The Parkinson 's Disease ( Pd )

Another cause can be the existence of Lewy bodies in the patients brain. Lewy bodies are bundles of certain substances among brain cells. Within Lewy bodies a protein termed alpha-synuclein is present (Mayo Clinic, 2014). Researchers say that synuclein is an immense factor in Parkinson’s disease. Environmental toxins can also increase the decay of neurons. A few of the toxins that have been associated with Parkinson’s disease consist of carbon disulfide, commonly found in many gases released from the earth’s surface, manganese, found in iron and steel, and carbon monoxide, which is the gas produced by cars (WebMD, 2014). All of these factors lead to patients showing signs and symptoms of Parkinson’s disease.

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).

Parkinson 's disease is a progressive neurologic degenerative disease of the Central Nervous system. The brain produces Dopamine and Norepinephrine, which are chemicals needed for smooth muscle movement and coordination, heart rate, and blood pressure. Dopamine and Norepinephrine are released by basal ganglions that are produced in a bundle of nerve cells in the brainstem called substantia nigra. In Parkinson 's patients, the substantia nigra are destroyed and neither of the chemicals can be released into the body. (3) The decrease in Norepinephrine causes heart arrhythmia and low blood pressure, causing the person to get dizzy upon standing or tire easily. The lack of Dopamine, the smooth muscle movement and coordination controller is now gone, or significantly decreased, resulting in the first signs of Parkinson’s disease, pill-rolling, a one handed tremor and a decreased appetite. (2)

Parkinson’s disease is a “neurodegenerative disorder of the basal nuclei due to insufficient secretion of the neurotransmitter dopamine” (Marieb & Hoehn, 2013, p. G-17). The cause of Parkinson’s disease is unknown, but many factors play a role in the development of Parkinson’s disease. One factor that has been found in an individual who has Parkinson’s disease causes over activity of targeted dopamine-deprived basal nuclei. This over activity is caused by the breakdown of neurons that release dopamine in the substantia nigra (Marieb & Hoehn, 2013). Another factor that is present in a person who has Parkinson’s disease, is the presence of lewy bodies in the brain stem ("What is lbd?," 2014). Lewy bodies are unusual

The major component shared by both Parkinson’s disease and dementia is the functioning of neurons, with a then understandable association. Dementia is caused by neuron demise or diminished capacity of communication with other cells, while Parkinson’s disease, neurons in the basal ganglia experience deterioration that disrupts the normal neurotransmitter dopamine balance where neurons waste and die. With this shared neuron deterioration, the prevalence of dementia associated with Parkinson’s disease is clearly understood. One-third of all patients with Parkinson’s disease will display dementia (LeMone, Burke, & Bauldoff, 2011) with indicators identical to Alzheimer’s form of dementia.

In Parkinson's Disease and Huntington's disease the nigra-striatum neural communication assemblage is severely hampered. PD results from a depletion in the amount of dopamine produced by the brain. At the onset of the disease, dopamine-secreting cells of the substania nigra, either because of genetic factors or environmental toxins, experience mass cell death. Thus, the nigra cells are unable to form synapses through which they secrete and relay dopamine to the striatum in a neural circuit within the basal ganglia (18).

PD is the second most common neurodegenerative disease featured pathologically by the progressive loss of dopaminergic neurons in the substantia nigra. The typical symptoms of PD include slowness of movements (bradykinesia), muscle stiffness (rigidity), tremor, and balance disturbance. Etiopathologically, PD is considered to be caused by the significant loss of dopaminergic neurons in the substantia nigra pars compacta and the subsequent dopamine depletion at the striatum. To date, there are only symptomatic treatments available for PD, particularly in the early stages of the disease. No therapy has been found that can cure or halt the progression of the disease.

Parkinson’s disease is a progressive disorder of the central Nervous system and affects both motor and nonmotor functions. parkinson 's is caused by a chemical imbalance within the brain. The brain produces a neurotransmitter called dopamine in the basal ganglia, which is structures linked to the thalamus in the base of the brain. If the Dopamine, Basal ganglia and Thalamus does not function properly then causes major damage,. A person having less and less dopamine, the individual has less and less ability to regulate their movements, body and emotions. Although there is no current cure available for Parkinson’s disease, the debilitating conditions can be lessoned through education, therapy, and a variety of treatments to improve their quality of life on the National Parkinson Foundation website.

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’s is a progressive neurodegenerative disease, primarily affecting voluntary, precise, and controlled movement. Parkinson’s occurs when cells in a part of the brain called the substantia nigra die off. These cells are responsible for producing dopamine. With less and less dopamine, a person has less and less ability to regulate their movements, body and emotions. The terms "familial Parkinson's disease" and "sporadic Parkinson's disease" are used to differentiate genetic from truly idiopathic forms of the disease.

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

PD pathology results from a degenerative process which reduces the function of dopaminergic substantia nigra (SN) neurons below a certain threshold until it manifests as clinical symptoms17. It should be noted that degeneration of the SN is not the sole location of degeneration – regions such as the locus coeruleus, raphe nuclei, basal forebrain, and frontal cortex undergo a similar process17. The pathology is still not fully understood, but the degenerative process has been found to stem from the glossopharyngeal, vagal, and olfactory cranial nerve nuclei and then ascend upwards through the brainstem18. The degeneration of these origin structures have been theorized to be responsible for the non-motor symptoms presented in PD18.

Parkinson’s disease is affected by the degeneration of dopaminergic neurons which is responsible to produce dopamine. Dopaminergic neurons have their cell bodies in substantia nigra pars compacta (SNpc) in basal ganglia (O’Sullivan and Schmitz, 2007). Basal ganglia are a collection of interconnected gray matter nuclear masses deep within the brain”. These gray matter masses are caudate, putamen, globus pallidus, subthalamic nucleus and the substantia nigra. Basal ganglia receive its input through striatum (O’Sullivan and Schmitz, 2007).

Parkinson’s Disease (PD) is a progressive and neurodegenerating disorder in the central nervous system that affects the motor skills of a patient. It is a long-term disorder that is common to old people ranging ages from the early 60s. Motor symptoms include shaking, rigidity, slowness in movement and difficulty to move limbs; all of these happen due to the result of dead cells coming from the substantia nigra, a region of the midbrain. It is understood that a dopamine deficiency is the root cause of this matter. The disease has no cure but recent studies suggest different kinds of treatments such as the anti-parkinson medication levodopa (L-DOPA).

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,