Parkinson's Disease Essay

James Parkinson first discovered Parkinson's Disease in 1817. Parkinson's Disease is a common neurologic disorder for the elderly. It is a disorder of the brain characterized by shaking and difficulty with walking, movement, and coordination. This disease is associated with damage to a part of the brain that controls muscle movement. Parkinson's Disease is a chronic illness that is still being extensively studied.

Diagnosis of Parkinson’s Disease is extremely important in terms of treating the symptoms before the disease gets worse. It is common for patients with PD to have motor symptoms such as gait disorder, which comes from muscle stiffness/rigidity, bradykinesia, postural imbalance, etc. Gait disorders can generally help determine how far the neurological disorder has affected the motor function and control of the individual. Many physicians in general clinics determine if a patient has PD or if it has progressed through evaluating the patients gait pattern, focused on a direct path walking. The problem with this way of diagnosis is that direct paths would generally require the clinic to have a space of 100-meter length for the patient to walk;

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 “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

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

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.

Parkinson disease (PD), also referred to as Parkinson’s disease and paralysis agitans, is a progressive neurodegenerative disease that is the third most common neurologic disorder of older adults. It is a debilitating disease affecting motor ability and is characterized by four cardinal symptoms: tremor rigidity, bradykinesia or kinesis (slow movement/no movement), and postural instability. Most people have primary, or idiopathic, disease. A few patients have secondary parkinsonian symptoms from conditions such as brain tumors and certain anti-psychotic drugs.

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).

Parkinson’s disease is caused by the destruction of dopamine-producing nerve cells in the midbrain (Substantia nigra). These nerve cells are used to coordinate smooth and regular body movement. In the absence of these cells, people often experience tremors (involuntary shaking or

Mitochondrial dysfunction and oxidative stress have been consistently observed in brains of PD patients. There is increasing pharmacological and genetic evidence sustain a link between PD and mitochondrial respiratory chain dysfunction, particular a deficit in mitochondrial complex I (Franco-Iborra et al., 2015). Accidental exposure to 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), an mitochondrial complex I inhibitor, has been known to result in acute and irreversible syndrome that was almost indistinguishable from PD (Calne and Langston, 1983; Langston and Ballard, 1983). Later on, mitochondrial complex I inhibition has been identified in the brains of sporadic PD patients (Schapira et al., 1990). In addition, chronic systemic inhibition of mitochondrial complex I by pesticide rotenone has been found to link to sporadic PD (Betarbet et al., 2000). Interestingly, mitochondrial complex I deficiency has been found not only in the postmortem substantia nigra but also in cerebral cortex (Schapira et al., 1990), which is consistent to the cortical glucose hypometabolism observed in PD patients. Indeed, the pathology of PD has been found to involve several brain regions other than the SNc and many neurotransmitters other than dopamine (Lang and Obeso, 2004a, b). PD models using MPTP and rotenone have now been used extensively in PD research (Beal,

Ketone bodies appear to have a conceivable neuroprotective role in NDD by decreasing oxidative stress through reducing ATP production via indirect inhibition, changing mitochondrial energy metabolism by altering cellular communication, increasing antioxidant activity and reducing neuronal death (Gano, Patel, Rho 2014). Interest in investigating the probable connection between ketone bodies produced via KD and oxidative stress and mitochondrial dysfunction is on the rise. Next, a review of three current original studies exploring ketone bodies effect on the progression of several of the most notable NDD’s: AD, PD, and ALS, respectively.

Parkinson’s Disease is known as one of the most common progressive and chronic neurodegenerative disorders. It belongs to a group of conditions known as movement disorders. Parkinson disease is a component of hypokinetic disorder because it causes a decreased in bodily movement. It affects people who are usually over the age of 50. It can impair an individual motor as well as non-motor function. Some of the primary symptoms of Parkinson’s disease are characterized by tremors or trembling in hands, legs and arms. In early symptoms the tremor can be unilateral, appearing in one side of body but progression in the disease can cause it to spread to both sides; rigidity or a resistant to movement affects most people with Parkinson’s disease,

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).

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

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,