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May is Huntington’s disease awareness month. We in the European Huntington Association would therefore like to draw attention to the disease. (For more information go to www.eurohuntington.org)
Did you know that Huntington’s Disease was recognized as an inherited disorder in 1872? A 22-year-old American doctor, George Huntington, wrote a paper on the disease – giving it its name “Huntington’s chorea”.
‘Chorea’ means “to dance”. The name comes from the involuntary movements that often follows with the disease.
Today, we simply call it ‘Huntington’s disease’, because there are more to it than just movements.
In many countries, the situation for people with Huntington’s disease is gradually improving. However, it often comes with stigma. Many family members don’t talk about the disease and hide the illness.
Unfortunately, there is still no known cure for the disease, but brilliant scientists work around the clock to develop treatments.
Scientists will probably find the answer to the puzzle of Huntington’s one day. Until then we will work to spread knowledge, raise awareness and break down stigma. Video Rating: / 5
Huntington’s disease (HD), also known as Huntington’s chorea, is a neurodegenerative disease that is mostly inherited.[7] The earliest symptoms are often subtle problems with mood or mental abilities.[1] A general lack of coordination and an unsteady gait often follow.[2] It is also a basal ganglia disease causing a hyperkinetic movement disorder known as chorea.[8][9] As the disease advances, uncoordinated, involuntary body movements of chorea become more apparent.[1] Physical abilities gradually worsen until coordinated movement becomes difficult and the person is unable to talk.[1][2] Mental abilities generally decline into dementia.[3] The specific symptoms vary somewhat between people.[1] Symptoms usually begin between 30 and 50 years of age but can start at any age.[3][4] The disease may develop earlier in each successive generation.[1] About eight percent of cases start before the age of 20 years, and are known as juvenile HD, which typically present with the slow movement symptoms of Parkinson’s disease rather than those of chorea.[3]
HD is typically inherited from an affected parent, who carries a mutation in the huntingtin gene (HTT).[4] However, up to 10% of cases are due to a new mutation.[1] The huntingtin gene provides the genetic information for huntingtin protein (Htt).[1] Expansion of CAG repeats of cytosine-adenine-guanine (known as a trinucleotide repeat expansion) in the gene coding for the huntingtin protein results in an abnormal mutant protein (mHtt), which gradually damages brain cells through a number of possible mechanisms.[7][10] Diagnosis is by genetic testing, which can be carried out at any time, regardless of whether or not symptoms are present.[5] This fact raises several ethical debates: the age at which an individual is considered mature enough to choose testing; whether parents have the right to have their children tested; and managing confidentiality and disclosure of test results.[2]
No cure for HD is known, and full-time care is required in the later stages.[2] Treatments can relieve some symptoms, and in some, improve quality of life.[3] The best evidence for treatment of the movement problems is with tetrabenazine.[3] HD affects about 4 to 15 in 100,000 people of European descent.[1][3] It is rare among Japanese, while the occurrence rate in Africa is unknown.[3] The disease affects men and women equally.[3] Complications such as pneumonia, heart disease, and physical injury from falls reduce life expectancy.[3] Suicide is the cause of death in about 9% of cases.[3] Death typically occurs 15–20 years from when the disease was first detected.[4]
The earliest known description of the disease was in 1841 by American physician Charles Oscar Waters.[11] The condition was described in further detail in 1872 by American physician George Huntington.[11] The genetic basis was discovered in 1993 by an international collaborative effort led by the Hereditary Disease Foundation.[12][13] Research and support organizations began forming in the late 1960s to increase public awareness, provide support for individuals and their families and promote research.[13][14] Research directions include determining the exact mechanism of the disease, improving animal models to aid with research, testing of medications and their delivery to treat symptoms or slow the progression of the disease, and studying procedures such as stem-cell therapy with the goal of replacing damaged or lost neurons.[12]
Huntington’s disease: Genetics, Neurology & Clinical Aspects, Diagnosis and Treatments
Huntington disease is a rare genetic disease that can give rise to involuntary movements like Huntington chorea.
**UPDATE: How Close are We to Curing Huntington Disease? Read my article on our Blog here: https://tinymedicine.org/?p=56
Today, we’ll explore the genetic basis of Huntington disease and the Neurological basis of chorea.
• This is the short arm of chromosome 4. It is the home of the Huntington gene which codes for the Huntington protein. All humans have two copies of this gene. It has a section called trinucleotide repeat, which is a sequence of three DNA bases, Cytosine, Adenine, and Guanine, repeated multiple times.
• A mutation in this gene can further increase the repeat count. If the repeat count is over 40, this will result in a very long Huntington protein called mutant Huntington protein. It can increase the decay of certain neurons in the brain.
• This gene is inherited as autosomal dominant. You get two copies of the gene from each parent. But since it’s dominant, one mutant copy is enough to give you the disease.
• The other important feature is its penetrance close to one hundred percent.
o It means that almost all the people with the mutant gene will develop the disease.
Symptoms typically arise after the age of 35-44. The age of onset depends on the number of the repeat count of the mutation. Symptoms may arise in the childhood itself if the repeat count is very high.
At first, they develop cognitive changes and mood changes like depression.
Later, the patients will develop speech and swallowing difficulty.
Finally, they will develop jerky, uncontrollable dancing like movements called chorea.
The brain learns and stores different motor patterns in the cerebral cortex. A structure called basal ganglia keeps these motor patterns switched off via a pathway called the indirect pathway. When you want to initiate a certain movement, the motor cortex signals the basal ganglia to activate the specific motor patterns. Activation occurs via a pathway called the direct pathway. In Huntington’s disease, neurons in the indirect pathway are decayed. Therefore the brain loses the ability to switch off the motor patterns. This results in uncontrollable movement such as chorea.
The presence of symptoms and positive family history is used to come to a clinical diagnosis. Genetic testing can confirm if an adult or an embryo carries the mutant Huntington Gene.
At the moment, there’s no cure for Huntington disease Drugs such as antipsychotics are given to control the movement. Supportive care includes occupational therapy, nutritional support and speech and language therapy. A new clinical trial tests a gene silencing drug to slow down the disease progression. But the hope for a complete cure is gene editing. Let’s hope the mankind will reach there soon.
Huntington’s disease is an incurable and fatal neurodegenerative disorder characterized by movement problems and a variety of other symptoms. It is a rare example of a neurological disorder that can be traced back to a mutation in a single gene. In this video, I discuss the symptoms and pathology of Huntington’s disease.
For an article (on my website) that discusses Huntington’s disease more in-depth, click this link: https://neuroscientificallychallenged.com/posts/know-your-brain-huntingtons-disease
TRANSCRIPT:
Welcome to 2 minute neuroscience, where I explain neuroscience topics in 2 minutes or less. In this installment I will discuss Huntington’s disease.
The symptoms of Huntington’s disease typically emerge during middle age and at first often involve subtle changes in personality, cognition, and movement. Eventually, the symptoms progress into substantial movement problems like chorea, which involves uncontrolled, spasmodic movements; impaired coordination and balance; muscle rigidity; and difficulty speaking and/or swallowing. Cognitive and psychiatric symptoms like dementia and depression occur as well. The disease is incurable and fatal.
These symptoms are associated with neurodegeneration, or the deterioration and death of neurons. A group of structures called the basal ganglia are strongly affected, but other regions of the brain experience neurodegeneration as well.
The pathology of Huntington’s disease can be traced back to a mutation in a single gene called huntingtin. The mutation that causes Huntington’s disease is a dominant mutation. Thus, if one parent has the disease, their child has a 50% chance of developing it, too. The huntingtin gene contains a DNA sequence that consists of three nucleotides (cytosine, adenine, and guanine) in repetition—a pattern known as a trinucleotide repeat. When the gene is mutated, an excess number of repeats can occur, and a mutated form of huntingtin protein is created. The higher the number of repeats, the greater the risk of disease, and all people with 40 or more repeats in the huntingtin gene will develop Huntington’s disease. Mutated huntingtin proteins have a tendency to group together, forming clusters within neurons that are not easily removed by brain enzymes. It has been hypothesized these clusters may play a role in the neurodegeneration seen in Huntington’s disease, for their accumulation in the brain is associated with increased neurodegeneration.
Reference:
Walker FO. Huntington’s disease. Lancet. 2007 Jan 20;369(9557):218-28. Video Rating: / 5
For more information and resources, please visit www.HDSA.org.
The Huntington’s Disease Society of America is the premier nonprofit organization dedicated to improving the lives of everyone affected by Huntington’s disease. From community services and education to advocacy and research, HDSA is the world’s leader in providing help for today, hope for tomorrow for people with Huntington’s disease and their families. In the battle against Huntington’s disease no one fights alone. At HDSA, family is everything.
Lesson on Graves’ Disease and Graves’ Ophthalmopathy: Signs and Symptoms, Diagnosis and Treatment. Graves’ disease is an autoimmune disorder caused by production of stimulatory autoantibodies to TSH receptors that lead to excessive production and release of thyroid hormones T4 and T3. High levels of T4 and T3 lead to HYPERthyroidism with characteristic HYPERthyroidism signs and symptoms including tachycardia, insomnia, anxiety and agitation, increased bowel movements and weight loss. Graves’ disease most often affects women in their 30s and 40s and is associated with other autoimmune disorders. Graves’ disease is associated with Graves’ opthalmopathy, an extra-ocular muscle disorder caused by autoattack on retro-orbital fibroblasts that leads to characteristic Graves’ signs and symptoms including proptosis, exophthalmos, and periorbital edema, and in significant cases, corneal abrasions and sight loss.
Treatment of Graves’ disease involves the use of thionamides, including methimazole and PTU, with methimazole being the first line choice of treatment due to significant side effects of PTU.
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Check out some of my other lessons.
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We sit down with Dr. Farah Karipineni, Endocrinology, Community Specialty Surgery Associates, to better understand Graves’ disease and how this immune system disorder affects the thyroid. Video Rating: / 5
Huntington disease is caused by a mutation in the HTT gene. Understanding how the mutation causes neurodegeneration might help researchers develop treatments that protect brain function. This animation describes the genetic defect that underlies Huntington disease. Created by the editors at Nature Reviews Disease Primers.
Learn more about Huntington disease with the Primer http://dx.doi.org/10.1038/nrdp.2015.5 and PrimeView http://go.nature.com/hPMENh Video Rating: / 5
This video contains a detailed and simplified explanation about hyperthyroidism and Graves Disease. We discuss some definitions around hyperthyroidism, the different causes, the universal features and the signs and symptoms that are unique to each cause, Graves disease, toxic multinodular goitre, thyroid storm and how we manage hyperthyroidism.
More written notes and diagrams about hyperthyroidism are available on the website at www.zerotofinals.com/hyperthyroid
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