How to Control Huntington’s Disease

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.

It is important to know that Huntington’s disease is not curable. There are treatments and medications that are being used to help decrease the symptoms of this disease and slow down the advancement of it. Physical therapy and counseling is being used frequently as a treatment for Huntington’s. Physically, the victim with Huntington’s disease or slowly progressing into having Huntington’s disease, need some form of physical therapy to help with having unstable and involuntary motor control. Physical therapy is consisted of physiotherapy, occupational therapy, and speech therapy. Physiotherapy focuses on the body’s main functional movements such as walking or standing. Occupational therapy focuses on finding new ways to

Huntington’s disease occurs from acquiring a defective gene IT15 found on chromosome four. A typical copy of this gene yields the protein huntingtin. However, when the defective gene is bigger than usual, it yields huntingtin in a larger quantity. The etiology becomes fickle when reasons concerning why this defective protein damages the portion of the brain that administers movement. Scientists reveal that the reasoning is due to a miniscule protein called Rhes, which is found in the brain portion that governs movement. Overall, the mutant protein huntingtin causes Huntington’s disease and the defective protein Rhes contributes, however more research and testing is needed to explicate how the Rhes protein augments the pathology. The pathology entails progressive degeneration of the spiny neurons within the basal ganglia, chiefly the putamen and caudate. As the disease advances, neuronal loss ensues in the

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.

George Huntington was not the first to describe the disease, but he was the first to present an account in concise clear detail. After Huntington’s research, the disease was known as Huntington chorea. Chorea meaning sporadic, involuntary movements. As time has progressed, research has as well, and this disease has come to be known as Huntington’s disease (HD). Huntington’s is a neurodegenerative disorder that is autosomal dominant, meaning the defective gene needs only be inherited from one parent. The cause of HD is a defect that occurs on chromosome 4 and as mentioned above is hereditary. This disease affects the cognitive, motor and emotional functions of the brain. Oliver Quarrell put in simpler terms the actions of the brain cells in a book he wrote stating the known facts of Huntington’s disease. Quarrell (1999) described a person with this disease to have, “some nerve cells, in specific areas of the brain, die back early” (p.2). The action of cells dying prematurely leads to two forms of Huntington’s; Adult

Huntington’s disease is a fatal genetic disorder that causes the progressive breakdown of nerve cells in the brain and eventually causes death. It is caused by a mutation in a gene that is responsible for producing the huntingtin protein. Over a period of time, physical and mental abilities gradually deteriorate, and there is currently

Huntington’s disease, also known as Huntington’s chorea, is a rare pathology among the nervous system. With fewer than 200,000 US cases per year is an inherited condition in which nerve cells in the brain break down over a period of time. This disease will usually start to effect people when they are in their 30s or 40s. Huntington’s usually results in psychiatric symptoms, progressive movement and thinking. No cure to this disease exists but physical therapy, drugs, and talk therapy can help manage symptoms.

Huntington’s Disease (HD) is a genetically inherited, progressive, autosomal dominant, fatal neurodegenerative disease that’s characterized by behavioral difficulties, decline of cognitive abilities, abnormal involuntary movements (chorea), and muscle spasms (dystonia) (1). These characteristics help diagnose patients with HD, but a genetic test can be done to prove that one has the disorder. The gene responsible is that which produces the huntingtin protein in chromosome 4; the defect causes extra repeats of the chemical code (2).

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.

Huntington’s disease (HD) is monogenic neurodegenerative disorder characterized by motor, cognitive and psychiatric abnormalities. It consists of two types: adult onset and juvenile onset. The most common form is adult onset in which a person’s symptoms usually occur between 35-44 years old with a mean survival time of 15-20 years after onset, while the less common form known as the juvenile form begins in adolescence with a mean survival time of 10-15 years after onset.1

Huntington’s disease (HD) is a fatal genetic neurodegenerative genetic disorder affecting the brain. It results in uncontrolled jerking movements (chorea), cognitive and behavioural changes. HD leads to incapacitation of the patient and ends fatal. However, death rarely results from HD itself. It is typically due to complications of HD. HD was originally called Huntington’s chorea, because of the involuntary movements that looked like jerky dancing. Chorea is the Greek word for dancing. The majority of HD patients start developing the disease around 30 to 40 or even later. If HD onsets before the age of 20, the condition is called juvenile Huntington’s disease. This form of HD has often expresses the symptoms different and progresses faster

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

Learning about Huntington's disease was one my favorite things of my observership. because I was able to help the Dr. with its research about the disease, and observe the physical exam but most important see patients with the disease. I am from Maracaibo, Venezuela, and the city is know for the largest population with Huntington's disease, they call it "el mal del Sambito" because of the choreography like movements. It was very nice, being to relate to the disease somehow.

Huntington’s disease is a rare genetic disorder that slowly kills nerve cells. The cause is the HTT gene in the fourth chromosome, being repeated more times than the healthy gene has. Due to the death of nerve cells, you can get dementia, loss of mental abilities and chorea witch is uncontrollable movements in the arms or other parts of the body. Other symptoms include violent outbursts, seizures, and dystonia or muscle problems like tremors. Also in adolescents having no perseverance and giving up right away.

Huntington's Disease is an inherited autosomal, dominant neurodegenerative disorder. The disease is characterized by a gradual worsening of neuromotor function, mood stability, and cognitive function. Manifestations include: chorea (disordered, involuntary movement), worsening behavioral changes, impaired gait, all leading to complete loss of cognitive faculties, loss of voluntary movement, speech/communication deficits, inability to perform ADLs, dysphagia, dysarthria and dementia. Onset of the disease is around 35 – 40 years of age. Death usually occurs within 10 - 15 years of this onset18.