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245				<h1><span>About</span>&nbsp;Huntington's Disease</h1>
246				<p><strong>Huntington’s disease (HD) is a rare, hereditary, degenerative disorder of the brain that was first described by George Huntington in 1872. Symptoms include motor (movement), behavioural (for example mood) and cognitive (for example understanding) disturbances, which in the majority of cases appear in mid-adult life. There are currently no therapies that effectively treat the underlying causes of HD, although there are treatments that can alleviate some of its symptoms and improve quality of life for those affected by it.</strong></p>
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254                                <h3 class="hidden-md-up">Symptoms & Disease<br>Progression</h3>
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256                                <h4>Learn more</h4><i class="fa fa-angle-down fa-4x" aria-hidden="true"></i>
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259                                <h3 class="hidden-md-up">Diagnosis &<br>Treatment</h3>
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264                                <h3 class="hidden-md-up">Inheritance &<br>What Causes HD?</h3>
265                                <h3 class="hidden-sm-down">Inheritance &<br>What Causes HD?</h3>
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269                                <h3 class="hidden-md-up">HD In<br>Daily Life</h3>
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300
301		<h1>HD History</h1>
302<p>HD is named after George Huntington, an American physician who described the disease in 1872. His description was based on observations of HD-affected families from the village of East Hampton, Long Island, New York (USA), where Dr Huntington lived and worked. HD was known as Huntington’s chorea and Saint Vitus’s dance in the past.</p>
303<h1><a id="symptoms" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>Symptoms &#038; Disease Progression</h1>
304<p><strong><div id="accordion-1" class="accordion no-js" role="tablist"></strong></p>
305<p><strong><h3 id="accordion-1-t1" class="accordion-title" role="tab" aria-controls="accordion-1-c1" aria-selected="false" aria-expanded="false">How Common is HD?</h3><div id="accordion-1-c1" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t1" aria-hidden="true"></strong></p>
306<p>HD is a rare disease that affects 5 to 10 per 100,000 people in the European population. A similar prevalence is found in countries whose populations are primarily of European descent, such as the USA. HD is less common in Asian and African countries, where the prevalence has been estimated at 1 per 100,000 people. Men and women are equally likely to inherit the HD expansion and to develop the disease.</p>
307<p><strong></div></strong></p>
308<p><strong><h3 id="accordion-1-t2" class="accordion-title" role="tab" aria-controls="accordion-1-c2" aria-selected="false" aria-expanded="false">What are the symptoms of HD?</h3><div id="accordion-1-c2" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t2" aria-hidden="true"></strong></p>
309<p>HD is characterised by a combination of motor (movement), behavioural (for example mood) and cognitive (for example understanding) disturbances, but other symptoms may also be reported. The symptoms of HD may vary in severity, age at onset and rate of progression from individual to individual – even between members of the same family. One person may have a very obvious movement disorder, but only mild behavioural symptoms and cognitive deterioration, while another may suffer from depression and anxiety for years before showing any abnormal movements. The onset of HD is described as ‘insidious’, since it is usually difficult to determine a date when it actually starts.</p>
310<ul>
311<li><strong><a id="diag" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>Motor Symptoms<br />
312</strong>The motor signs of HD are a mixture of chorea, bradykinesia and dystonia, which notably affect posture, balance and gait. Chorea comes from the Greek word choreia, which means dance and refers to the involuntary movements often seen in HD. Having trouble initiating voluntary movements (bradykinesia), and sustained muscle contractions that cause abnormal postures and torsions or twisting (dystonia), are other common motor signs in HD. Oculomotor (eye movement) abnormalities and difficulties with swallowing are also common, and speech becomes more slurred over time.</li>
313</ul>
314<ul>
315<li><strong>Personality and behavioural changes</strong><br />
316The most common psychiatric symptoms of HD are apathy, anxiety, depression, irritability, outbursts of anger, impulsiveness, obsessive-compulsive behaviours, sleep disturbances and social withdrawal. More rarely, mania and schizophrenia – including delusions (false beliefs) and hallucinations (seeing, hearing or feeling things that do not really exist) – have been reported. Affected individuals may experience suicidal thoughts, especially in early stages of the disease. Most HD patients and their carers perceive the behavioural symptoms to be more distressing than the motor or cognitive impairments caused by the disease.</li>
317</ul>
318<ul>
319<li><strong>Cognitive impairments</strong><br />
320HD is characterised by the gradual impairment of comprehension, reasoning, judgement and memory. Cognitive symptoms include slower thinking and difficulty concentrating, organising, planning, making decisions and answering questions, as well as short-term memory and problem-solving deficits and an impaired ability to absorb and understand new information.</li>
321</ul>
322<ul>
323<li><strong>Other symptoms in HD</strong><br />
324There are a number of other changes that may occur during the course of HD, including loss of appetite, weight loss, loss of self
324-esteem, loss of sex drive, and urinary and fecal incontinence.</li>
325</ul>
326<p></div></p>
327<p><strong><h3 id="accordion-1-t3" class="accordion-title" role="tab" aria-controls="accordion-1-c3" aria-selected="false" aria-expanded="false">When do HD symptoms appear?</h3><div id="accordion-1-c3" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t3" aria-hidden="true"></strong></p>
328<p>Most individuals who carry the HD expansion develop symptoms in mid-adult life – that is, between 35 and 55 years of age. Approximately 10% do so before the age of 20 (they have juvenile HD) and another 10% after the age of 55. In general, HD develops very gradually, so that it may go undiagnosed for many years. On average, disease duration is 15 to 20 years from diagnosis, but this varies between individuals and can also depend on the quality of care that the patient receives.</p>
329<p></div></p>
330<p><strong><h3 id="accordion-1-t4" class="accordion-title" role="tab" aria-controls="accordion-1-c4" aria-selected="false" aria-expanded="false">What determines age at symptom onset?</h3><div id="accordion-1-c4" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t4" aria-hidden="true"></strong></p>
331<p>The determinants of age at onset are complex and the subject of ongoing investigations. When looking at large groups of HD patients, scientists find a correlation between the trinucleotide repeat number and the age at onset of symptoms (figure below). This means that, in general, the higher the number of CAG repeats, the earlier the onset of symptoms (figure below). However, for any given CAG repeat number, the variability in age at onset may be up to 30 years, as shown in the figure below. This is probably due to the effects of genes other than <em>HTT</em> (so-called genetic modifiers), and to environmental factors such as lifestyle and diet. Taking this altogether, it’s very difficult to accurately predict the precise age at onset in any given person carrying the HD expansion.</p>
332<figure id="attachment_2882" style="width: 557px" class="wp-caption aligncenter"><img class="wp-image-2882 size-full" src="/wp-content/uploads/2016/08/AAO-vs-CAG.jpg" alt="AAO vs CAG" width="557" height="467" /><figcaption class="wp-caption-text"><em>If your HTT gene contains 40 or more CAG-repeats you will develop symptoms of HD within a normal lifespan but when exactly you will experience the first symptoms is difficult to say. HD symptoms generally tend to start earlier with longer CAG repeats but the variability reported is up to 30 years in a group of people who all carried a CAG repeat of 45.This tells us that it is not only the length of the CAG repeat that determines age at onset but also other factors that still remain to be identified. Figure adapted from: Andrew, S. E. et al. The relationship between trinucleotide (CAG) repeat length and clinical features of Huntington’s disease. Nature Genetics 4, 398–403 (1993).</em></figcaption></figure>
333<p></div></p>
334<p><strong><h3 id="accordion-1-t5" class="accordion-title" role="tab" aria-controls="accordion-1-c5" aria-selected="false" aria-expanded="false">What are the different stages of HD progression?</h3><div id="accordion-1-c5" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t5" aria-hidden="true"></strong></p>
335<p>According to a classification developed by neurologist and HD specialist Ira Shoulson of Georgetown University in the USA, the progression of HD can be divided into five stages:</p>
336<ul>
337<ul>
338<li><strong>Early Stage</strong>: the person is diagnosed as having HD and can function fully both at home and at work.</li>
339<li><strong>Early Intermediate Stage</strong>: the person remains employable but at a reduced capacity. S/he is still able to manage daily affairs despite some difficulties.</li>
340<li><strong>Late Intermediate Stage</strong>: the person can no longer work or manage household responsibilities. S/he needs considerable help or supervision to handle daily financial affairs. Other daily activities may pose slight difficulties but s/he usually only needs minor help.</li>
341<li><strong>Early Advanced Stage</strong>: the person is no longer independent in daily activities but is still able to live at home if supported by family or professional carers.</li>
342<li><strong>Advanced Stage</strong>: the person requires complete support in daily activities and professional nursing care is usually needed.</li>
343</ul>
344</ul>
345<p>The <a href="https://pubmed.ncbi.nlm.nih.gov/35716693/" target="_blank" data-wpel-link="external" rel="external noopener noreferrer" class="wpel-icon-right">Huntington’s Disease Integrated Staging System<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> (HD-ISS) is a biologically and evidence-based framework developed by Sarah Tabrizi of University College London (UK) and colleagues to help progress ph
345armaceutical research. The four stages of the HD-ISS (0 to 3) aim to objectively describe the trajectory of HD over the lifespan, starting from birth. It is hoped that the HD-ISS will allow evaluation of new therapeutic approaches in the very early stages of HD, even before clinical signs are apparent. In facilitating early stage HD research, the potential for new treatments and interventions to slow disease progression and increase clinical benefit is maximised.</p>
346<p></div></p>
347<p><strong><h3 id="accordion-1-t6" class="accordion-title" role="tab" aria-controls="accordion-1-c6" aria-selected="false" aria-expanded="false">Do the symptoms of juvenile HD differ from those of the adult form?</h3><div id="accordion-1-c6" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t6" aria-hidden="true"></strong></p>
348<p>When HD starts early in life (before the age of 20), involuntary movements (chorea) are less prominent as a symptom than slowness of movement (bradykinesia) and stiffness (dystonia). Early features of juvenile HD include marked behavioural changes, difficulties with learning and speech, and decline in performance at school. Epileptic seizures are occasionally reported, being more common in young patients. In general, the juvenile form of the disease progresses more rapidly than the adult form.</p>
349<p></div></p>
350<p><strong><h3 id="accordion-1-t7" class="accordion-title" role="tab" aria-controls="accordion-1-c7" aria-selected="false" aria-expanded="false">What are the symptoms when HD starts late in life?</h3><div id="accordion-1-c7" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t7" aria-hidden="true"></strong></p>
351<p>When HD starts late in life, chorea tends to be a more prominent sign than slowness or stiffness. In such cases, it is likely to be more difficult to establish a family history, because the individual’s parents may already have died, perhaps before they themselves showed signs of the disease</p>
352<p></div></p>
353<p><strong><h3 id="accordion-1-t8" class="accordion-title" role="tab" aria-controls="accordion-1-c8" aria-selected="false" aria-expanded="false">Causes of death</h3><div id="accordion-1-c8" class="accordion-content" role="tabpanel" aria-labelledby="accordion-1-t8" aria-hidden="true"></strong></p>
354<p>People with HD do not die as a direct result of the disease, but rather from medical problems that arise as a result of the body’s weakened condition. These include pneumonia (which accounts for one third of all deaths in HD patients), choking, heart failure, head injury as a result of falls, and nutritional deficiencies. Suicide risk is notably increased, accounting for up to 7% of all patient deaths.</p>
355<p></div></p>
356<p><strong></div></strong></p>
357<h1><a id="diagnosis" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>Diagnosis &#038; Treatment</h1>
358<div id="accordion-2" class="accordion no-js" role="tablist"></p>
359<p><strong><h3 id="accordion-2-t1" class="accordion-title" role="tab" aria-controls="accordion-2-c1" aria-selected="false" aria-expanded="false">How is HD diagnosed?</h3><div id="accordion-2-c1" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t1" aria-hidden="true"></strong></p>
360<p>HD is diagnosed by a combination of clinical assessments and a genetic test. Clinical diagnosis is based on a person’s medical and family history, as well as on standard examinations that make use of clinical rating scales to assess the frequency and severity of the symptoms of HD. The results of the clinical diagnosis are usually confirmed by genetic screening for the <em>HTT</em> expansion (known as diagnostic or confirmatory genetic testing). If a person does not show any symptoms, but is at risk of the disease, asymptomatic genetic testing (known as predictive genetic testing) will determine whether or not they carry the expansion.</p>
361<p></div></p>
362<p><strong><h3 id="accordion-2-t2" class="accordion-title" role="tab" aria-controls="accordion-2-c2" aria-selected="false" aria-expanded="false">What clinical assessment tools are used to diagnose HD?</h3><div id="accordion-2-c2" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t2" aria-hidden="true"></strong></p>
363<p>The clinical assessment tools used to diagnose HD and measure aspects of the presentation are not the same in all clinics in all countries. However, the tool most commonly used is the Unified Huntington’s Disease Rating Scale (UHDRS), which is divided into motor, behavioural, cognitive and functional sub-sections. In addition, the Problem Behaviours Assessment for Huntington’s Disease (PBA) is often used for assessing the severity and frequency of behavioural abnormalities (such as depressed mood, apathy and irritability), while a variety of tests such as the Mini-Mental State Examination (MMSE) and the Mattis Dementia Rating Scale are used to supplement the sub-section of the UHDRS that assesses cognitive impairments.</p>
364<p></div></p>
365<p><strong><h3 id="accordion-2-t3" class="accordion-title" role="tab" aria-controls="accordion-2-c3" aria-selected="false" aria-expanded="false">What is the procedure for predictive genetic testing?</h3><div id="accordion-2-c3" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t3" aria-hidden="true"></strong></p>
366<p>Living with the knowledge that you are at risk of HD can be very worrying. You may feel that you would prefer to know for certain if you are carrying the expansion. In that case, genetic counselling and psychological support are highly recommended, because they allow you to explore your options and to discu
366ss your concerns. In general, predictive testing is not recommended for those younger than 18 – the age at which, it is hoped, a person has the maturity to cope with the awareness that they carry the expansion. In exceptional cases, however, it may be deemed reasonable to perform the confirmatory genetic test in children – if they show signs of juvenile HD, for example – or in women younger than 18 if they are pregnant. If you decide to get tested, a blood sample will be taken from a vein in your arm and your DNA will be extracted from it in the lab. Depending on the local service, the result will be ready in two-to-eight weeks. <a href="http://onlinelibrary.wiley.com/doi/10.1111/j.1399-0004.2012.01900.x " target="_blank" data-wpel-link="external" rel="external noopener noreferrer" class="wpel-icon-right">Guidelines for the predictive genetic testing procedure<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> were updated by the EHDN <a href="http://www.ehdn.org/geneticcounseling/" target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">Genetic Testing and Counselling Working Group</a> in 2012.</p>
367<p></div></p>
368<p><strong><h3 id="accordion-2-t4" class="accordion-title" role="tab" aria-controls="accordion-2-c4" aria-selected="false" aria-expanded="false">What does the genetic test detect?</h3><div id="accordion-2-c4" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t4" aria-hidden="true"></strong></p>
369<p>The genetic test determines the number of CAG repeats in the <em>HTT</em> gene. The test can reveal whether you carry the HD expansion, but it cannot ascertain when the disease will begin, how rapidly it will progress, or which symptoms you might develop. The genetic test for HD is considered to be close to 100% accurate. The results from the DNA analysis are usually double-checked using two separate blood samples. In addition, blood from a parent of the affected person (or, if that is not available, from another family member) may also be tested to provide confirmation of the original diagnosis.</p>
370<p></div></p>
371<p><strong><h3 id="accordion-2-t5" class="accordion-title" role="tab" aria-controls="accordion-2-c5" aria-selected="false" aria-expanded="false">Is it possible for a person who carries the HD expansion<br />
372to ensure that they do not pass HD on to their child?</h3><div id="accordion-2-c5" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t5" aria-hidden="true"></strong></p>
373<p>Yes. This can be achieved using a modern diagnostic procedure called pre-implantation genetic diagnosis (PGD) – also known as embryo screening – that is used in combination with in vitro fertilisation (IVF), and involves screening embryos prior to their implantation in the womb. The technique ensures that only embryos inheriting normal copies of the gene are implanted. Hence, even if one of them carries the HD mutation, PGD makes it possible for a couple to conceive a child that does not carry the mutant <em>HTT</em> gene, – regardless of whether the carrier is the man or the woman. However, PGD is not permitted in some countries under embryo protection laws, and it is also important to note that the chances of a pregnancy coming to term after PGD/IVF are lower than in the case of “natural” conception. In some countries it is possible to test unborn foetuses that were conceived naturally, and to choose abortion once the foetus’ genetic status is known.</p>
374<p></div></p>
375<p><strong><h3 id="accordion-2-t6" class="accordion-title" role="tab" aria-controls="accordion-2-c6" aria-selected="false" aria-expanded="false">May I test my unborn child?</h3><div id="accordion-2-c6" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t6" aria-hidden="true"></strong></p>
376<p>Prenatal (before birth) diagnosis is only available when those requesting it can show that their case fulfils certain medical and legal criteria, which are country-specific. There are two standard procedures for prenatal diagnosis. The first is amniocentesis (also called the amniotic fluid test), in 
376which amniotic fluid containing fetal cells is collected via a needle inserted through the mother’s abdominal wall, usually after the 14<sup>th</sup> week of pregnancy. The second is chorionic villus sampling, which involves the collection of a sample of the chorionic villi (placental tissue) and can be conducted earlier – between the 10<sup>th</sup> and 13<sup>th</sup> weeks of pregnancy. It is, however, riskier for the foetus.</p>
377<p></div></p>
378<p><strong><h3 id="accordion-2-t7" class="accordion-title" role="tab" aria-controls="accordion-2-c7" aria-selected="false" aria-expanded="false">Are there any treatments for HD?</h3><div id="accordion-2-c7" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t7" aria-hidden="true"></strong></p>
379<p>There are currently no <a id="thera" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>therapies that can effectively treat the underlying causes of HD. However, basic and clinical research has dramatically increased our knowledge of HD in recent years, and many <a href="/hd-clinicians-researchers/previous-ongoing-research/#clinicalstudies/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">studies are now underway</a> that are investigating its pathogenesis, with a view to identifying drugs that will postpone disease onset or slow its progression. Treatments are already available that alleviate certain symptoms of the disease (symptomatic treatments), and so improve patients’ quality of life. These are divided into pharmacological (drug) and non-pharmacological (non-drug) treatments.</p>
380<p></div></p>
381<p><strong><h3 id="accordion-2-t8" class="accordion-title" role="tab" aria-controls="accordion-2-c8" aria-selected="false" aria-expanded="false">What are the pharmacological options for treating HD symptoms?</h3><div id="accordion-2-c8" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t8" aria-hidden="true"></strong></p>
382<p>Chorea, bradykinesia, irritability, apathy, depression, anxiety and sleep disturbances have all been reported to be the most distressing symptoms of HD. There are several options for managing these symptoms using drugs. However, many medicines can cause side effects, and some may counteract the therapeutic effects of others. In addition, the same medication may have different effects in different individuals. Treatment must be personalised by an <a href="/find-a-clinic/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">experienced HD specialist</a>, according to the patient’s symptoms and his or her response to the drugs in question.</p>
383<p></div></p>
384<p><strong><h3 id="accordion-2-t9" class="accordion-title" role="tab" aria-controls="accordion-2-c9" aria-selected="false" aria-expanded="false">How can non-pharmacological treatments help?</h3><div id="accordion-2-c9" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t9" aria-hidden="true"></strong></p>
385<p>Non-pharmacological treatments (such as psychotherapy, and cognitive, physical, speech, respiratory and occupational therapies) may improve the psychological and physical symptoms of HD. For instance, improvements have been reported in mood, motor control, speech, balance, swallowing and gait after these therapies. It is well known that physical exercise improves both physical and mental health, enhancing general wellbeing, and exercise has been shown to alleviate the symptoms of depression. There is accumulating evidence that it may also help slow the progression of the movement impairment in HD. For example, some physiotherapy programmes have been shown to result in benefits in terms of motor symptoms, gait and balance. The EHDN <a href="http://www.ehdn.org/physiotherapy-wg/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">Physiotherapy Working Group</a> has published a <a href="/clinical-guidelines/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">guidance document</a> for physiotherapists working with HD patients.</p>
386<p></div></p>
387<p><strong><h3 id="accordion-2-t10" class="accordion-title" role="tab" aria-controls="accordion-2-c10" aria-selected="false" aria-expanded="false">Can a special diet alleviate the symptoms of HD?</h3><div id="accordion-2-c10" class="accordion-content" role="tabpanel" aria-labelledby="accordion-2-t10" aria-hidden="true"></strong></p>
388<p>The benefits of a diet rich in vitamins, co-enzymes and other compounds have been the subject of much discussion, but remain to be proven clinically. However, as weight loss is a problem for some HD patients, especially in the later stages of the disease, it is important to ensure a healthy diet throughout the course of the disease. At later stages a high-calorie diet may become necessary. Referral to a dietician may be helpful.</p>
389<p></div></p>
390<p></div>
391<h1><a id="inheritance" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>Inheritance &#038; What Causes HD</h1>
392<div id="accordion-3" class="accordion no-js" role="tablist"></p>
393<p><strong><h3 id="accordion-3-t1" class="accordion-title" role="tab" aria-controls="accordion-3-c1" aria-selected="false" aria-expanded="false">What causes HD?</h3><div id="accordion-3-c1" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t1" aria-hidden="true"></strong></p>
394<p>HD is caused by a change (an expansion) in the gene (<em>HTT</em>) that encodes a protein called huntingtin. As a result of this expansion, the gene is translated into an altered form of the protein, something that results in the malfunction and death of nerve cells (neurons) in specific areas of the brain. The exact mechanisms of the disease are multifaceted and highly complex, in agreement with the multiple functions of the huntingtin protein. Researchers are working on getting a better understanding of the underlying disease causing mechanisms to develop disease modifying therapies.</p>
395<p></div></p>
396<p><strong><h3 id="accordion-3-t2" class="accordion-title" role="tab" aria-controls="accordion-3-c2" aria-selected="false" aria-expanded="false">What is the underlying cause of HD?</h3><div id="accordion-3-c2" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t2" aria-hidden="true"></strong></p>
397<p>In 1993, scientists identified the mutation that causes HD. The <em>HTT</em> gene is located on chromosome 4 and encodes a protein called huntingtin. The gene contains a sequence of three nucleotides (the basic units of DNA), cytosine-adenine-guanine (CAG), that is repeated several times. This so-called trinucleotide repeat can vary in length. If a person has 40 CAG repeats or more in one copy of the <em>HTT</em> gene, s/he will develop HD within a normal lifespan – that is, in mid-adult life. Since the expansion that causes HD is present in all cells of the body from conception, and can be passed on to subsequent generations, HD is a hereditary disease.</p>
398<p><figure id="attachment_2885" style="width: 450px" class="wp-caption aligncenter"><img class="wp-image-2885" src="/wp-content/uploads/2016/08/Huntingtin-mutation.png" alt="Huntingtin mutation" width="450" height="338" /><figcaption class="wp-caption-text"><em>The Huntingtin gene (HTT) is located on chromosome 4. The HTT gene contains a repeat of three basic DNA units called C-A-G. If the repeat expands to contain 40 or more C-A-G repeats the person carrying the expanded gene will develop Huntington’s disease within a normal lifespan</em>.</figcaption></figure></p>
399<p></div></p>
400<p><strong><h3 id="accordion-3-t3" class="accordion-title" role="tab" aria-controls="accordion-3-c3" aria-selected="false" aria-expanded="false">What does the length of the <em>HTT</em> CAG repeat mean?</h3><div id="accordion-3-c3" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t3" aria-hidden="true"></strong></p>
401<p>As the number of CAG repeats increases, that particular section of DNA becomes more unstable. This means that the number of repeats in this section can increase or decrease when it is passed down to the next generation. As long as the number of CAG repeats in the <em>HTT</em> gene is lower than 27, the section is stable. If the number of repeats is between 27 and 35 (the so-called intermediate repeat length), that individual will not develop HD and the section is considered normal. However, a CAG repeat number of 27 or more is unstable and liable to increase when passed on to the next generation, meaning that those children carry a risk of developing HD. Individuals with a CAG repeat number between 36 and 39 may develop HD, but only very late in life, if at all. This is known as the reduced-penetrance repeat length range. When the number of CAG repeats is higher than 39, a person will develop HD within a normal lifespan – most often in mid-adult life. In rare cases the CAG expansion can be exceptionally long, leading to disease onset in adolescence or childhood (juvenile HD). Patients who develop the disease before the age of 10 often have more than 80 CAG repeats.</p>
402<p>
403<table id="tablepress-3" class="tablepress tablepress-id-3">
404<thead>
405<tr class="row-1 odd">
406	<th class="column-1">CAG repeat length</th><th class="column-2">Disease causing?</th><th class="column-3">Consequences for offspring?</th><th class="column-4">Name</th>
407</tr>
408</thead>
409<tbody class="row-hover">
410<tr class="row-2 even">
411	<td class="column-1">Below 27</td><td class="column-2">No</td><td class="column-3">None</td><td class="column-4">Normal repeat length</td>
412</tr>
413<tr class="row-3 odd">
414	<td class="column-1">27 - 35</td><td class="column-2">No</td><td class="column-3">Repeats of 27 and more can be unstable and might increase when passed on to offspring</td><td class="column-4">Intermediate repeat length</td>
415</tr>
416<tr class="row-4 even">
417	<td class="column-1">36 - 39</td><td class="column-2">Maybe</td><td class="column-3">Yes, offspring have a 50% probability of inheriting the expanded gene</td><td class="column-4">Reduced penetrance repeat length</td>
418</tr>
419<tr class="row-5 odd">
420	<td class="column-1">40 and above</td><td class="column-2">Yes</td><td class="column-3">Yes, offspring have a 50% probability of inheriting the expanded gene</td><td class="column-4">Fully penetrant repeat length</td>
421</tr>
422</tbody>
423</table>
424<!-- #tablepress-3 from cache --></p>
425<p></div></p>
426<p><strong><h3 id="accordion-3-t4" class="accordion-title" role="tab" aria-controls="accordion-3-c4" aria-selected="false" aria-expanded="false">What is a gene?</h3><div id="accordion-3-c4" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t4" aria-hidden="true"></strong></p>
427<p>Genes are found on our chromosomes inside every cell in our body. A gene is a stretch of DNA that c
427ontains the code for a particular protein; the DNA is transcribed into messenger RNA (mRNA), which is then translated into the protein. Most usually, everyone inherits two copies of each gene – one from the mother, one from the father. In HD the important gene is the <em>HTT</em> gene, which encodes the huntingtin protein. When a child inherits an expanded version of the <em>HTT</em> gene then that child will also develop HD. The parent himself may already have the disease or this can develop later in age.</p>
428<p><figure id="attachment_2886" style="width: 400px" class="wp-caption aligncenter"><img class="wp-image-2886" src="/wp-content/uploads/2016/08/gene.jpg" alt="Print" width="400" height="341" /><figcaption class="wp-caption-text"><em>Genes are located along the length of the chromosomes like beads on a string (depicted as coloured lines). Most usually everyone inherits two copies of each gene – one from the mother and one from the father.</em></figcaption></figure></p>
429<p></div></p>
430<p><strong><h3 id="accordion-3-t5" class="accordion-title" role="tab" aria-controls="accordion-3-c5" aria-selected="false" aria-expanded="false">What is a protein?</h3><div id="accordion-3-c5" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t5" aria-hidden="true"></strong></p>
431<p>Proteins are large molecules made up of building blocks called amino acids. The exact sequence of amino acids in a particular protein is determined by the DNA sequence of the corresponding gene. Genes therefore function as blueprints – sets of instructions to cells that tell them how to build specific proteins. The <em>HTT</em> gene contains instructions on how to build the huntingtin protein. Proteins are the molecules that do the work inside cells – they perform a large number of essential processes, such as enzyme reactions or structural support. If a protein functions abnormally or is missing due to an expansion in the gene that encodes it, then it can affect the cell and, ultimately, the whole organism, sometimes causing disease.</p>
432<p></div></p>
433<p><strong><h3 id="accordion-3-t6" class="accordion-title" role="tab" aria-controls="accordion-3-c6" aria-selected="false" aria-expanded="false">The huntingtin protein</h3><div id="accordion-3-c6" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t6" aria-hidden="true"></strong></p>
434<p>The huntingtin protein is a very large protein that is made or “expressed” to varying degrees in every cell of the human body; the highest levels are found in the brain. Huntingtin seems to be a very important protein because the absence of it is lethal to mouse embryos. At one particular end of the huntingtin protein there is a stretch of repeats of one particular amino acid called glutamine. This distinctive feature, known as the polyglutamine repeat, normally consists of up to 35 glutamine units. In people who carry the HD expansion, however, it contains at least 36 repeats and it is this polyglutamine expansion that results in a protein that malfunctions.</p>
435<p></div></p>
436<p><strong><h3 id="accordion-3-t7" class="accordion-title" role="tab" aria-controls="accordion-3-c7" aria-selected="false" aria-expanded="false">How is HD passed on?</h3><div id="accordion-3-c7" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t7" aria-hidden="true"></strong></p>
437<p>HD is a dominant hereditary disease. This means that a person born with one copy of the mutant <em>HTT</em> gene will develop HD even though s/he is also carrying a normal copy of the gene. An HD expansion carrier, whether symptomatic or not, can pass on either a normal or a mutant copy of the gene with a 50% probability of each (provided that s/he only carries the expansion on one of the two copies of the <em>HTT</em> gene). Medical techniques can ensure that an affected individual only passes on the normal <em>HTT</em> gene to his or her children. On the other hand, a person who has not inherited the mutant <em>HTT</em> gene will not develop the disease, and his or her children will not be at risk of it either. The HD expansion cannot skip a generation. However, it can happen that an expansion carrier dies before showing symptoms, and that his or her children do not realise they are at risk of developing the disease.</p>
438<p></div></p>
439<p><strong><h3 id="accordion-3-t8" class="accordion-title" role="tab" aria-controls="accordion-3-c8" aria-selected="false" aria-expanded="false">Brain areas involved in HD</h3><div id="accordion-3-c8" class="accordion-content" role="tabpanel" aria-labelledby="accordion-3-t8" aria-hidden="true"></strong></p>
440<p>Certain functions of the brain such as the ability to move, think and talk gradually deteriorate in HD as crucial nerve cells become damaged and die. The part of the brain most affected by HD is the striatum, which is a component of the basal ganglia and located deep in the brain’s central region. The striatum is primarily involved in planning and controlling movements, but also in many other processes, including cognition and emotions. As HD progresses, it affects the cortex (the outermost wrinkled part of the brain), contributing to cognitive deterioration. In general, HD causes atrophy of the whole brain over time, impairing the individual’s general functional capacity.</p>
441<p><figure id="attachment_2887" style="width: 600px" class="wp-caption aligncenter"><img class="wp-image-2887" src="/wp-content/uploads/2016/08/shutterstock_329843900.jpg" width="600" height="471" /><figcaption class="wp-caption-text"><em>The striatum is a brain structure located deep in the brain’s central region and is the part of the brain most affected 
441in HD early on.</em></figcaption></figure></p>
442<p></div></p>
443<p></div>
444<h1><a id="hd" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize"></a>HD In Daily Life</h1>
445<div id="accordion-4" class="accordion no-js" role="tablist"></p>
446<p><strong><h3 id="accordion-4-t1" class="accordion-title" role="tab" aria-controls="accordion-4-c1" aria-selected="false" aria-expanded="false">How does HD affect daily life?</h3><div id="accordion-4-c1" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t1" aria-hidden="true"></strong></p>
447<p>Testing positive for the HD expansion may affect many different aspects of a person’s life, including the decision as to whether or not to have children, planning for the future, rethinking priorities, negotiating appropriate housing, and informing other family members that they too may be at risk of the disease. <a href="http://hdyo.org/ " target="_blank" data-wpel-link="external" rel="external noopener noreferrer" class="wpel-icon-right">Young adults<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> in particular may need to consider the implications of a positive test result for their education, training and employment. As the disease progresses, it gradually affects a person’s ability to live independently. Working, social life and general daily activities become problematic, and patients become increasingly dependent on help from relatives and health and social care professionals. Local <a href="https://eurohuntington.org/huntingtons-disease-associations/ " target="_blank" data-wpel-link="external" rel="external noopener noreferrer" class="wpel-icon-right">patient advocacy groups<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> and <a href="/find-a-clinic/" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">clinical centres</a> can be contacted at any time, and will provide support.</p>
448<p></div></p>
449<p><strong><h3 id="accordion-4-t2" class="accordion-title" role="tab" aria-controls="accordion-4-c2" aria-selected="false" aria-expanded="false">Are there any strategies for coping better with HD?</h3><div id="accordion-4-c2" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t2" aria-hidden="true"></strong></p>
450<p>Efficient strategies for coping with HD have to be personalised and depend on the affected person, the stage of the disease and the family context. HD develops very slowly, so that in general there is time to adapt to the changes it brings about. For carers and loved ones, a better understanding of the behavioural and cognitive impairments associated with the disease may help them to develop strategies for accommodating these changes and maintaining a good relationship with the affected person. Helpful information and advice is available from <a href="/find-a-clinic/" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">HD specialists</a> and <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">patient advocacy groups<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a>.</p>
451<p></div></p>
452<p><strong><h3 id="accordion-4-t3" class="accordion-title" role="tab" aria-controls="accordion-4-c3" aria-selected="false" aria-expanded="false">How do I contact the EHDN?</h3><div id="accordion-4-c3" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t3" aria-hidden="true"></strong></p>
453<p>If you go to <a href="/about-ehdn/ehdn-structure/#lanco/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">this page</a> you will find a list of language area coordinators who can help you. Alternatively, you may use the contact form provided <a href="https://ehdn.org/contact-us/" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">here</a>.</p>
454<p></div></p>
455<p><strong><h3 id="accordion-4-t4" class="accordion-title" role="tab" aria-controls="accordion-4-c4" aria-selected="false" aria-expanded="false">How do I get an appointment with a specialist?</h3><div id="accordion-4-c4" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t4" aria-hidden="true"></strong></p>
456<p>This differs from one European country to another but most often you need to obtain a referral from your general practitioner before you can see a specialist doctor. You can contact your <a href="/about-ehdn/ehdn-stru
456cture/#lanco/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">local EHDN language coordinator</a> who will help you.</p>
457<p></div></p>
458<p><strong><h3 id="accordion-4-t5" class="accordion-title" role="tab" aria-controls="accordion-4-c5" aria-selected="false" aria-expanded="false">Is there any way I can speak to a specialist without attending a clinic?</h3><div id="accordion-4-c5" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t5" aria-hidden="true"></strong></p>
459<p>Independent advice about HD can be obtained from the <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">patient advocacy groups in your country<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a>.</p>
460<p></div></p>
461<p><strong><h3 id="accordion-4-t6" class="accordion-title" role="tab" aria-controls="accordion-4-c6" aria-selected="false" aria-expanded="false">How do I become involved in HD research?</h3><div id="accordion-4-c6" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t6" aria-hidden="true"></strong></p>
462<p>The EHDN plays a key role in the worldwide clinical study <a href="https://www.enroll-hd.org" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">Enroll-HD<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a>. It is an observational study that does not involve intervention. This means that it does not test experimental therapies per se. Any member of a family affected by HD can take part in Enroll-HD including unaffected companions. The Enroll-HD participants undergo clinical assessments during their annual visits and HD mutation carriers may be eligible to take part in clinical trials of symptomatic or disease-modifying treatments as and when these become available.</p>
463<p>Enroll-HD is accessible via many HD study sites around the world. To find out whether there is a site near you, please <a href="https://www.enroll-hd.org/study-sites-and-locations-browse-the-map/#find-a-platform-clinic-browse-map/?view_449_per_page=1000&#038;view_449_page=1" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">look here<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> or approach your EHDN <a href="/about-ehdn/ehdn-structure/#lanco/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">language coordinator</a>, who will be able to inform you about research activities in your region. Your local <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">patient advocacy group(s)<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> will be able to provide you with general information about participating in research. For more information about HD research, please look <a href="/hd-clinicians-researchers/previous-ongoing-research/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">here</a> or visit the <a href="http://www.hdbuzz.org" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">HDBuzz<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> webpage with HD research news written by HD researchers in lay language and translated into most languages.</p>
464<p></div></p>
465<p><strong><h3 id="accordion-4-t7" class="accordion-title" role="tab" aria-controls="accordion-4-c7" aria-selected="false" aria-expanded="false">Are there support groups that specialise in HD?</h3><div id="accordion-4-c7" class="accordion-content" role="tabpanel" aria-labelledby="accordion-4-t7" aria-hidden="true"></strong></p>
466<p>Yes, a number of <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">patient advocacy groups<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> provide support for individuals and families affected by HD. These can be contacted via your general practitioner or HD specialist or you can contact them directly. The <a href="http://eurohuntington.org/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">European Huntington’s disease Association<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> (EHA) keeps a <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">list of patient advocacy groups<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a> that might be useful for you.</p>
467<p></div></p>
468<p></div>
469<p>For any other questions, please contact your EHDN <a href="/about-ehdn/ehdn-stru
469cture/#lanco/ " target="_blank" data-wpel-link="internal" rel="follow noopener noreferrer" class="wpglobus-menu-item-url-nolocalize">language coordinator</a> or your <a href="https://eurohuntington.org/huntingtons-disease-associations/" data-wpel-link="external" target="_blank" rel="external noopener noreferrer" class="wpel-icon-right">local patient advocacy group<i class="wpel-icon fa fa-external-link" aria-hidden="true"></i></a>.</p>
470<p style="text-align: right;">
471<p style="text-align: right;">April, 2024</p>
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748
749<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/ultimate-social-media-icons/js/shuffle/modernizr.custom.min.js?ver=4.6.29'></script>
vendor: 1 bytes, line 749
749
750<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/ultimate-social-media-icons/js/shuffle/jquery.shuffle.min.js?ver=4.6.29'></script>
vendor: 1 bytes, line 750
750
751<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/ultimate-social-media-icons/js/shuffle/random-shuffle-min.js?ver=4.6.29'></script>
vendor: 1 bytes, line 751
751
752<script type='text/javascript'>
753/* <![CDATA[ */
754var sfsi_icon_ajax_object = {"nonce":"fcf76b9238","ajax_url":"https:\/\/ehdn.org\/wp-admin\/admin-ajax.php","plugin_url":"https:\/\/ehdn.org\/wp-content\/plugins\/ultimate-social-media-icons\/"};
755/* ]]> */
756</script>
vendor: 1 bytes, line 756
756
757<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/ultimate-social-media-icons/js/custom.js?ver=2.9.1'></script>
vendor: 1 bytes, line 757
757
758<script type='text/javascript' src='https://ehdn.org/wp-content/themes/understrap-child/js/child-theme.min.js?ver=0.1.0'></script>
vendor: 1 bytes, line 758
758
759<script type='text/javascript' src='https://ehdn.org/wp-content/slick/slick.min.js?ver=1.6.0'></script>
vendor: 1 bytes, line 759
759
760<script type='text/javascript' src='https://ehdn.org/wp-content/slick/slick-init.js?ver=1.6.0'></script>
vendor: 1 bytes, line 760
760
761<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/page-links-to/js/new-tab.min.js?ver=2.9.8'></script>
vendor: 1 bytes, line 761
761
762<script type='text/javascript' src='https://ehdn.org/wp-includes/js/hoverIntent.min.js?ver=1.8.1'></script>
vendor: 1 bytes, line 762
762
763<script type='text/javascript'>
764/* <![CDATA[ */
765var megamenu = {"effect":{"slide":{"in":{"animate":{"height":"show"},"css":{"display":"none"}},"out":{"animate":{"height":"hide"}}}},"timeout":"300","interval":"100"};
766/* ]]> */
767</script>
vendor: 1 bytes, line 767
767
768<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/megamenu/js/maxmegamenu.js?ver=2.2.3.1'></script>
vendor: 1 bytes, line 768
768
769<script type='text/javascript'>
770/* <![CDATA[ */
771var WPGlobus = {"version":"1.8.7","language":"en","enabledLanguages":["en","es","fr","da","it","cs","pl","nl","no","sv","ru","pt","de"]};
772/* ]]> */
773</script>
vendor: 1 bytes, line 773
773
774<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/wpglobus/includes/js/wpglobus.min.js?ver=1.8.7'></script>
vendor: 1 bytes, line 774
774
775<script type='text/javascript' src='https://ehdn.org/wp-includes/js/wp-embed.min.js?ver=4.6.29'></script>
vendor: 1 bytes, line 775
775
776<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/tablepress/js/jquery.datatables.min.js?ver=1.7'></script>
vendor: 1 bytes, line 776
776
777<script type='text/javascript' src='https://ehdn.org/wp-includes/js/jquery/jquery.form.min.js?ver=3.37.0'></script>
vendor: 1 bytes, line 777
777
778<script type='text/javascript' src='https://ehdn.org/wp-includes/js/underscore.min.js?ver=1.8.3'></script>
vendor: 1 bytes, line 778
778
779<script type='text/javascript' src='https://ehdn.org/wp-includes/js/backbone.min.js?ver=1.2.3'></script>
vendor: 1 bytes, line 779
779
780<script type='text/javascript'>
781/* <![CDATA[ */
782var ninja_forms_settings = {"ajax_msg_format":"inline","password_mismatch":"The passwords provided do not match.","plugin_url":"https:\/\/ehdn.org\/wp-content\/plugins\/ninja-forms\/deprecated\/","datepicker_args":{"dateFormat":"dd\/mm\/yy"},"currency_symbol":"$","date_format":"dd\/mm\/yy"};
783var thousandsSeparator = ",";
784var decimalPoint = ".";
785var ninja_forms_form_25_settings = {"ajax":"0","hide_complete":"1","clear_complete":"1"};
786var ninja_forms_form_25_calc_settings = {"calc_value":"","calc_fields":[]};
787var ninja_forms_password_strength = {"empty":"Strength indicator","short":"Very weak","bad":"Weak","good":"Medium","strong":"Strong","mismatch":"Mismatch"};
788/* ]]> */
789</script>
vendor: 1 bytes, line 789
789
790<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/ninja-forms/deprecated/js/min/ninja-forms-display.min.js?nf_ver=3.0.34.2&#038;ver=4.6.29'></script>
vendor: 1 bytes, line 790
790
791<script type='text/javascript'>
792/* <![CDATA[ */
793var accordionShortcodesSettings = [{"id":"accordion-1","autoClose":true,"openFirst":false,"openAll":false,"clickToClose":true,"scroll":true},{"id":"accordion-2","autoClose":true,"openFirst":false,"openAll":false,"clickToClose":true,"scroll":true},{"id":"accordion-3","autoClose":true,"openFirst":false,"openAll":false,"clickToClose":true,"scroll":true},{"id":"accordion-4","autoClose":true,"openFirst":false,"openAll":false,"clickToClose":true,"scroll":true}];
794/* ]]> */
795</script>
vendor: 1 bytes, line 795
795
796<script type='text/javascript' src='https://ehdn.org/wp-content/plugins/accordion-shortcodes/accordion.min.js?ver=2.3.1'></script>
vendor: 1 bytes, line 796
796
797<script type="text/javascript">
798jQuery(document).ready(function($){
799$('#tablepress-3').dataTable({"stripeClasses":['even','odd'],"ordering":false,"paging":false,"searching":false,"info":false});
800});
801</script>
801
802</body>
803</html>

Line numbers count LF bytes from the start of the resource, as the search results do. Vendor segments are library code the classifier recognised; they are stored but not indexed. Bytes are shown as Latin1 characters, one per byte.