would be regulated by the nucleus. Depending on the type of neuron, afferent or efferent, nuclei interpret, send, and receive messages from other nuclei in their respective part of the nervous system. Although the function of the huntingtin protein is currently unknown, scientists have been able to infer through experimentation that mHtt interacts with both huntingtin’s interactor protein (HIP-1) and huntingtin’s associated protein (HAP-1) which can only be found in the brain. This finding can explain why only cells in the brain die when a patient has the abnormal amount of glutamine residues in the huntingtin protein despite the protein being found in every cell of the patient’s body. The number of C-A-G repeats in the huntington gene determines how the huntingtin protein interacts with HIP-1 and HAP-1. In a normal huntington gene, there are less than thirty-six glutamine residues of the repeating C-A-G triplet. When that number surpasses thirty-six, the huntingtin protein consequently binds less to HIP-1 and more to HAP-1. One of many theories attempting to explain the death of neurons in HD patients discusses how the abnormal mHtt gene causes neurons to go through apoptosis (cell-suicide) at a much more accelerated rate than normal. The theory explains how HD patients’ neurons have neuronal inclusions of the abnormal huntingtin protein that only contain a segments of the full protein suggesting that at some point the protein is cut into fragments, with some within and outside of the nucleus. The apoptosis directed by the nucleus would, in theory, cause all of the organelles to cease their regular functions and die of the affected cells. Neither physical therapy nor talk therapy will help the nuclei of the abnormal cells perform their regular tasks. What the therapies offer, however, are methods to make life less painful for the affected patients and their family members/friends. Physical therapy can help limit chorea and allow for more controlled movement for patients in the later stages of the disease while talk therapy may help family members and patients in the earlier stages of the disease recognize and cope with the diagnosis. WORKS CITED Davidson, Michael W. "Molecular Expressions Cell Biology: The Cell Nucleus."Molecular Expressions Cell Biology: The Cell Nucleus. Florida State University, 1 Oct. 2000. Web. 29 Sept. 2016. Liou, By Stephanie. "HOPES." The Basic Neurobiology of Huntington’s Disease (Text and Audio). Stanford University, 26 June 2010. Web. 29 Sept. 2016. "What Is Huntington's Disease?" Huntingtons Desease Society of America What Is HD Comments. Huntington's Disease Society of America, n.d. Web. 29 Sept. 2016.