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The huntingtin protein is widely expressed in the central nervous system. HuntingtonOs Disease
(HD) is a late-onset and progressive neurodegenerative disease of the central nervous system with
autosomal dominant inheritance. Particularly, finding early changes in gene expression may well lead
us to better therapies. The clinical symptoms of HD involve motor dysfunction, behavioural
disturbances and cognitive decline. It is now taken as the probable way of the management of HD.
Drug developers are also aware that this strategy could be useful for common disorders, such as high
cholesterol. This gene codes for the huntingtin protein wherein the normal or wild-type variant has a
series of CAG repeats which code for glutamine residues. Apart from affecting the disease
penetrance, studies have also shown that the longer the CAG repeat, the earlier the onset of the
disease symptoms. With CAG repeats of 60 or more, a patient may have disease onset at childhood
or adolescence, a condition known as Juvenile Huntington’s disease. Some studies and trials are
targeting the mutant huntingtin gene, such as by degrading its alleles’ mRNAs. In addition,
personality of the patients becomes more centered and unmotivated (WebMD, 2011). Third, low
abundance miRNA biomarkers can be amplified and then detected in a clinical setting by real-time
quantitative PCR (qPCR). It is an important area of research, especially for those in the field of
genetics, as elucidating the factors that lead to its pathogenesis may provide clues on how to
eventually cure it. Last year, drugmaker Roche's Genentech unit said that an experimental drug
sharply reduced the amount of illness-inducing protein measured in people's spinal fluid. About
30,000 people in the United States carry the deadly gene. The first page of the PDF of this article
appears above. It is characterized by cognitive motor and psychiatric disturbance. 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. As a result, current approaches are directing to the
HTT gene expression silencing. This test will be measuring your electrical activity into your brain.
Evers et al. (2018) delivered engineered miRNA targeting human Htt to mouse and minipig HD
models through adeno-associated virus vector 5 (AAV5-miHTT) to verify the therapeutic effect of
this technique. She says she can't even let herself hope that the treatment will work for her. By
comparing the expression levels of 56 candidate miRNAs, they concluded that miR-34b and miR-
1285 were upregulated in m HTT-Exon-1 -transfected human teratocarcinoma cell line, which is a
model of mHtt -induced transcription is supported by immune complex 2 -positive, nuclear
immunostaining and the reduction in pluripotent and neuron-specific transcript levels, including
known mHtt targets (BDNF). Frozen embryos are people and you can be held legally responsible if
you destroy them, according to the Alabama Supreme Court. Let us write or edit the research paper
on your topic. These bases include adenine (A), thymine (T), cytosine (C) and guanine (G). It is a
family disease that is common in most countries, and the rate at which it is spreading is also
worrying, since there is no absolute treatment for this disease. Still, there are various clinical or
laboratory-based testing which can be employed to assist the problem in Huntington’s disease
diagnosis. Among these differentially expressed miRNAs, 26 were regulated by the REST, TP53,
and E2F1 transcription factors ( Sinha et al., 2012 ). Moreover, Johnson and Buckley (2009) found
that some critical neuronal miRNAs (e.g., miR-9, miR-124, and miR-132) were downregulated in the
brains of HD patients and mouse models, potentially disrupting mRNA regulation and neuronal
function. 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. Symptoms of
Huntington’s disease HD symptoms are usually mild and assumed for a long time before it fully
develops.
This interferes with work and daily living, as patients become prone to falling and can no longer
carry out their usual activities such as dressing and cooking (Roos 2). In HD patients, this sequence
normally repeats itself several times, and the number of repeats becomes larger in the subsequent
generations. Also, new technologies have emerged to allow us to investigate molecular changes in
the human brain. The first page of the PDF of this article appears above. The pregnancy may be
terminated if the embryo is found to have the gene for Huntington disease, although the mother
could decide otherwise (Roos 6). Note that in mouse models of disease one can isolate cells, not just
nuclei, from freshly removed brains, but that is impossible in frozen tissues. It is also advisable for
people carrying the gene for Huntington’s disease to go for vitro fertilization. In general, cognitive,
psychiatric, and motor elements aggravate at this stage. Antidepressants may improve the symptoms
of depression, and psychotherapy is mainly expected to alleviate cognitive dysfunction. In general,
cognitive, psychiatric, and motor elements aggravate at this stage. Some of the common symptoms
of early-onset are as mentioned below: Seizures Clumsiness Slow movements Drooling Rigid
muscles Frequent falling What are the Main Causes of Huntington Disease. Dementia can result
owing to many underlying pathologies which include Alzheimer's disease, Huntington's disease and
Creutzfeldt-Jacob disease. Chorea lessens at this stage, however, Parkinsonism increases, which
consists of slowness, stiffness, tooth grinding, and peculiar limb postures. 3. How do you get
Huntington’s disease. The severity of the disease also depends on the number of CAG repeats in a
DNA. The effect of AAV5-miHTT therapy was dose-dependent and reduced the Htt protein by
inhibiting the formation of mHTT aggregates in the striatum and cortex. About 30,000 people in the
United States carry the deadly gene. Moreover, if these movements are disconnected and have
haphazard distribution and timing, they propose the diagnosis of huntington's disease. IT15. Thus,
the reader develops the sense of the discovery as a link in a. 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. These parts of the brain control planning, personality, movement and planning.
MiRNAs in the peripheral circulation have been extensively investigated as biomarkers for early
diagnosis and monitoring of disease progression ( Pan et al., 2016 ). In addition, changes in miRNAs
levels may be associated with disease prognosis, such as Alzheimer’s disease ( Zhao et al., 2020 ).
They've resisted the option for a decade, but are now running into competition with each other.
Although the study of CSF biomarkers is not as extensive as that for peripheral biomarkers, Reed et
al. (2018) suggested a clinical basis for using CSF miRNAs as biomarkers for HD patients, especially
for the early diagnosis of pre-symptomatic HD patients. Most of the clinical trials on Huntington’s
disease basically fall on the following categories: (1) symptomatic or palliative therapies, (2) anti-
degenerative therapies, (3) restorative or reparative therapies, and (4) molecular targets in specific
and radical therapies (Kanazawa 213). This results in the production of a mutant huntingtin (mHTT)
protein with an abnormally long polyglutamine repeat ( Jacobsen et al., 2010 ). The pathogenic gene,
Htt, located on chromosome 4p16.3 and was identified in 1993 ( Bates et al., 2015 ). HD is related
to the unstable expansion of CAG triplet repeats in exon 1 of Htt. Although you cannot cure it, it has
some ways with which you can easily cope this disease as well as its major symptoms. Introduction
about Huntington disease Huntington’s disease (HD) is defined as a form of a fatal genetic disorder
in which you will experience some sort of progressive breakdown of your brain nerve cells. Still,
there are various clinical or laboratory-based testing which can be employed to assist the problem in
Huntington’s disease diagnosis. There are two types of Huntington’s disease: adult-onset
Huntington’s disease, which is the most common, and an early-onset form, which begins in
childhood or adolescent stages of development (Lawrence, 2009). Note that not all genes are
expressed in all cell types, so, for example, the expression of genes in liver cells are different from
those expressed in muscle cells. Brain imaging testing can even be used for detecting the physical
changes inside your brain.
Among these differentially expressed miRNAs, 26 were regulated by the REST, TP53, and E2F1
transcription factors ( Sinha et al., 2012 ). Moreover, Johnson and Buckley (2009) found that some
critical neuronal miRNAs (e.g., miR-9, miR-124, and miR-132) were downregulated in the brains of
HD patients and mouse models, potentially disrupting mRNA regulation and neuronal function.
There are two types of huntington's disease: adult-onset huntington's disease, which is the most
common, and an early-onset form, which begins in childhood or adolescent stages of development
(Lawrence, 2009). The authors also determined that miR-10b-5p levels were significantly associated
with CAG length in postmortem HD brain tissue ( Hoss et al., 2015a ). Furthermore, they found that
miR-10b-5p was elevated in the plasma of individuals with HD, which might be a promising clinical
diagnostic marker to predict the age and severity of HD onset ( Hoss et al., 2015b ). Upload Read
for free FAQ and support Language (EN) Sign in Skip carousel Carousel Previous Carousel Next
What is Scribd. Bases usually pair together, and combine with other pairs to form coded messages.
Yes 2 No 0 Facebook Twitter Pinterest WhatsApp Previous article Surprising Difference between
Dentists and Periodontists. These bases include adenine (A), thymine (T), cytosine (C) and guanine
(G). Other advanced research projects aimed at Huntington's and other diseases use a technique
called RNA interference to accomplish a similar result. To browse Academia.edu and the wider
internet faster and more securely, please take a few seconds to upgrade your browser. The affected
person is no longer unbiased at this 4 th stage, however nevertheless can stay in their home with an
assist from both household and professionals, though their wishes may additionally be higher met at
a prolonged care facility. Some of the starting signs of adult-onset are as mentioned below: Poor
coordination Irritation Depression Minor involuntary movements Hallucinations Difficulty in
understanding Trouble in making decisions As the disease began to progress on the next stage, some
of the basic symptoms which you can face are as mentioned below: Confusion Loss of memory
Changes in speech Changes in personality Difficulty in walking Trouble in speaking or swallowing
Lack of cognitive abilities 2. However, due to the ubiquitous presence of huntingtin, astrocytes are
also dysfunctional, a. The heredity probability from a parent who has the condition is 50%, when
both parents have the condition; the children will have the disease and will pass it to their children
(Folstein, 1989). Stage 5: Advanced stage The advanced stage lasts between eleven and 26 years
from sickness onset. It is characterized by cognitive motor and psychiatric disturbance. Normally,
there are 10-29 repeats of the CAG, which is expanded up to 121 in patients with Huntington disease
(Kumar, Kalonia, and Kumar 2). In recent years it has become clear that HD can be regarded as a
systemic disorder affecting many organs and tissues causing peripheral as well as brain pathology 2.
It is now taken as the probable way of the management of HD. Difficulties can also reflect in the
physical production of speech and the process of swallowing, an observation key in aggravated
cases of Huntington's disease. Genetic testing can easily search for it in case if you are having a
faulty gene. This level on which this ailment has been progressing is completely depending on person
to person body nature. Most of the clinical trials on Huntington’s disease basically fall on the
following categories: (1) symptomatic or palliative therapies, (2) anti-degenerative therapies, (3)
restorative or reparative therapies, and (4) molecular targets in specific and radical therapies
(Kanazawa 213). Conclusion This is an end of the discussion about what Huntington Disease wiki is
all about and how you can better perform its diagnosing to deal with this worst condition. Although
most of the therapies are at a pre-clinical stage, phase II-III clinical trials have been performed for
each pathophysiological mechanism of the disease. Predictive testing is available; however, it should
be done with caution in patients who are at risk for the disease but have no clinical disease
expression ( Tibben, 2007 ). Occupational therapy is best used to evaluate all your daily activities as
well as recommend devices that might help you with some bathing activities, movement, or getting
dressed. Scientists have developed several methods to jam this signal. Prenatal diagnosis may also
be done for parents aware of whether or not they have Huntington’s disease. This disease causes
progressive damage to brain cells in the cerebral cortex and basal ganglia (WebMD, 2011). They
surmised that increased miR-10b-5p might play a pathological role in the expanded polyglutamine
repeat of HD and was associated with the pathology of this disease.
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. Conclusion Huntington’s disease is a
condition that leads to disability, which gets worse as it progresses. 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. Privacy Policy Password recovery Recover your
password your email Search Home Cookies Policy Terms and Conditions Privacy Policy Disclaimer
About Us Contact US Sign in Welcome. Exportin 5 and Ran GTPase transport the pre-miRNAs to
the cytoplasm. Several years have elapsed since the HD mutation was discovered, and analyses of
peripheral tissues from HD patients have helped to understand the molecular pathogenesis of the
disease and revealed that the molecular mechanisms through which mutated htt leads to cell
dysfunction are widely shared between central nervous system (CNS) and peripheral tissues. A
psychiatrist often checks your major signs of impaired thinking. Predictive testing is available;
however, it should be done with caution in patients who are at risk for the disease but have no
clinical disease expression ( Tibben, 2007 ). Bucha et al. (2015) showed that increased miR-214
expression in HD cells could target mitofusin2 (MFN2), thereby altering mitochondrial morphology
and deregulating the cell cycle. Keep on browsing if you are OK with that, or find out how to
manage cookies. This test will be measuring your electrical activity into your brain. Thus each child
of the affected person usually has 50% chances of inheriting the huntington's disease. He or she
typically keeps traditional pre-disease degrees of independence when it comes to day-to-day things
to do such as finances, home responsibilities, and activities of everyday living, which encompass
eating, dressing, bathing, etc. This is 100% legal. You may not submit downloaded papers as your
own, that is cheating. Also you. Until today, absolute treatment of this disease has not been found,
however, there are treatments that help in managing the symptoms. Treatment of this disease also
depends on the nature of the symptoms. It is, therefore, necessary for families and care takers of
Huntington’s disease patients to give them 24-care, close supervision and assistance. It's a huge
increase and the majority of the injured riders were not wearing helmets. Chorea lessens at this
stage, however, Parkinsonism increases, which consists of slowness, stiffness, tooth grinding, and
peculiar limb postures. They've resisted the option for a decade, but are now running into
competition with each other. This can bring a sort of effect on your emotions, physical movements as
well as cognitive abilities. Upload Read for free FAQ and support Language (EN) Sign in Skip
carousel Carousel Previous Carousel Next What is Scribd. Recent studies have suggested promising
roles of miRNAs as biomarkers and potential therapeutic targets for HD. These results suggested
that increased miR-10b-5p and miR-486-5p plasma levels might be clinically relevant for the
diagnosis of HD ( Hoss et al., 2015b ). They lack the ability to groom themselves, organize their
surroundings, and have memory loss. 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. Fertility clinics in Alabama are contemplating next steps after the state Supreme
Court ruled that frozen fertilized eggs are children — and discarding them would be a crime. They
further showed that miR-212, miR-132, miR-128, and miR-218 might be significantly associated
with Htt CAG repeat expansion, thus suggesting that these miRNAs may be involved in the
differential sensitivity to CAG length expansion ( Langfelder et al., 2018 ). Children who inherit HD
gene may not show symptoms of this disease in early ages, but later in their lives. The need for
humanitarian aid in Gaza is enormous, but trying to decipher how much aid is getting into the
territory and where it's going can be tricky. Subsequently, Chang et al. (2017) examined miRNA
expression levels in the peripheral leukocytes of 36 HD patients, eight pre-symptomatic HD carriers,
and 28 healthy controls. In summary, Huntington’s disease is a significant inherited disease.
For example, miRNAs in plasma can bind to high-density lipoprotein to form stable structures in
peripheral blood ( Noren Hooten et al., 2013 ). Thus, miRNAs in the peripheral circulation may be
important biomarkers for detecting HD because they can exist stably outside cells. There are two
types of Huntington’s disease: adult-onset Huntington’s disease, which is the most common, and an
early-onset form, which begins in childhood or adolescent stages of development (Lawrence, 2009).
Dementia can result owing to many underlying pathologies which include Alzheimer's disease,
Huntington's disease and Creutzfeldt-Jacob disease. It has also been shown that some people
develop this condition even if there is no family history of HD. Magnetic resonance imaging (MRI)
scanning process makes the use of magnetic fields to record the brain images with a high level of
detail. Some of the starting signs of adult-onset are as mentioned below: Poor coordination Irritation
Depression Minor involuntary movements Hallucinations Difficulty in understanding Trouble in
making decisions As the disease began to progress on the next stage, some of the basic symptoms
which you can face are as mentioned below: Confusion Loss of memory Changes in speech Changes
in personality Difficulty in walking Trouble in speaking or swallowing Lack of cognitive abilities 2.
Until today, absolute treatment of this disease has not been found, however, there are treatments that
help in managing the symptoms. Treatment of this disease also depends on the nature of the
symptoms. It is, therefore, necessary for families and care takers of Huntington’s disease patients to
give them 24-care, close supervision and assistance. The miR-146a can also target human and mouse
Htt gene. New clinical studies on managing and treating this disease will be of significant help to
future patients. These repeats code for a glutamine tract in the HD gene product huntingtin (htt),
which is a protein expressed in almost all tissues. The disease is caused by a polyglutamine repeat
expansion located in the N-terminal region of the huntingtin protein. Because of the mutation, it
accumulates and triggers a cascade of oxidative injury, transcriptional dysregulation, mitochondrial
dysfunction, and energy depletion which ultimately leads to increasing neuronal dysfunction (Kumar,
Kalonia, and Kumar 2). Thus, LTL might be a reliable biomarker to track HD progression. Stage 2:
Early intermediate stage The early intermediate stage of this Huntington’s can stay between 3-13
years from ailment onset. 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. Non-specific partial inhibition of wtHtt and mHtt gene expression was
effective in animals with HD, and no apparent adverse effects were detected. In case if you are
experiencing different symptoms, then doctors will most probably recommend you with some
genetic testing process. Until now actual remedy for the HD is not available. This review is based on
the pathophysiology of HTT on HD. It usually presents with abnormal movements, psychiatric
symptoms, and cognitive dysfunction. The Boeing executive who oversaw the troubled 737 Max
program, Ed Clark, has left the company. Furthermore, the mutant HTT gene is occupied in the HD
associated changes of neurotransmission for enabling the neurodegeneration. It's part of a broader
management shakeup after a door plug panel blew off a jet in midair last month. At this stage,
sufferers generally do not ride impaired motor symptoms, however, they may additionally experience
slight cognitive signs and symptoms and psychiatric changes. You can even call it the form of an
autosomal dominant disorder of Hungtington’s disease chromosome. The behavioral and psychiatric
symptoms such as depression and aggression are also treated with neuroleptics, such as olanzapine,
which is the preferred drug. Huntington’s disease life expectancy which is mostly 20 years right
through the onset symptoms with some secondary signs of pneumonia and heart failure leading to
death. The typical dyskinesia of the disease is chorea-like involuntary movement. Pdf Huntington S
Disease A Clinical Review Huntington disease peer reviewed article. The authors also determined
that miR-10b-5p levels were significantly associated with CAG length in postmortem HD brain tissue
( Hoss et al., 2015a ). Furthermore, they found that miR-10b-5p was elevated in the plasma of
individuals with HD, which might be a promising clinical diagnostic marker to predict the age and
severity of HD onset ( Hoss et al., 2015b ).