Writing a thesis can be a daunting task, especially when it comes to a complex and sensitive topic

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in a thesis. The disease is caused by a genetic mutation and affects the brain's nerve cells, leading to
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The Standard of Care Working Group We are aware of the need for peer-reviewed evidence of best
practice to be available to those who create guidelines. However, in HD patients, it is repeated 36 to
120 times. Examining cells from different striatal regions may also give us insights into changes in
gene expression as HD progresses. Huntingtons disease HD is a rare neurodegenerative disease of
the central nervous system characterized by choreatic movements behavioral disturbances and
neuropsychiatric sequelae. The authors have no other relevant affiliations or financial involvement
with any organization or entity with a financial interest in or financial conflict with the subject
matter or materials discussed in the manuscript apart from those disclosed. The glial cells have
structural and support functions while the neurones are specialist cells that transmit information. Any
child, who does not inherit a copy of HD gene from parents, can never develop this condition, and
he or she cannot pass it to the next generations. This enables researchers to study the disease
progression and investigate new options for treatments. Working groups exist to encourage new
collaborative work, and the Standards of Care (SoC) working group is one of these to use the
expertise of families and clinicians involved in HD. There is loss of myelin, the fatty sheath that
surrounds and insulates axons, the neuronal processes through which neurons communicate with
each other. It is an autosomal dominant disorder that is categorized by motor dysfunctions,
behavioral and cognitive deficits. In order to understand and potentially treat neurological diseases,
scientists need to understand the structure and functioning of the healthy brain, and then explore
what is happening in the brain of patients with neurological diseases. Clinical researches such as the
use of stem cells- specialized group of cells which are capable of producing other cells- will help in
developing new brain cells, which can be transplanted into the patient’s brain so as to enhance their
balance, thinking, swallowing and other outlooks (HDSA, 2008). When this DNA repeat is
translated into protein it makes an abnormally long tract of the amino acid glutamine, repeated
within the huntingtin protein. It is mainly labeled to be a disease of the old people but it may occur
in the younger age groups as well. Our website is not intended to be a substitute for professional
medical advice, diagnosis, or treatment. During meiosis, the two identical homologous chromosomes
containing the set of alleles split. Although it comes from a single gene, it interacts with many other
proteins inside the brain, including those involved in transcription, cell signalling and intra-cellular
transportation. Medical researchers and other scientists are also promising to introduce RNA
interference (RNAi), which is capable of stopping the functions of the targeted cells in the body.
Often, some symptoms can be subtle, or they might not be as noticeable as the more disruptive
effects of the condition. You might decide to consider genetic testing, along with genetic counseling.
The cost of neurological disease to individuals, families and society is enormous. The brain is integral
in everything from our existence and normal functioning through to the creative and intellectual
thought that enables humans to work and interact in such diverse and marvellous ways. Fetuses can
also be tested, giving parents the option to terminate the pregnancy if the baby is found to be a
carrier. The cardiovascular continua in cardiovascular disease. To review the existing literature on the
prevalence of Huntingtons disease HD in the US and Canada and to estimate the number of people
in the US currently affected by this disease. Thus, efforts should continue to ensure that effective
therapies are studied and tested to help mitigate HD. Cantle Medicine, Biology 2015 TLDR This
dissertation will detail work performed in characterizing the cellular and molecular determinants of
HD pathogenesis in novel mouse models developed in the Yang lab, using conditional genetics to
define cells in the cortex and striatum as essential to developing HD phenotypes, and assessed
molecular signatures in these cells that are dependent on the mutant huntingtin protein. Scientists and
medical researchers should also double their efforts to develop and improve drugs that will retard the
development of this disease in both children and adults. These groups are not all inclusive of those
within the MCN, and so several aspects of care have not been addressed by the group. ? Social work
The essential role of social workers in the provision of community and financial support is recognized.
Heart Disease Diabetes Cancer Sorting through the evidence. Upload Read for free FAQ and support
Language (EN) Sign in Skip carousel Carousel Previous Carousel Next What is Scribd. Parents who
carry this defective gene are also advised to seek genetic counseling, so as to find ways of limiting its
spread to their children (Lemiere, 2004). However if the mutation causes a change in the amino acid
sequence that is formed during translation, this will affect the protein that is formed and its function.
Perandones I. Munoz-Sanjuan Medicine 2014 TLDR The preclinical and clinical development
molecular therapies targeting HTT expression and the modulation of biological mechanisms thought
to contribute to disease pathogenesis via novel therapeutic agents are reviewed. See Full PDF
Download PDF See Full PDF Download PDF Related Papers HUNTINGTON'S DISEASE:
GENETICS, PATHOGENIC MECHANISMS, ANIMAL MODELS AND THERAPEUTICS Ankur
Gupta Download Free PDF View PDF Molecular Basis of Huntington’s Disease and Brain Imaging
Evidence Antonia Plerou Huntington’s disease as a neurodegenerative disease is characterized by
motor and cognitive impairment. Reason for this disease is expansion of the polyglutamine (due to
the more CAG repeat) in the amino-terminal region of the exon 1 of the Huntingtin gene (HTT).
Huntington disease HD is an adult-onset autosomal dominant disorder characterized by progressive
deterioration of intellectual function bradykinesia rigidity and progressive chorea. Symptoms of
Juvenile Huntington’s disease Juvenile Huntington’s disease develops before the age of twenty.
Download Free PDF View PDF See Full PDF Download PDF Loading Preview Sorry, preview is
currently unavailable. Other symptoms include hallucinations, paranoia, restlessness, psychosis, loss
of judgment, speech changes, loss of memory, confusion, personality, and behavioral disturbances.
Huntingtin is found in many of the body's tissues, with the highest levels of activity in the brain. If
you have a chance of developing Huntington’s disease due to a known family history of the
condition, you may want to discuss your risk with your healthcare provider and with your family.
This means that parents, who usually have less number of repeats, show mild symptoms, which may
later become more severe in their later lives. When the chain is long enough, the disease manifests in
children as young as one year of age. (In children the disease has different features: lack of
movement, a rigid body and seizures). Although it comes from a single gene, it interacts with many
other proteins inside the brain, including those involved in transcription, cell signalling and intra-
cellular transportation. Huntingtons disease is a devastating inherited neurodegenerative disease
characterised by progressive motor cognitive and psychiatric symptoms. Huntington disease HD is
an adult-onset autosomal dominant disorder characterized by progressive deterioration of intellectual
function bradykinesia rigidity and progressive chorea. The disease is inherited in an autosomal
dominant fashion by an increased number of CAG repeats on the short arm of chromosome 4p163 in
the Huntingtin gene. Behavioral Symptoms These include loss of initiative and drive. Although it is
well established that psychiatric symptoms are common in Huntingtons disease 1-5 research and
clinical emphases have been on motor and cognitive aspects of the disorder. Until now actual remedy
for the HD is not available. The htt protein appears to be a scaffolding protein that orchestrates the
complex assembly of multiple intracellular proteins involved in multiple processes, including
vesicular movement and cell metabolism. Encased in the protection of the skull and bathing in the
cerebrospinal fluid, the spongy 1.5kg mass of brain tissue is the most complex organ in the human
body. Thought you might appreciate this item(s) I saw in Current Opinion in Neurology. In this
review we describe the symptomatic and neuroprotective therapies in HD that are currently in a pre-
clinical or clinical stage. They found that people with mainly motor symptoms had more damaged
and lost cells in the primary motor cortex, which is the part of cerebral cortex responsible for
movement. Parkinsons disease and Huntingtons disease are both model diseases. As one example of
this, we have found that astrocytes in the HD brain can be grouped by their gene expression patterns
into those we believe are farther along in a pathological spectrum than others. The clinical symptoms
of HD involve motor dysfunction, behavioural disturbances and cognitive decline. One of these is
single nucleus RNA sequencing (snRNAseq).
It is an autosomal dominant disorder that is categorized by motor dysfunctions, behavioral and
cognitive deficits. However, because its deleterious effects generally appear after carriers have had
their children, it survives. Therefore, in successive generations, the age of onset becomes increasingly
younger. The mutation’s damaging effects accumulate in the brain over time. With ten thousand
million (1010) neurones or nerve cells inside the brain, and the potential for each of these nerve cells
to be in contact with up to 1000 other cells, the communication potential is immense. Heart Disease
Diabetes Cancer Sorting through the evidence. Identification of neuropathological mechanisms that
underlie the selective striatal and cortical neurodegeneration has allowed for the development of
novel neuroprotective therapies that may improve HD patients' quality of life and enhance their
survival. Intestinal diseases: celiac disease, inflammatory bowel disease, short bowel. Huntington
disease causes the degeneration of nerve cells in brain. To review the existing literature on the
prevalence of Huntingtons disease HD in the US and Canada and to estimate the number of people
in the US currently affected by this disease. To understand the person with HD, a neuropsychology
evaluation is required. A single abnormal gene can lead to the development of this disease. They
found that people with mainly motor symptoms had more damaged and lost cells in the primary
motor cortex, which is the part of cerebral cortex responsible for movement. In the present day,
about 30,000 North Americans have Huntington's disease which is about 5 to 8 out of every
100,000. Those with mainly mood and cognitive symptoms had more cell loss in their anterior
cingulate cortex, which plays an important role in mood and cognitive impairment (Fig. 9).
Parkinsons disease and Huntingtons disease are both model diseases. There are many areas where
further work is required to clarify the extent of such involvement, and to assess the value for each
family. Regular assessment and documentation of stage of disease is essential for this process. The
Journal of Huntingtons Disease is a peer-reviewed medical journal that will be launched in 2012 and
will cover research on Huntingtons disease and related disorders. A child born of HD parents has 50-
50 chance of developing this disease. The neurological examination of HD does not require a formal
neurological background and can be taught to other healthcare professionals with appropriate training
and experience in clinical examination. Others, like the one responsible for HD, involve changes to
longer sections of the gene. Audit of the work and research of the benefits or otherwise of the MCN
should take place. In part, this reflects the fact that in many countries there are no specialist clinics
for this patient group, and statistically significant data about care from large patient groups are
lacking. Role of NMDA Receptor-Mediated Glutamatergic Signaling in Chronic and Acute
Neuropathologies. Parkinsons disease is the most common of several akinetic-rigid syndromes and
Huntingtons disease is only one of an ever growing number of trinucleotide repeat disorders. Early
deficits can result in family conflict, marital discord and loss of employment before a formal
diagnosis of HD is made, usually based on neurological features. The researchers found large families
with HD, each emanating from a single individual who had the disease, and established detailed
pedigrees. How HD is inherited HD is a disease that is passed from parents to children through
misspelling or mutation in the normal gene, and it is found in every part of the world. Inflammatory
bowel disease (IBD) Crohn’s disease (CD).
A quantifiable and reliable biomarker for monitoring disease progression is crucial for clinical studies
of neuroprotection, and this remains an area of active research. Pdf Huntington S Disease A Clinical
Review Huntington disease peer reviewed article. Because the allele associated with the mutation is
dominant, a person only needs to inherit one copy of the mutated allele to inherit the disease (Fig.
1). Dr. Moawad regularly writes and edits health and career content for medical books and
publications. Because symptoms usually appear after childbearing age, people have often potentially
passed the disease to their children by the time their own symptoms appear. The mutation underlying
disease is the expansion of the highly polymorphic CAG repeat tract in the first exon of the HD gene
In fact, HD belongs to a group of disorders for which the causative mutation is the expansion of
CAG repeats in the respective genes. It is possible to do this to some extent from a fresh human
brain, but more difficult, and one cannot use already banked material. Thought you might appreciate
this item(s) I saw in Current Opinion in Neurology. The disease is genetically dominant; that is, only
one of our two HTT genes needs to be mutated to produce HD, and each child of a person with HD
has a 50% chance of receiving the mutant gene. It is essential for proper cell division and
programmed cell death (a normal part of the life cycle of cells). We are certain that there is not a
random distribution. Much of the research focuses on how specific molecules and cells are disrupted,
and how they give rise to the movement disorder, psychiatric symptoms and cognitive deficits,
which culminate in dementia. As a result, some mutations make no change to the amino acid
sequence that results from translation of the gene. While the Centre has teams looking into many
different diseases, in this resource we will explore the work led by Professor Faull relating to
Huntington’s disease, a neurological disorder caused by a gene mutation which has devastating
consequences for the patient and their family. There are other exciting developments on the cards
with clinical trials underway for a drug that can potentially silence the huntingtin gene, preventing
the disease from manifesting. When you have an infectious disease, pathogens have gotten inside
your body and caused harm. Huntington disease causes the degeneration of nerve cells in brain. Find
this author on Google Scholar Find this author on PubMed Search for this author on this site L.M.
Levy From the George Washington University Medical Center, Department of Radiology,
Washington, DC. Genes are made up of deoxyribonucleic acid (DNA): which is a molecule that
exists as spiral ladder (HDSA, 2008). There are two main ways in which the epigenome can
influence which genes are turned on and off; DNA methylation and histone modification (Fig. 10).
In both cases the epigenetic change alters the packaging of the DNA. This has opened up new
options for people from HD families. Again, this visualisation can give us insights into where the
earliest changes are in the brains. IT15. Thus, the reader develops the sense of the discovery as a link
in a. Huntington’s disease is fatal, usually resulting in death due to complications within 20 years
after diagnosis. It is believed that this is caused by a new genetic mutation, a process that usually
occurs during sperm development (Lemiere, 2004). Parkinsons disease is the most common of
several akinetic-rigid syndromes and Huntingtons disease is only one of an ever growing number of
trinucleotide repeat disorders. Fetuses can also be tested, giving parents the option to terminate the
pregnancy if the baby is found to be a carrier. The differing number of repeats is linked to two types
of variation that are seen in the disease symptoms (the phenotype): the onset of disease and how
quickly it progresses. Distribute the alleles to each corresponding row or column. A normal gene is
usually composed of three DNA bases, made up of the sequence CAG.
Although it comes from a single gene, it interacts with many other proteins inside the brain,
including those involved in transcription, cell signalling and intra-cellular transportation. The effect
of genes on determining an individual’s characteristics depends on whether it is dominant or
recessive. The definition of best practice is controversial, but using groups of individuals with
considerable clinical experience of the management of HD within their field has been the approach
of this group. Rebecca Peterson, M. D. Associate Professor Department of Radiology University of
Ottawa. Anatomy. Normal PA. Normal Lateral. The Chest X-ray in Disease. When this DNA repeat
is translated into protein it makes an abnormally long tract of the amino acid glutamine, repeated
within the huntingtin protein. Amongst Asian and African peoples the prevalence is much lower; in
Japan, for example, it is only 0.5 per 100,000. Thought you might appreciate this item(s) I saw in
Current Opinion in Neurology. This paper provides a description of Huntington’s disease including
its causes, symptoms, and treatment. Huntingtons disease HD is a rare neurodegenerative disease of
the central nervous system characterized by choreatic movements behavioral disturbances and
neuropsychiatric sequelae. These parts of the brain control planning, personality, movement and
planning. A discussion of a popular press article which reviews this research can be found here.
Those with mainly mood and cognitive symptoms had more cell loss in their anterior cingulate
cortex, which plays an important role in mood and cognitive impairment (Fig. 9). The htt protein
appears to be a scaffolding protein that orchestrates the complex assembly of multiple intracellular
proteins involved in multiple processes, including vesicular movement and cell metabolism. The
Journal of Huntingtons Disease is a peer-reviewed medical journal that will be launched in 2012 and
will cover research on Huntingtons disease and related disorders. Cantle Medicine, Biology 2015
TLDR This dissertation will detail work performed in characterizing the cellular and molecular
determinants of HD pathogenesis in novel mouse models developed in the Yang lab, using
conditional genetics to define cells in the cortex and striatum as essential to developing HD
phenotypes, and assessed molecular signatures in these cells that are dependent on the mutant
huntingtin protein. Medline Google Scholar 10 Craufurd D, Thompson JC, Snowden JS. Disorders
such as stroke, epilepsy, Alzheimer’s, Parkinson’s, Huntington’s, motor neurone disease, multiple
sclerosis and deafness affect thousands of New Zealanders every year. This is 100% legal. You may
not submit downloaded papers as your own, that is cheating. Also you. Verywell Health's content is
for informational and educational purposes only. In this review we describe the symptomatic and
neuroprotective therapies in HD that are currently in a pre-clinical or clinical stage. Therefore, the
SoC group comprises clinicians from various disciplines and many different countries within Europe
as well as the USA. These issues could be caused by Huntington’s disease or by another neurological
or psychiatric condition. Hester Franks Academic F2 Supervisors Professors Hawkey and
Macdonald. The cause of this disease is natural, and it spreads from parents to their children.
Symptoms usually appear at ages between 30 and 50 (but there some cases of juvenile HD) Only
those people with family history of this disease can receive the genes for HD and this disease does
not escape a generation. There are differing approaches to such clinics, and differing opinions about
what is necessary at such a clinic. Upload Read for free FAQ and support Language (EN) Sign in
Skip carousel Carousel Previous Carousel Next What is Scribd. The Journal of Huntingtons Disease is
a peer-reviewed medical journal that will be launched in 2012 and will cover research on Huntingtons
disease and related disorders. Download Free PDF View PDF HUNTINGTON'S DISEASE:
UNDERSTANDING THE PATHOPHYSIOLOGY THROUGH THE HUNTINGTIN GENE Editor
iajps Huntington's Disease (HD) is a progressive neurodegenerative disorder. While the genome does
not change during a lifetime (other than through mutation), the chemical markers of the epigenome
can change as the environment of the individual changes.