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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 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.
Huntington’s disease is a genetic disorder caused by a breakdown of nerve cells in the brain. The disease affects an individual’s ability to move, their mood, and how they think. There’s currently no cure for Huntington’s disease, but there are types of gene therapy approaches that may offer hope for managing or slowing symptoms.
Huntington’s disease is a genetic, neurodegenerative disease with a devastating impact on individuals and entire families. Despite knowing the exact cause of Huntington’s disease since 1993, there still remains much unknown about this complex brain disease.
In this animation, Lauren Byrne, a Research Fellow at the UCL Huntington’s Disease Centre shares her personal experience with Huntington’s. She takes us inside the brain to explore the mechanism of this disease leading to the cognitive, behavioural and motor symptoms in Huntington’s.
This is a Roche video developed in collaboration with Ed Wild, also from UCL Huntington’s Disease Centre, George Yohrling from the Huntington’s Disease Society of America, and Roger and Brenda Wylie, a family living with Huntington’s disease.
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UVA Neurologist Madaline Harrison, MD explains the signs of Huntington’s Disease.
Huntington’s disease is a rare genetic disorder that causes programmed degeneration of brain cells, called neurons, in certain areas of the brain. This talk explores the diagnosis, stages of the disease, and its treatment. The Stanford Huntington’s Disease and Ataxia Clinic has been named a Center of Excellence by the Huntington’s Disease Society of America. This talk reflects the treatment standards offered at Stanford.
Speaker: Veronica Santini, MD Clinical Instructor, Neurology and Neurological Sciences, Stanford University Medical Center
This video explains the genetics behind Huntington’s disease (HD) in a simple way. If you have any further questions about the genetics of HD email us at questions@hdyo.org Please consider making a donation to HDYO here: https://en.hdyo.org/eve/about/587
Dr. Claudia Testa provides an overview of genetic testing options for Huntington’s Disease, including pre-symptomatic, symptomatic and reproductive choices.
The Parkinson’s and Movement Disorders Center at VCU Health offers clinical, research, and outreach services for movement disorders. Learn more on our website at http://parkinsons.vcu.edu/index.html Video Rating: / 5
