Huntington’s disease is a neurodegenerative disorder that slowly breaks down somatic tissues. This degeneration causes a mass amount of chorea, change in mental functioning, change in behavior, decreased memory, along with other serious psychological problems. Since the mechanism of the disease is still not fully understood, there is no cure for the disease, but there are several therapies and medications available. All of the medication and treatment available only help to manage symptoms; they are just stalling the progression of the symptoms but not the overall disease. Medications that have shown an ability to slow the effect of symptomatic onset of Huntington’s disease are currently being tested in clinical trials. One of these medications …show more content…
Being diagnosed with Huntington’s disease is equivalent to being told the long painful process that will eventually kill you. This is why there is a suicide rate of about 25% for those diagnosed with Huntington’s disease. There are counseling option available such as group sessions or personal doctors in order to help people cope with the idea of death. Along with counseling, there are also a number of antidepressants such as fluoxetine, citalopram and paroxetine that can help improve mood. A major problem with these drugs is that many of their side effects increase the chorea within users. These side effects are the main reason why the smallest dosage possible is prescribed, if prescribed at all. (NHS). Family members of Huntington disease victims also often need similar counseling because they have to watch their loved one go through this degeneration. …show more content…
This is a common repeat that all people have, 35 or less is considered normal, but if the repetition goes beyond that it is linked to Huntington’s disease. (U.S. Library of Medicine). In order to help treat this disease as a whole, I would propose a drug that can help to limit the number of CAG repetitions during production. One way of doing this is to have the drug target the ribosomes during their production of amino acid chains. If it can be possible to limit the CAG repetition here to no more than 35, then is can be possible to prevent Huntington’s disease before it happens. Since a person can be tested at any point in their life, this drug can be taken if a person tests positive in order to prevent the onset of Huntington’s disease. Another way to try and treat the disease is to have the drug target the rough endoplasmic reticulum, which manages the folding of proteins and recognizing any errors within its process. If the drug can promote the rough ER to target proteins with a large CAG repeat for degradation, then the protein cannot reach a toxic level. This type of treatment could be used to prevent the disease or halt the process if it has already
Huntington’s Disease is a brain disorder affecting movement, cognition, and emotions (Schoenstadt). It is a genetic disorder generally affecting people in their middle 30s and 40s (Sheth). Worldwide, Huntington’s disease (affects between 3-7 per 100,000 people of European ancestry (Schoenstadt). In the United States alone, 1 in every 30,000 people has Huntington’s disease (Genetic Learning Center). Huntington’s Disease is a multi-faceted disease, with a complex inheritance pattern and a wide range of symptoms. There is also much research being done in the field of Huntington’s disease, because as of 2012, this disease is untreatable. THESIS.
Huntington's Disease is a genetic autosomal disorder which effects the brain. It affects about 1 in 20,000 individuals. The symptoms of the disease do not start to occur until after or around 40 years of age. With the onset of the disease the patient starts to gradually deteriorate intellectually, this deterioration also causes involuntary movements. Scientists have only recently found the section of the gene which causes Huntington's disease, and this is allowed them to devise pre-symptomatic tests. However, a cure for the disease is yet to be found.
Huntington’s disease may be irreversible but it can be treated with proper treatment may slow down the effects of the disease and medical attention. In children who have symptoms of Huntington’s disease, some of the symptoms would be a rapid deteriorating in school performance, lack of swift movements, behavior changes etc...
Huntington's Disease (HD) is an autosomal dominant, progressive, neurodegenerative disorder (Walker, 2007 and Harmon, 2007). The gene that causes the disease is located on the fourth chromosome and causes an abnormal number of repeats in the patient's genetic code (Harmon, 2007). Huntington's Disease can have devastating effects on patients' quality of life. The first symptoms of HD generally start between the ages of 30 and 45 and patients are typically asymptomatic prior to this time (Terrenoire, 1992 and Walker, 2007). However, the disease progresses with subtle changes in motor control, personality, and cognition. Patients eventually develop distinct
In 2008, the FDA approved tetrabenazine, which is used to help treat chorea. This was the first drug approved to treat symptoms of HD ("Huntington's Disease: Hope Through Research," n.d.). Additionally, the use of antipsychotic drugs are used to help lessen the extremity of involuntary movements and help moderate the individuals temperament ("Huntington's Disease: Hope Through Research," n.d.). In contrast, the use of antipsychotics are not used to help treat dystonia and may actually worsen these symptoms by causing stiffness in movement ("Huntington's Disease: Hope Through Research," n.d.). Many individuals with HD also suffer from depression and may be prescribed fluoxetine, sertraline, or nortriptyline ("Huntington's Disease: Hope Through Research," n.d.). Mood swings and anxiety are controlled with the use of tranquilizers and/or lithium ("Huntington's Disease: Hope Through Research,"
Huntington's disease is an autosomal dominant disorder, which is found on the # 4 chromosome. George Huntington discovered it in 1872. It mainly has an effect on the nervous system. There are around 210,000 bases between D4S180 and D4S127. The disease itself is found in 2% of people in their childhood, and in 5% of the people they were older then 60. (Miller p 16) In the majority of the affected people the disease is detected between the ages of 35-45. In males the disease begins around the time of their childhood. However, in females it begins later in life. This severe symptom has a tendency for the condition to worsen as it is passed on from generation to generation. Huntington’s disease is paternally
Huntington’s Disease is a dominant, autosomal, neurodegenerative disease that results from excess CAG repeats on the human chromosome 4. These CAG repeats code for a protein named Huntingtin, and patients of Huntington's Disease have a mutated form of it. Symptoms begin to appear in one’s middle ages and continue to progress over a span of about 20 years. It leads to loss of mental ability and muscle coordination, as well as increasing one’s vulnerability to depression. Those who develop Huntington’s Disease cannot be cured, but there is treatment to reduce the mental and physical effects. Genetic advancements in both testing and treating Huntington’s Disease have provided hope for families with a history of this disease, but it has
Huntington’s Disease is an inherited disease of the brain where the nerve cells break down over time. Huntington’s disease can also be called HD or Huntington’s Chorea, due to over 90% of patients having Chorea as well as HD. Chorea is an abnormal body movement disorder, which affects people with HD when it comes to muscle spasms, and involuntary movements. HD is a very rare disease, fewer than 200,000 cases in the U.S. per year. If an immediate family member has HD, you have a 1 in 2 (50%) chance of inheriting the disease. After the condition appears, patient usually lives for 15 to 18 years, HD is a guaranteed death. HD can cause cognitive amnesia, memory loss, behavioral issues (irritability, lack of restraint, etc.), psychological problems (delirium, depression, paranoia, etc.), anxiety, apathy, mood swings, and many more.
Frank (2014) explains that the treatments for Huntington’s usually target hyperkinetic movement disorders, including chorea, dystonia, ballism, myoclonus, and tics. Tetrabenazine (TBZ) is considered one of the most effective agents for chorea, explains Frank (2014), however other medications like dopamine antagonists, benzodiazepines, and glutamate antagonists are also viable candidates towards treating chorea symptoms. Several studies that Frank (2014) presents show that atypical drugs like olanzapine, quetiapine, and aripriprazole show very positive results in treating chorea. In “Huntington’s disease” (2016) various medications are cited that may help alleviate behavioral and psychiatric symptoms such as fluoxetine, sertraline, nortriptyline for depression, lithium for mood swings or pathological excitement, and also cites that other medications may be needed to address obsessive-compulsive rituals in some individuals. Both Frank (2014) and “Huntington’s disease” (2016) advise that side effects need to be taken into consideration when prescribing particular medications, for example Frank (2014) writes that “providers should consider if there will be a positive or negative effect of the agent on psychiatric issues associated with HD, such as irritability, depression, anxiety, mania, apathy, obsessive–compulsive disorder, or cognitive
Huntington's disease is a neurodegenerative hereditary condition which causes problems in muscle coordination, behavioral symptoms and leads mental deterioration (Hammond and Tatum 2010). Symptom varies among persons of same family. The most punctual side effects are frequently unpretentious issues with state of mind or insight.
No treatments can alter the course of Huntington's disease. But medications can lessen some symptoms of movement and psychiatric disorders. And multiple interventions can help a person adapt to changes in his or her abilities for a certain amount of time.
Symptoms for Huntington’s disease usually become apparent later in life, between the ages of 30 and 50, but in unusual and severe cases can be visible from as early as age 2. There are three distinct types of symptoms defective huntingtin kills off brain cells, Cognitive, Psychiatric, and Movement disorders. Cognitive Disorders include difficulty in focusing on tasks, a tendency to get stuck on a thought, lack of control that can result in outbursts, lack of awareness of self-behavior, slowness in processing ideas, and difficulty in learning. Psychiatric disorders from Huntington's Disease, is most often depression, however they can also be obsessive compulsive disorder (OCD), or repeating actions over and over again, mania, or overactivity and hyperactive behavior, bipolar disorder, which is uncontrolled alternating behaviors of depression and mania. Movement disorders include jerking movements, muscle problems, slow eye movements, impaired posture and balance, difficulty with the speech or swallowing, as the tell- tale symptoms for Huntington's Disease . As a result of the above symptoms, it is also common for people with Huntington’s is drastic weight loss (Huntington's
Huntington’s disease (HD) is a rare and fatal disease known as a polyglutamine neurodegenerative disorder effecting only 4-10 per 100,000 people of European decent (Driver-Dunckly et. Al 2007). This means there is a problem with the trinucleotide that codes for glutamine, cytosine-adenine-guanine (CAG). In the case of HD there is an extreme overproduction of the CAG repeats in the protein huntingtin. Accumulation of this mutated form of the protein in neurons causes cell atrophy which in turn causes the brain to malfunction. The disease was first described by Dr. George Huntington in 1872, however it wasn’t until 1993 that the cause of the disease was actually discovered (Bertram et. Al 2005).HD is characterized by symptoms effecting the afflicted
Huntington’s disease, or Huntington’s chorea, is a neurodegenerative genetic disorder that affects muscle proficiency and proceeds to psychological decline and behavioral symptoms (Huntington’s Society, 2013). Symptoms are similar to what is seen with Parkinson’s disease, nevertheless they vary between different individuals and its progression is almost always foreseeable. Those who are suffering from Huntington’s often see symptoms anywhere between the ages of 30-50, however it has been seen in individuals as young as two and as old as 70( Huntington’s Society, 2013). Along with the progression of the disease the severity of the symptoms increase and can be separated into three different stages. In the first stage there are usually slight uncontrolled muscle movements, lack of concentration and mood changes. As the severity worsens they may need assistance proceeding with everyday activities such as walking talking and even swallowing. Irregular jerking movements of the limbs are more consistent and more noticeable to others. In
There are many studies trying to slow the progression of this disease. There was one study completed in Maryland that aimed to see if the use of lithium carbonate, with or without divalproex, would increase the brain-derived neurotrophic factor (BDNF) in the spinal fluid of patients with Huntington’s Disease. Lithium carbonate is used to treat Bipolar Disorder, while divalproex is used to treat mood disorders and seizure disorders. Both have been linked to the increase of BDNF. During the study, participants would have three spinal taps to measure for increases in their BDNF levels. The study was completed in March 2005 and was last updated in 2008, with no results posted.