Anti Parkinson's Disease Research Paper

Ramig and colleagues (2001) performed a study to examine the long-term effects of using Lee Silverman Voice Treatment (LSVT) to improve vocal function in individuals with Parkinson’s Disease (PD). Ramig and colleagues (2001) compared LSVT to received respiratory therapy (RET) to control for extraneous variables. Subjects were recruited from a variety of sources which helped to reduce recruitment bias (Ramig et al., 2001). Individuals with any laryngeal pathology unrelated to PD were excluded from the study (Ramig et al., 2001). All 33 subjects were stratified based on: age, time post-diagnosis, stage of disease, score on the unified Parkinson’s disease rating scale, and clinical ratings on speech and voice severity (Ramig et al., 2001). Subjects were then randomly divided into 2 groups and received either LSVT or RET provided in four one-hour weekly sessions for four weeks (Ramig et al., 2001).

Parkinson's Disease is a literally crippling neurodegenerative disorder, manifested in about 1% of the aged population. People who have Parkinson's Disease gradually lose control of their movements; specific symptoms include, "tremor, slowness of movement, stiffness, difficulty in walking, and loss of balance." (1) Evidence strongly suggests that Parkinson's Disease is the result of severe cell loss in the substantia nigra. This brain structure is principally involved in the production of dopamine. (2) Dopamine, among other functions, is the neurotransmitter involved in initiation of movement. Hence, the link between dopaminergic cell loss and cessation of voluntary movement, as manifested

Parkinson disease (PD) is one of the most common neurologic disorders. and it affects approximately 1% of individuals older than 60 years old. Parkinson’s disease is a condition that progresses slowly by treatment. In addition, loss of pigmented dopaminergic neurons of the substantianigra pars compacta and the presence of Lewy bodies and Lewyneurites are the two major neuropathologic findings in Parkinson disease (Hauser, 2016).

There is also no actual known cause of the disease. But in your case because of the car accident that you had a few weeks ago The MRI that we took of your brain shows that your brain was hit pretty hard and the nerve cells of your basal ganglia have become impaired which means you will start to produce a lot less dopamine. An MRI is a painless test used to see the inside of the body without using X-rays. It uses a large magnet, safe, low- energy radio waves and a computer to produce 2d or 3d pictures. Radio waves are passed into your body and are absorbed by some of the tissues, which in turn retransmit the radio waves. The magnet is then turned on and off. The computer picks up this information and generates a picture. Diseased tissue gives off a different signal from healthy tissue and the machine detects this. The positives of having an MRI is that it provides a detailed picture of any part of the body and also means that some of the less pleasant tests do not have to be done. The negatives of having an MRI are very little, they include, being slightly uncomfortable if you are claustrophobic, otherwise the test should have gone very smoothly. Also because you are over the age of 50 this can come in role of the disease. The damage of your brain and your age a very high risks of developing Parkinson’s. Through our research, our understanding the possible causes of Parkinson’s disease is increasing all the time. We also know that you have Parkinson’s because of the symptoms you have been showing. In This disease there are four categories- tremors, stiffness, slowness of movement, and impaired balance and coordination. The nonmotor symptoms, which are symptoms that are not visible are- memory loss, depression, diminished sense of smell. All of these symptoms develop slowly and gradually progress over time. Also remember that each person is very different and are affected differently and

Although the etiology of idiopathic Parkinson's disease (PD) is unknown, it is characterized by the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of ventral midbrain region [9]; [1]. Its prevalence is associated with age. Approximately 1% of the population is affected at 65–70 years of age, which increases to 4–5% in 85-year-olds [2]. Various epidemiological studies and pathological analyses have demonstrated that mean age of onset in sporadic PD, which accounts for about 95% of cases of Parkinsonism is 70 years [7]; [3]. Familial form of Parkinson’s disease is linked to genetic mutations and has prevalence rate of 4%. Familial Parkinson’s disease patients develop early-onset disease before the age of 50

Parkinson's disease affects the way you move. It happens when there is a problem with certain nerve cells in the brain. Normally, these nerve cells make an important chemical called dopamine. Dopamine sends signals to the part of your brain that controls movement. Some conspiracy theories makes us happy by creating a picture where hitler was finally reduced to a trembling, almost rigid person with the mood swings of a woman at her worst PMS, shambling through a burnt, destroyed, and pillaged Nazi regime because he was inflicted by parkinson's disease in the final days of his life. Although it is rumored that hitler really had this disease. It was highly unlikely that he died from it due to the fact that parkinson's disease does not kill by

Attempts to cure or slow down the progression of Parkinson’s disease have largely failed; researchers in this paper maintain this is obviously a direct result of the lack of insight into the pathogenesis of the disease. Parkinson’s disease is the product of the deaths of a number of dopaminergic (dopamine-secreting) neurons in the substantia nigra pars compacta region (SNc) of the brain. But what causes these deaths? In the paper “‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease,” Chen and researchers find that older neurons in the SNc are unusually reliant on calcium channels and that after blocking these channels, the cells are “rejuvenated” and begin acting like their juvenile counterparts; as a

Medical treatment has been the pillar of the treatment for PD, the main pharmacological drug is an alternate form of a neurotransmission found in our brain called dopamine. This alternate form can give what is missing to patients with Parkinson's and it is called levodopa. It was first used in the mid-20th century, however, the long-term use of the drug will bring severe side effects and a decrease in the effectiveness of the drug, forcing the healthcare team to introduce more and different drugs to the regimen (Olanow and Shapira, 2010). Giving moral support and therapy is very important, but all the hope and faith is the response to the pharmacological treatment. Without the correct treatment, the disease will rapidly

disease” (Atchison & Dirette, 2012, p. 213). The disease is a complex hypokinetic type with

Parkinson disease (PD) is a progressive neurodegenerative disorder characterized mainly by physical and psychological disabilities. This disorder was named after James Parkinson, an English physician who first described it as shaking palsy in 1817 (Goetz, Factr, and Weiner, 2002). Jean- Martin Charcot, who was a French neurologist, then progressed and further refined the description of the disease and identified other clinical features of PD (Goetz, Factr, and Weiner, 2002). PD involves the loss of cells that produce the neurotransmitter dopamine in a part of the brain stem called the substansia nigra, which results in several signs and symptoms (Byrd, Marks, and Starr, 2000). It is manifested clinically by tremor,

Parkinson’s Disease is a very complex and interesting disease. Parkinson’s is a nervous system disorder that disrupts the person’s movement and thinking. Parkinson’s is named after James Parkinson. Parkinson was a doctor from London. He studied many of the symptoms, and at the time, he got little recognition for his studies. He tried to get medical schools to study with him, but they would not listen. He died in 1824, and it wasn’t until 1861, until his studies got attention. The person that recognized Parkinson’s studies was Jean Martin Charcot. He was a French neurologist. He and his colleagues called the disease Parkinson’s Disease after James Parkinson. (http://www.everydayhealth.com/parkinsons-disease/history-of-parkinsons-disease.aspx) 6/10/2009

The first new human prion is discovered in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold, they multiply and cause disease. The resulting illness is MSA, a neurodegenerative disease similar to Parkinson's.

Stem cells from human exfoliated deciduous teeth (SHED) consist of multipotent stem cells that could differentiate into various types of cells, including DAergic neuron-like cells. A study shows that SHED could be applied for neurodegenerative disease treatments, namely Parkinson's disease (PD) transplantation therapy. PD leads to malfunction of neurons in substantia nigra in the brain resulting in a lower level of production of dopamine. Dopamine is a neurotransmitter responsible for signal delivery. Insufficient dopamine has an adverse effect on controlling

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by aberrant α-synuclein aggregates within neurons causing damage or neuronal death in different regions of the brain with most disease development occurring in the substantia nigra (NIH.PARK). α-synuclein positive Lewy bodies are another hallmark of PD development (NIH.PARK). Damage or death of neurons leads to a decrease in dopamine production which is required for smooth control of muscle movement (NIH.PARK2, NIH.PARK). Clinically presenting symptoms manifest over time and are characterized by muscle rigidity, tremors and delayed movement however, cognitive changes have also been observed (NIH.PARK2, NIH.PARK). Almost all cases of PD develop sporadically with a small

Parkinson’s disease is a disorder of the nervous system that affects movements. It gradually develops with an unnoticed, but well-known sign, of a tremor in one hand. It may also cause stiffness or slowing in movement.