Acute Parkinson's Disease

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 “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 path physiology of Parkinson’s disease is the pathogenesis if Parkinson disease is unknown. Epidemiologic data suggest genetic, viral, and environmental toxins as possible

Therefore, the rotenone model might be an invaluable tool for investigating the molecular basis of Lewy body formation and the link between this phenomenon and nigrostriatal dopaminergic neuronal death. This model gives excellent experimental support to the environmental hypothesis of PD pathogenesis. Furthermore, the finding that the severity of the rotenone-induced striatal dopaminergic damage is highly variable within rats, ranging from none to nearly complete (Betarbet et al., 2000; Sherer et al., 2003a), unequivocally demonstrates that the inter-individual susceptibility to rotenone reflects genetic differences among rats, providing insights into the interaction between environmental and genetic influences on PD pathogenesis (Perier et al., 2003). Generally speaking, the model shows that a lifetime exposure to toxic environmental factors, combined with individual genetic differences (for example, in the function of complex I) and the ability to metabolize xenobiotics (Menegon et al., 1998) may underlie many cases of idiopathic PD (Sherer et al., 2003a). The rotenone model provides experimental evidence that modest systemic defects induced by the pesticide in the brain (e.g., the systemic inhibition of complex I) can, indeed, cause parkinsonism. The observation that complex I was uniformly

Parkinson’s disease “is described as a common disorder of the brain caused by a progressive deterioration of the areas that produce the neurotransmitter dopamine” (Fischer, 1999). It affects the nervous system, more specifically it affects the nerve cells in your brain that secrete dopamine. Dopamine is a chemical that is responsible for the movement and coordination of the musculoskeletal system.

Phrmacodynamics: Pramipexole is a nonergot dopamine agonist with high relative in vitro specificity and full intrinsic activity at the D2 subfamily of dopamine receptors, binding with higher affinity to D3 than to D2 or D4 receptor subtypes. The relevance of D3 receptor binding in Parkinson's disease is unknown. The precise mechanism of action of Pramipexole as a treatment for Parkinson's disease is unknown, although it is believed to be related to its ability to stimulate dopamine receptors in the striatum. This conclusion is supported by electrophysiologic studies in animals that have demonstrated that Pramipexole

A previous literature review(8)reported that there is an obvious link between cigarette smoking and PD. Furthermore,where direct animal studies predict a possible protective effect of smoking on the development of PD and it's symptoms, nevertheless the mechanism by which this occurs is un-clear. Therefore the mechanism by which smoking may impart a neuroprotective effect remains to be clarified in an animal model. Determining the underlining mechanism by which smoke imparts its effects may aid in defining the etiology and pathogenesis of PD, and it may be utilized in

(2014). Considerations on the role of environmental toxins in idiopathic Parkinson’s disease pathophysiology. Translational Neurodegeneration 3 (10). doi: 10.1186/2047-9158-3-10

If nothing else, the lesson that can be taken from the connection between Hebb’s postulate in 1949 and the discovery of LPT in 1973 is that the advancements in the neurobiological field of medicine can applied to previous theories and start to offer new ways to alleviate the symptoms that come with diseases such as Huntington’s and Parkinson’s. In a groundbreaking study, the alleviating effects of both THC and CBD were studied on rats who were injected with 6-hydroxydopamine (Lastres-Becker, Molina-Holgado, Ramos, Mechoulam, and Fernandez-Ruiz, 2005). This drug has been found to induce Parkinson’s disease-like conditions. Based on previous studies on the effectiveness of these cannabinoids on protecting neurons from neurotoxicity, the

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).

Since it is already known that Parkinsons is a neurodegerative disorder but the etiology is uncertain as regards what exactly can contribute to its original progression the need for Parkinson induced models is critical. 6-Hyroxydopamine (6-OHDA) is a compound specifically designed to determine the molecular mechanisms of neuronal death. 6-OHDA is the most widely used neurotoxin for both in vivo and in vitro studies to model the common Parkinson trait of nigral degeneration. 6-OHDA is a synthetic hydroxylated analogue compound of the normal endogenous neurotransmitter dopamine. The very first biological effects of 6-OHDA were demonstrated by (Porter et al., 1963) and (Stone et al., 1963) however the compound was first isolated in 1959 by Senoh (Senoh and Witkop, 1959).

Pathophysiology: HD causes atrophy of the striatum and cerebral cortex of the brain (John Hopkins University, 2015). Scientists do not know how HD demyelinates nerve cells (John Hopkins University, 2015). HD’s pathophysiology is still not clear among medical professionals and researchers. The Division of Neuropathology at John Hopkins University reports, “As valuable as they are, animal and cell models of HD are not enough on themselves to unravel the pathogenesis of HD and discover an effective treatment” (para. 1).

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,

Rotenone is the most intoxicating member of the rotenoid family and is typically found in tropical plants. It is both an herbicide and insecticide having a half-life of 3-5 days depending on light conditions and degrade quickly in soil and water (Hisata 2002). The toxicity of rotenone comes from its high lipophilia and it can easily cross the blood brain barrier. It is mainly used in rats since, so far, the studies attempting to lesion in mice or monkeys have not been successful (Ferrante et al. 1997; Thiffault et al. 2000). Recently, some studies have tested the toxicity of rotenone when administrated intragastric (Pan-Montojo et al. 2010) or directly in the brain (Alam et al. 2004).