Faulty Gene That Causes Huntington's Disease

Huntington’s disease destroys the organs that carry the functions of the central nervous system. Kalat (2013) states, “Huntington disease (also known as Huntington disease or Huntington’s Chorea) is a severe neurological disorder that strikes about 1 person in 10,000 in the United States” (A.B. Young, 1995, p. 258).Individual’s develop the symptoms in their middle age, but even if it is a rare disorders juveniles as well as children before the age of ten can develop the disease. Huntington’s disease is hereditary disease that is passed on from a parent. Huntington’s disease is of the lack of the chromosome 4, if one of the parents carries the gene, they can pass that gene to their

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

Huntington’s disease is an autosomal, dominant inherited disorder caused by a polyglutamine expansion at the amino-terminal on the huntingtin protein. It causes a progressive degeneration of spiny nerve cells in the striatum and cortex of the brain, impairing a person’s functional and cognitive abilities. Polyglutamine repeats of 36 are found to be non-threating but sequences containing an additional two or three repeats are associated with Huntington’s disease.

Huntington’s disease is a neurological (nervous system) condition caused by the inheritance of an altered gene. A neurological disorder is a disease that can affect the central and peripheral nervous systems. Huntington’s disease is an incurable genetic brain disorder. The disease is an autosomal dominant disease, meaning a child only needs to inherit the gene from one parent to develop Huntington’s. Nerve cells become damaged when someone holds the HTT gene that produces a protein called huntingtin, as too much of this protein damages cells, and causes various parts of the brain to gradually deteriorate. Huntington’s disease causes changes in the central area of the brain, the basal ganglia, which can affect movement, emotions, and mental

neurologist named Geoge Huntington during the late 19th century. HD is a brain disorder that greatly affects a person's ability to think, speak, and move functionally (MedicineNet). The causes behind this disease were uncovered in the basal ganglia, a nuclei group linked to the thalamus, the center of the brain responsible for sensory and motor relay. The basal ganglia obtains the same control of physical movement, but is also responsible for human emotion and cognitive ability. In HD, there is a mutation on chromosome 4, which, without dysfunction, holds over 1,000 genes and creates over 186 million copies of different DNA building materials, or base pairs (Mandal, Ananya). DNA is shaped like a spiral ladder and creates different base pairs out of adenine, guanine, cytosine, and thymine. The combination of these bases determine a cell's function. Chromosome 4 creates CAG; however, all base pairs come with a maximum limit of copies that it can create. In HD, CAG is endlessly repeated, which then encodes the protein, huntingtin (Mandal, Ananya). There are results in damage of the basal ganglia, and, eventually, overall neurological

Huntington’s disease (or Huntington’s chorea) is a hereditary degenerative disease that affects the cerebral cortex and basal ganglia. It is a progressive brain disease that targets the ability to move, loss of the ability to think, and emotional problems. The most common form of Huntington’s is adult onset, appearing in the thirties or forties. As the disease advances,

Human beings have two copies of genes that provide genetic information to produce Huntington, which is a protein. The two copies are usually labeled HTT (Hayes & Reichsman, 2009). A portion of this gene is as a result of a repetitive section referred to as a trinucleotide repeat that changes in terms of length from one person to the other, as well as between different generations. In case the repeat section of the gene is present in a gene that is considered healthy, then an active mutation might lead to an increment in the repeat sections, which might in turn lead to a gene that is defective (Marks & Neill, 2007). Subsequently, the length of the repeat portion might reach a given level where it leads to the production of altered and defective proteins

Huntington’s disease is a progressive neurodegenerative disease that causes uncontrolled physical movements and mental deterioration. Huntington’s destroys the brain leading to changes in personality and even cognitive functioning. A faulty gene is responsible for this disease. This faulty gene generates a malformed protein which is accountable for the immediate damage. This damage leads to a slow decline and eventually death. Unfortunately there is no cure and only minor treatments to manage

Huntington’s chorea, or more commonly known as Huntington’s disease (HD), is a neurodegenerative disorder that affects both men and women. Although previously thought to be a relatively rare disease, new research discoveries show that it’s actually more common than not; while the onset of symptoms typically occurs in a person’s 40s and 50s, research has also shown that individuals in their 70s, 80s and even 90s have enough repeats in the HTT gene to develop mild HD symptoms. (Samson, 2016) Through the selective degeneration of neurons and with the loss of neurons from the striatum and cerebral cortex, Huntington’s disease affects the nervous system by impacting movement, cognitive abilities, as well as neuropsychiatric symptoms. Unfortunately

For our gene and protein lab, my group decided and I to research the deadly, yet rare, disease, known as Huntington's disease. Huntington's disease is an extremely rare condition when your nerve cells in your brain break down overtime. Also, “HD” has a treatment that could aid someone, but it unfortunately cannot be cured. Huntington’s Disease typically begins when someone is thirty or forty years of age and can last years to a life time.

Named after George Huntington, Huntington’s Disease is a hereditary neurodegenerative disease. It “causes the death of specific neurons in the brain, leading to jerky movements, physical rigidity, and dementia (First).” The mutation was first mapped to chromosome 4 in 1983, becoming the first disease gene to be mapped using DNA polymorphisms (First). In 1993, a group of investigators found the gene that causes Huntington’s Disease. It is caused by a mutation in a gene located on chromosome 4 (Mennitto). The gene contains an abnormally large number of CAG (Mennitto). The gene may lengthen when passed from father to child, but not mother to child (Mennitto).

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.

Huntington's disease is a genetic disease. It is an autosomal dominant disorder which means that a single defective gene copy will cause the disease because it inherits the defect in a single gene caused by a mutation in the HD (also known as HTT) gene on chromosome 4.

Huntington’s Disease (HD) is defined as being a progressive neurodegenerative condition which can be characterized by cognitive, motor and behavioral problems (Mestre, Ferreira, Coelho, Sampaio, & Costa, 2009). It is an autosomal dominant disease, meaning that if a child’s parent is affected by HD, there is a 50% chance the child will be affected as well. Huntington’s disease (first known as Huntington’s Chorea) was first documented and studied in 1872 by George Huntingon, MD (Aubeeluck & Wilson, 2008, p. 146; Bourne, Clayton, Murch, & Grant, 2006). Almost 150 years later there is still little known about this disease, which contains no cure in sight.

Huntington disease (HD) is a genetic disorder characterized by the progressive loss of neurons in the brain. It is caused by expansion of CAG repeats in exon 1 of the huntingtin gene, affecting initially the striatum and progressively the cortex. OS is known to play a role in this disease by promoting mutant Huntingtin aggregation and mutant Huntingtin-dependent cell death by mimicking proteasomal malfunction [24]. Several laboratories have demonstrated the existence of oxidative damage in HD brains [30–33] and those antioxidants slow down disease progression [34]. In HD, the initial cause of oxidative insult is the presence of mutant Htt, which has been shown to increase levels of ROS in neuronal and nonneuronal cells [18]. The level of 8-hydroxydeoxyguanosine,