Huntington 's Disease ( Hd ) Is A Neurodegenerative Disease

McMahon , et al, 2014). Another factor that can play into S.A.D. is melatonin, which helps with sleep and wake cycles. Rosenthal, et al, notes how the pineal gland, the gland that produces melatonin, will react to dark surroundings with drowsiness that can lead people to being lethargic (as cited in Melrose, 2015). When melatonin increases and serotonin decreases, the offset of the proteins can cause circadian rhythms to be disrupted, which is the bodies “24 hour” clock. Researcher Melrose writes that “…circadian rhythms respond to the rhythmic light-dark changes that occur daily and throughout each of the seasons.” (2015). People with S.A.D. disorder normally find that their circadian rhythms are off beat and timed differently with day lengths, for example feeling tired in the middle of the day while being wide awake or feeling wide awake when it would normally be time to sleep.

Huntington 's Disease (HD) is a progressive brain disorder caused by a defective gene. This disease causes changes in the central area of the brain, which affect movement, mood and thinking skills. Nerve cells become impaired, causing several segments of the brain to fail. The disease disturbs movement, behavior and perception the affected people abilities to walk, think, reason and talk are slowly weakened to a point that they eventually become entirely dependent on other people for care. HD is a disease that affects the brain in many different ways. One of the ways the HD affects the brain is that it causes the person who has it to become forgetful and moody. Huntington 's disease also causes a decline in thinking and reasoning skills, including memory, concentration, judgment and ability to plan and organize.

According to Genetic Science Learning Center, it has been stated that approximately 1 in every 30,000 Americans have been affected with Huntington Disease and is considered one of the most common brain disorders due to heredity (Genetic Science Learning Center). This disease was discovered by a 22-year-old American doctor, named George Huntington, in 1872. Huntington wrote a paper called On Chorea which was published in the Medical and Surgical Reporter, and the disorder later become known as Huntington Chorea, but is now commonly known as Huntington Disease (What Is The History of Huntington’s Disease?). Huntington disease-like Syndrome (HDL) is a condition that resembles a lot like Huntington disease (HD) (Huntington disease-like Syndrome).

Huntington’s disease is a hereditary disorder that affects a person’s nervous system and kills brain cells. It is caused by a defective gene on chromosome four, which is one of the chromosomes that holds our genetic code. This disease has been known to cause problems with the body’s abilities to produce energy from nutrients taken in from the body. Patients that have more advanced stages of Huntington’s Disease commonly experience increased weight loss.

Researchers used luciferase on fireflies to study this mechanism. The result showed some significant results about how this “clock gene” affect behaviors. With enough enzyme, researchers can repress the DNA at the clock gene and completely change the behavior of any animal. The gene also provided some explanations for how light exposure can change human’s behaviors. From the talk, Dr. Herzog mentioned that the VIP (vasoactive intestinal polypeptide) cells in the suprachiasmatic nucleus can respond to light. Therefore, when the light shifts our daily behavior, it means that the VIP cells must be activated somehow in the SCN. The activation of VIP results in a chain of reactions inside the suprachiasmatic nucleus and cause a shift in circadian

Huntington 's disease is a dynamic, neurological disorder. Tragically, it doesn 't demonstrate manifestations until people have reached they’re 30 's or more. 'Children whose parent 's have this genetic disorder have a 50-50 ' ( ) possibility of acquiring the trait.

Huntington’s disease (HD) is a late-onset, usually between 35 and 50 years old, neurodegenerative disorder prevalent in 3-7 per 100,000 people of European ancestry1. The disease, inherited in an autosomal dominant pattern2, is characterized by motor disturbance, intellectual decline, and psychiatric manifestations3. The disease is difficult to detect at an early stage of an individual’s life since its symptoms appear in the third to fifth decade of life. To better understand the disease, investigations were done to identify the gene that is linked with the disease. The researchers in this paper relied on the polymorphic protein markers or enzymes which they excluded in the 20% of the genome. However, the lack of additional markers made it impossible to test the remaining part of the genome.

Huntington’s disease is a progressive, degenerative disease like Alzheimer’s and Parkinson’s. It is characterized by tremors, uncontrolled movements, emotional issues, and cognitive problems or loss of the ability to think properly. The mutation of the huntingtin protein causes brain cell death that directly influences mood changes and mental problems. Diagnosis of HD uses different methods to determine HD symptoms and mutation of the relevant protein.

Most of the carriers of Huntington disease are usually childhood victims (Donaldson, Marsden, Schneider, & Bhatia, 2012).

According to Cunha, (2010) article Huntingtons Disease, there is no treatment to stop Huntington’s disease. The physicians may prescribe a lot of medication to control the emotional and movement problems. The U.S Food and Drug Administration approved tetrabenazine in August 2008 to treat the HD making it the first drug approved in U.S to treat the disease. To help reducing the choreic movements and help to control hallucinations, delusions and violent outburst, use Antipsychotic drugs such as haloperidol or clonazepam. However, the Antipsychotic are not prescribed for other form of muscle contraction called dystonia associated with HD that can worsen the condition causing stiffness. Also, it have a severe side effects including sedation so it should take in lowest doses. Physicians may prescribe fluoxetine, sertraline, nortriptyline for depression. Tranquilizers help to control anxiety and lithium may prescribed to severe mood swings and pathological excitement. Some individuals with HD need medications to treat the obsessive-compulsive. Other drugs used to treat symptoms of HD have side effects such as fatigue, restlessness and hyperexcitability.

The name suprachiasmic comes from the fact that it is located just above the optic chiasm (Kalat, 2013). The SCN generates circadian rhythms itself based on genetics. If neurons in the SCN are detached from the rest of the brain, they still generate a rhythm. (Earnest, Liang, Ratcliff, & Cassone, 1999). Though SCN cells can sustain a rhythm on their own, interation between SCN cells and other parts of the brain aid in producing a rhythm in sync with one’s daily life (Long, Jutras, Connors, & Burwel, 2005). In studying hamsters’ circadian rhythms it was found that a mutation causes hamsters’ SCN to generate a 20-hour rhythm instead of a 24-hour rhythm. When the researchers removed the SCN tissue from the hamsters with a 20-hour rhythm into a normal hamster with a 24-hour rhythm, they then produced a 20- hour rhythm. Likewise, when they transplanted the tissue from the hamster with a normal 24-hour rhythm into the hamster with the mutated gene they no longer produced a 20-hour rhythm, they then produced a 24- hour rhythm (Ralph, Foster, Davis, & Menaker, 1990)

Circadian rhythm disorders are interruption in a person’s circadian rhythm which an internal body clock that manage 24-hour cycle of biological growth in animals and plants. The main characteristic of circadian rhythm disorders is a repeated or occasional interruption of sleep patterns. The interruption results from either a failure in the internal body clock or a disparity between the internal body clock and the external environment concerning the period and duration of sleep. As a result of the circadian disparity, individuals may have disruption or interruption to the normal circadian rhythm which cause the patients to experience too much daytime sleepiness, insomnia or both of

Circadian Rhythms are controlled by the suprachiasmatic nucleus (SCN), a group of cells found in hypothalamus. The SCN allows the body to adapt day-night changes through the release of melatonin which rises at night and falls in daytime. Melatonin treatment is used to fix desynchronized

A) Huntington’s Disease has been the focus of various research experiments for many years. Thanks to the consistent research that has been done in this field, we have come to learn many things about

Bimonthly, a random sample of 5 mice will be taken and analyzed for levels of expression of peripheral clock genes in the form of PER proteins in the cytoplasm of cells [5]. The relative levels of the proteins in the cytoplasm will be compared between the three test conditions and analyzed to determine the effects of a high fat diet on the sleep cycle. Each sample of mice will be euthanized and a sample of Epididymal adipose tissue will be taken [6]. Proteins and primary RNA transcript will be extracted from adipose tissue via a TRIzol extraction kit following the protocol published by The Institute for Genomic Research [6]. The sample taken from these mice will have varying levels of PER and CLOCK protein. To help further quantify the relative amounts of these proteins in the extracted sample an ELISA assay will be used. [7]. An ELISA assay will require the purified sample, an antibody specific to the CLOCK protein, and a substrate specific to the antibody [7]. The CLOCK specific antibody will react with the relative amounts of protein extracted from the sample, which, by the addition of a substrate, will be translated into a measurable signal. Once completed, the signal will be analyzed by a plate reader, which uses a program to measure the intensities between the various samples and quantifies the