What Is The Difference Between Parkinson’s Disease And Huntington’s Disease

Cerebral Dopamine Neurotrophic Factor And Mesencephalic Astrocyte

In 2003, a protein called mesencephalic astrocyte-derived neurotrophic factor was characterized and demonstrated to promote survival of embryonic dopaminergic neurons in vitro . Then, a homologous protein called CDNF was discovered with a protective role for dopaminergic neurons. Several studies evidence the protective role of CDNF and MANF in dopaminergic neurons against the injury caused by -syn oligomers . The intrastriatal injection of CDNF prevents the loss of TH-positive neurons in a 6-OHDA-lesioned rat model of PD , and protected dopaminergic neurons in 6-OHDA and MPTP mouse models of PD . MANF has been tested in the 6-OHDA-lesioned rat model showing beneficial effects . CDNF and MANF diffuse to the brain significantly better than GDNF, and CDNF was more efficient in reducing amphetamine-induced ipsilateral rotations in the 6-OHDA rat PD model in comparison with GDNF treatment . In 6-OHDA-lesioned monkeys, PET imaging showed a significant increase of DA transporter ligand-binding activity in lesioned animals treated with CDNF .

The first phase III clinical trial using CDNF in PD patients is being conducted since 2017. In this study, an implanted drug delivery system for Ipu of recombinant human CDNF is used in patients with idiopathic mild-advanced PD . Additionally, another phase III clinical trial to evaluate the beneficial effects of CDNF in PD patients is still on course . Currently, the delivery of CDNF for HD treatment has not been described.

What Is Parkinsons Disease

Parkinsons disease is a degenerative disorder of the central nervous system mainly affecting the motor system. The motor symptoms of Parkinsons disease result from the degeneration of dopamine generating cells in the substantia nigra in the midbrain. The causes of this cell death are poorly understood. Early in the course of the disease, the most obvious symptoms are shaking, rigidity, slowness of movement and difficulty in walking and gait. Later, thinking and behavioral problems arise, with dementia commonly occurring in the advanced stages of the disease. Depression is the most common psychiatric symptom. Other symptoms include sensory, sleep problems and emotionally related problems.

Parkinsons disease is more common in older people, and most cases occur after the age of 50 when it is seen in young, it is called young onset Parkinsons disease.Diagnosis is by medical history and physical examination. There is no cure for PD, but medications, surgery, and multidisciplinary management can provide relief from the disabling symptoms. The main classes of drugs useful for treating motor symptoms are levodopa, dopamine agonists, and MAO-B inhibitors. These drugs too can cause disabling side effects. Deep brain stimulation has been tried as a treatment modality with some success.

Differences Between Parkinsons And Huntingtons Diseases And Their Role For Prioritization Of Stem Cell

Volume 13, Issue 5, 2013

Page: Pages: 15

Abstract

The problems of allocation of scarce resources and priority setting in health care have so far notbeen much studied in the context of stem cell-based therapeutic applications. If and when competitive costeffectivestem cell-based therapies are available, the problem of priority setting – to whom should stem cellbasedtherapies be offered and on what grounds – is discussed in this article using the examples ofParkinsons Disease and Huntingtons Disease . The aim of this paper is to examine the presentlyknown differences between PD and HD and analyze the role of these differences for setting priorities of stemcell-based therapeutic applications to treat these diseases. To achieve this aim, we present the theoreticalframework used in the analysis compare PD and HD in terms of health related and non-health relatedconsequences of these diseases for patients, their relatives and third parties analyze the ethical relevanceof observed differences for priority setting given different values and variables compare PD and HD interms of social justice related consequences of stem cell-based therapies and analyze the ethicalrelevance of these differences for priority setting given different values and variables. We argue that the stepsof analysis applied in this paper could be helpful when setting priorities among treatments of other diseaseswith similar differences as those between PD and HD.

Current Molecular Medicine

Affiliation:

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What Is The Life Expectancy For People With Huntingtons Disease

The life expectancy of a person that has Huntington disease will depend on when do the symptoms start. Doctors estimate that it takes approximately 15 to 20 years for the persons death when they develop symptoms. It is important to note that the estimation does not take into account that the patient commits suicide before they suffer from a fatal condition.

Studies have also shown that patients that inherit the disease from their father have an earlier onset of symptoms. This would mean that those who got the gene from their fathers will probably have a lower life expectancy.

Professionals define another form of juvenile Huntingtons disease, which happens to people younger than 20 years old. This particular form has a shorter disease duration since the symptoms appear as early as eight years old or less. It also has a different progression of symptoms comparing it to the regular disease. Rigidity is the main symptom, instead of chorea, and seizures are another common thing for these patients. Besides, there is cognitive decline and dementia, sadly, at this very early age, showing the worse of the disease progression.

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Huntingtons Vs Parkinsons: Differences And Similarities

Symptoms Huntingtons Disease Symptoms Parkinsons Disease Symptoms Dementia With Parkinsons and Huntingtons Causes What Causes Huntingtons Disease? What Causes Parkinsons Disease? Possible Link to Alzheimers Diagnosis Huntingtons Diagnosis Parkinsons Diagnosis Seek Out Specialists Treatment Huntingtons Treatment Depression With Huntingtons Disease Parkinsons Treatment Prevention A Word From Verywell Frequently Asked QuestionsFAQsVideos

Parkinsons disease and Huntingtons disease are both neurodegenerative diseases. These types of diseases occur when nerve cells in the brain or peripheral nervous system deteriorate and die off over time.

While there is some overlap between Parkinsons and Huntingtons, in that they both affect movement, there are distinct differences. The main difference between these diseases is in their genetic makeup.

Huntingtons is an inherited disorder caused by a genetic abnormality. Parkinsons occurs when the nerve cells in the brain dont produce enough dopamine, which can be caused by a combination of genetic and environmental factors.

Learn more about the different symptoms, causes, diagnosis, and treatment for these conditions.

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How Do Treatments Differ

MS treatments can ease your symptoms during an attack or slow down the diseaseâs effects on your body.

Steroids like prednisone calm the inflammation that damages your nerves.

Plasma exchange is another therapy if steroids donât work. Your doctor will use a machine to remove the plasma portion of your blood. The plasma gets mixed with a protein solution and put back into your body.

Some people with both diseases who take anti-inflammatory medicines like steroids see their Parkinsonâs symptoms get better.

Disease-modifying treatments slow down MS nerve damage and disability. They include:

National Institute for Neurological Disorders and Stroke: âTremor Fact Sheet.â

Neurology: âParkinsonâs Disease in Multiple Sclerosis A Population-Based, Nationwide Study in Denmark .â

Mayo Clinic: âMultiple Sclerosis: Overview,â âMultiple Sclerosis: Symptoms and Causes,â âMultiple Sclerosis: Treatment,â âParkinsonâs Disease: Causes,â âParkinsonâs Disease: Definition,â âParkinsonâs Disease: Risk Factors,â âParkinsonâs Disease: Symptoms.â

Christopher Reeve Foundation: âHow the spinal cord works.â

National Association for Continence: âParkinsonâs Disease.â

National Multiple Sclerosis Society: âMS Symptoms,â âWho Gets MS? .â

National Parkinson Foundation: âNon-Motor Symptoms.â

Multiple Sclerosis Trust: âLhermitteâs sign.â

Johns Hopkins Medicine: âPlasmapheresis.â

FDA.

Depression With Huntingtons Disease

Due to the nature and lower life expectancy of Huntingtons disease, it is common for a diagnosis to lead to depression. Patients with Huntingtons are at a higher risk of suicide.

If you are struggling with your Huntingtons diagnosis or prognosis, contact the Substance Abuse and Mental Health Services Administration National Helpline online or call 1-800-662-4357 to seek help.

If you are having suicidal thoughts, dial 988 to contact the 988 Suicide & Crisis Lifeline and connect with a trained counselor. If you or a loved one are in immediate danger, call 911.

For more mental health resources, including a helpful list of links and hotline numbers, see our National Helpline Database.

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Human Fetal Tissue As A Source Of Progenitor Cells

The first study demonstrating that dopaminergic neurons could be replaced using fetal tissue was performed using 6-hydroxydopamine -lesioned rats that were implanted with DA-rich ventral mesencephalic tissue from rat fetuses . These studies were followed by the generation of the first non-human primates PD model: monkeys lesioned with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine . This model manifested several of the patients symptoms, and transplanting primate fetal mesencephalic tissue into their striatum showed to alleviate these symptoms . These studies set foot for the first PD cell replacement therapy in humans. These clinical trials were performed using dopaminergic neuron precursors from human fetal tissue, which were transplanted into the striatum of PD patients . Transplanted tissue presented no negative effects at the transplantation site, was functional and survived in the transplanted brain region, but clinical benefits were variable .

Table 3. Common animal models of Parkinsons Disease.

Table 4. Common animal models of Huntingtons disease.

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Activation Pattern In Control Subjects

The pattern of brain activation induced by unilateral high-frequency passive vibratory stimulation in our control cohort is in keeping with previous PET data on elementary somatosensory function, as reviewed recently by Paulesu and colleagues . Our study confirms that this rather crude sensory stimulus produces strong activation in cortical areas S1 and S2. The pattern of normalized group rCBF increases in our study was markedly lateralized to the contralateral hemisphere, similar to previous reports . Transcallosal connections have, nevertheless, been demonstrated in posterior S1 , adjoining parietal cortex and secondary sensory cortical areas and, likewise, previous PET and functional MRI experiments have provided evidence for bilateral sensory cortical processing in humans. However, it remains an issue of further inquiry with higher temporal resolution imaging modalities, how ipsilateral sensory area recruitment is affected by habituation and/or other task-related issues. For instance, evoked potential recordings in cats indicate that habituation occurs more rapidly in S2 compared with S1 areas .

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Can Parkinson’s Disease Be Cured

No, Parkinson’s disease is not curable. However, it is treatable, and many treatments are highly effective. It might also be possible to delay the progress and more severe symptoms of the disease.

A note from Cleveland Clinic

Parkinson’s disease is a very common condition, and it is more likely to happen to people as they get older. While Parkinson’s isn’t curable, there are many different ways to treat this condition. They include several different classes of medications, surgery to implant brain-stimulation devices and more. Thanks to advances in treatment and care, many can live for years or even decades with this condition and can adapt to or receive treatment for the effects and symptoms.

What Tests Will Be Done To Diagnose This Condition

When healthcare providers suspect Parkinsons disease or need to rule out other conditions, various imaging and diagnostic tests are possible. These include:

• Positron emission tomography scan.

New lab tests are possible

Researchers have found possible ways to test for possible indicators or Parkinsons disease. Both of these new tests involve the alpha-synuclein protein but test for it in new, unusual ways. While these tests cant tell you what conditions you have because of misfolded alpha-synuclein proteins, that information can still help your provider make a diagnosis.

The two tests use the following methods.

• Spinal tap. One of these tests looks for misfolded alpha-synuclein proteins in cerebrospinal fluid, which is the fluid that surrounds your brain and spinal cord. This test involves a spinal tap , where a healthcare provider inserts a needle into your spinal canal to collect some cerebrospinal fluid for testing.
• Skin biopsy. Another possible test involves a biopsy of surface nerve tissue. A biopsy includes collecting a small sample of your skin, including the nerves in the skin. The samples come from a spot on your back and two spots on your leg. Analyzing the samples can help determine if your alpha-synuclein has a certain kind of malfunction that could increase the risk of developing Parkinsons disease.

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Does Huntingtons Disease Cause Chorea

Most cases of Huntingtons disease will result in the person developing chorea. Chorea involves involuntary movements, muscle jerks, or tics.

Chorea is not limited to Huntingtons disease, and other neurological conditions can also cause it. An accurate diagnosis is important so that a person experiencing chorea can receive appropriate treatment.

Dystonia Vs Dyskinesia Whats The Difference Between These Two

There are two main types of movement disorders- dystonia and dyskinesia. While they may share some common symptoms, the two disorders are caused by different mechanisms and require other treatments.

In this article, we will take a closer look at each disorder and explore the differences between them.

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Cellular Replacement Therapies For Pd And Hd

In 1967, in an important breakthrough, Cotzias et al. demonstrated that the administration of a precursor of DA, L-dopa, improved motor function in PD patients, leading to the thought that the cure for PD was discovered. Also in the 1960s, tetrabenazine was introduced as an antipsychotic but also showed beneficial effects for the treatment of hyperkinetic motor symptoms, like chorea in HD patients . To date, it is known that these drugs do not reverse disease progression and in many cases do not have the desired effects. This has brought the idea that local production of DA and GABA, and therefore the replacement of the neurons that produce it, would be the ideal treatment for these diseases. The fact that the major symptoms present in PD and HD patients are due to the loss of dopaminergic and GABAergic neurons in specific brain regions, respectively, means that replacing these specific cell types could help relieve some of the symptoms present in patients. This has given rise to different branches of investigations seeking cellular replacement-based therapies, which have shown promising results in animal models for these diseases as well as in affected patients .

Cellular Reprogramming For Pd And Hd

In the adult brain, NSCs are present in the subventricular zone of the lateral ventricle and the subgranular zone of the dentate gyrus. These NSCs are capable of generating neuroblasts, which differentiate into mature neurons . Despite the presence of a niche for the generation of new neurons, these cells have limited migration to remote regions, like the SN and striatum. Hence, the idea to generate new local neurons from preexisting cells has been studied for the last 10 years. Initial studies have demonstrated that fibroblasts can be reprogrammed to dopaminergic neurons through the ectopic expression of transcription factors . Considering the reprogramming of cells for the treatment of neurodegenerative diseases, astrocytes were initially considered as an attractive alternative and their reprogramming to neurons forming functional synapses was demonstrated .

Recently, using AAV-based reprogramming of striatal astrocytes, Wu et al. demonstrated that astrocytes could be converted to MSNs in the striatum of R6/2 and YAC128 mice. Converted neurons expressed specific MSNs markers, showed electrophysiological properties, and projected their axonal terminals to the GP and SNpr. All these findings were accompanied by a reduction in striatal atrophy, attenuation of the phenotypic deficit, and an extended life span of R6/2 mice with converted MSNs .

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Possible Link To Alzheimers

Though Alzheimers, Huntingtons, and Parkinsons are distinctly different diseases, some evidence has emerged that shows a common link between the three.

All three diseases have proteins within the cells that do not assemble properly. Though the molecular and cellular changes that occur in each disease vary greatly, this protein degradation has been shown to precede early clinical signs in each disease. This is promising news, as more studies are being done to determine whether this can either predict or prevent these neurodegenerative diseases.

Pluripotent Stem Cells As A Source Of Differentiated Cell

Pluripotent stem cells are an unlimited source of cells with the potential to give rise to any type of cell of the body. Cells differentiated from embryonic stem cells and induced pluripotent stem cells are widely used as in vitro models for many diseases, including neurodegenerative diseases, and also as a source of cell-replacement therapies. Initial studies demonstrated that, when midbrain-derived dopaminergic neurons where grafted in the striatum of rodent models of PD , long-term survival of these cells was observed, which were tyrosine hydroxylase -positive neurons, completely reversed amphetamine-induced rotational behavior and lacked neuronal overgrowth . Importantly, midbrain human dopaminergic neurons grafted in MPTP-lesioned non-human primates survived in the grafted area, expressed TH, extended fibers to the surrounding striatum, and did not present neuronal overgrowth .

As highlighted previously, since HD is caused by a genetic mutation, and differentiated MSNs progenitors come from HD patients, it is imperative to correct the mutation present in these cells, along with the replacement of the target neurons and other cell types, like interneurons and glial cells, as they may provide a healthy and functional environment for the new neurons to integrate to the local circuitry and survive. Currently, no clinical trials are assessing the use of PSCs in HD patients.

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Comparison Table Between Huntingtons And Parkinsons