6-OHDA Model

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).

Sayer begins to consider LDOPA as a possible cure for the patients. Sayer considers LDOPA due to its reputation as a “miracle drug” in Parkinson’s patients. LDOPA functions as a precursor to the catecholamines dopamine, epinephrine, and norepineprine and, as a precursor, serves to treat Parkinson’s patients by increasing their levels of dopamine.

Parkinson’s disease is a progressive neurological condition which occurs when the brains nerve cells that contain/produce dopamine die, without the chemical

In the past twenty years, many drugs have been developed to treat the disease. Although the cause of Parkinson's disease is still unknown, scientists have been developing methods of treatment and therapy. The idea is to replace dopamine in the brain, which is accomplished, to some extent, with the administration of L-Dopa. In conjunction with other drugs, L- Dopa "inhibits the enzymes that break down L-dopa in the liver, thus making a greater part of it available to the brain" (5). This treatment is very successful, but it only hinders the disease for a time and it is by no means a cure. That leaves us with stem-cells and the role they play in treatment of Parkinson's disease.

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

And there this field is always developing new techniques to slow or stop the progression of this aggressive degenerative process. It is now under investigation the use of gene therapy combined with surgical approaches. It was pointed out by Kang, Papasian, Chang, and Lee (2003) the exact mechanisms of the degeneration that takes place in Parkinson's may not be well understood, especially the main cause that unleashed the neuronal alteration, however to prevent the progression it is important to understand the general process of cellular death (p.339). At this point of the disease the patient is already being treated by a multidisciplinary patient, and now more than ever it is key for the clinician to keep by the patient's side guiding him through the rough path, being a light and a support for him and for his family. Don't let the person feel overwhelmed by the weight of being sick. Always keep in mind the holistic approach of the patient and giving support in all the aspects of his life, only this way we could give relief and peace of

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

The neurodegenerative disease is the disease in which the neurons become degenerate and causing death of neurons. The Alzheimer’s disease is the first most common neurodegenerative disease. The Alzheimer’s disease is firstly described by Alois Alzheimer in (1907) because of this it named Alzheimer’s. The Parkinson’s disease is the second most common neurodegenerative disease National Institute of Environmental Health Sciences (NIEHS). Alzheimer’s disease is the first most common neurodegenerative disease and the (Yanker, 1996) studied the Alzheimer’s disease neuronal degeneration and the mechanism of this disease. The dopamine neurons degenerate when the neurotoxin induced in the Caenorhabditis elegans (Francis et al., 1999). The 95% Parkinson’

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).

A newer model for toxin-induced Parkinsonism is based on the herbizide rotenone. Rotenone is the most potent member of the rotenoids, a family of natural cytotoxic compounds extracted from various parts of Leguminosa plants. Like MPTP, rotenone is highly lipophilic and brain distribution is heterogeneous paralleling regional differences in oxidative metabolism (Talpade, Greene et al. 2000). In mitochondria, rotenone impairs oxidative phosphorylation by inhibiting nicotinamide adenine dinucleotide (NADH)-ubiquinone reductase activity through its binding to the PSST subunit of the multipolypeptide enzyme complex I of the electron transport chain (Schuler and Casida 2001). Aside from its action on mitochondrial respiration, rotenone also inhibits

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,

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by the classical motor symptoms: resting tremor, bradykinesia, akinesia, rigidity and postural instability. Although the complete PD pathogenesis is not well understood, we have gained a better understanding of its etiology, pathology, and molecular mechanisms, thanks to the use of animal models. Importantly, none of the current available models is able to fully recapitulate PD symptoms and pathology. Each model is based on the production of one or few pathological processes of PD, which are either artificially induced in a way that is seldom relevant to the disease (like toxin models), or that produces only a small part of the pathology (like genetic models).