IndexAbstract and AcknowledgmentsIntroductionTypes of Parkinson's diseaseTreatments of Parkinson's diseaseConclusionsReferencesAbstract and AcknowledgmentsA literature review of Parkinson's disease studies around the world was included in this project. The studies mentioned above concern the treatment of Parkinson's disease, gene expression and alternative methods. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay IntroductionParkinson's disease is a neurodegenerative disease that has caused the loss of nerve cells responsible for the production of dopamine (C2H11NO2) in the area called the substantia nigra in the brain first defined by James Parkinson. The chemical dopamine is a neurotransmitter responsible for signal transduction between the brain and nerve cells. Bradykinesia, defined as the slowing of movements in cases of dopamine deficiency or injury, leads to resting tremors, postural instability and abnormal movements, defined as the absence of movement. . Because nerve cell loss is slow, it is usually seen at older ages and is more common in men. It is a chronic disease. Although what causes the loss of these nerve cells is still being studied, it is thought to be caused by environmental factors and genetic disorders. Types of Parkinson's diseaseThere are two types of parkinsonism: primary parkinsonism and secondary parkinsonism in Parkinson's disease. Primary parkinsonism is called idiopathic Parkinson's disease. This means that the cause of the disease is unknown. This type of parkinsonism involves the use of drugs that work to increase the amount of dopamine in the brain or to change dopamine. On the other hand, the cause of secondary parkinsonism is generally known and does not respond well to dopaminergic medications. This is an important difference to help distinguish secondary parkinsonism from primary parkinsonism. The cause of secondary parkinsonism is generally known and does not respond well to dopaminergic medications. This is an important difference to help distinguish secondary parkinsonism from primary parkinsonism. Drug-induced parkinsonism, vascular parkinsonism, normal pressure hydrocephalus (NSA), corticoscopic degeneration (CBD), progressive supranuclear (PSP), and multiple system atrophy (MSA) are the known causes of secondary parkinsonism. (Fénelon G)Treatments of Parkinson's diseaseAlthough there is no clear cure for Parkinson's disease today, the intended treatment is for the patient to be able to carry out their personal work independently. The important thing is that these conditions are provided and that the symptoms are controlled. For this purpose, drugs are used that contribute to dopamine deficiency, a dopamine-like effect and prevent the degradation of dopamine in the brain. Such drugs include levodopa. Levodopa is converted into dopamine in the human body and brain. Furthermore, physical therapy practices are important for patients' well-being and facilitate patients' adaptation to daily life. Adenosine A2A Antagonist Researchers tested the A2A receptor antagonist KW-6002 for antiparkinsonian activity in primates administered MTPT (the chemical that creates the Parkinson's effect). L-Dopa is a common treatment that causes complications, including loss of drug effectiveness and the onset of dyskinesia. They may increase antiparkinsonian activity when KW-600 and L-dopa are applied together. This means that KW-600 can reduce the dosage of L-Dopa. Accordingly, this study presents that A2A receptor antagonist is an agentantiparkinson which does not cause dyskinesia or complications. COMT inhibitor treatment (catechol-O-methyl transferase inhibitors) COMT inhibitor therapy aims to increase the effect of levodopa on Parkinson's disease patients and reduce downtime. In this study, the efficacy and safety of the COMT inhibitors, tolcapone and entacapone, compared to placebo were evaluated. The results showed that entacapone reduced rest time compared to placebo. Tolcapone reduced downtime more and provided more significant results. In addition to positive results, diarrhea was found with tolcapone, entacapone increased constipation and dizziness. Both caused side effects of nausea, vomiting, and dyskinesia. Another negative result is that tolcapone causes three cases of fatal liver toxicity. The negative results have raised doubts about the reliability of tolcapone. Kinesiotherapy This study investigated the effect of kinesitherapy on Parkinson's disease. Manual muscle testing (MMT) was applied to patients with Parkinson's disease who continued to use medications. Significant results were obtained in the muscle strength of patients who received kinesitherapy. These results demonstrated that kinesitherapy had a positive effect on Parkinson's disease. Gene therapy Drug treatments are useless in long-term Parkinson's disease and as a result patients require deep brain stimulation (DBS). Because the underlying pathogenic process cannot be changed after DBS, patients' motor symptoms cannot be fully treated, and patients continue to be in the medical treatment process. Symptom control or pathogenic corrections are aimed at with gene therapy. Comment from [email protected]: Bu kısmın hepsi bir makaleden mi alındı? Buraya bi başka makleden de alıntı yapıp referansı zenginleştirelim. It is necessary to know the necessary temporal and spatial properties of gene expression and the pathogenesis of the disease. The vectors for this treatment surround the blood brain barrier, target anatomical regions for therapy, and avoid areas where transgene expression is not required. This study focused on the application of gene therapy to the brain region relevant to patients with Parkinson's disease. As a result, infiltration into border areas and perivascular spaces was prevented in continued studies. Furthermore, complete transduction of the targeted structure was achieved. Finally, it is believed that the development of technology will make a great contribution to this field.Vitamin C, Vitamin E and KarotenIn a study on the effects of taking vitamin C, vitamin E and karoten on Parkinson's disease it was found that vitamin E protects from Parkinson's disease, but vitamin C and karoten do not have an effect like vitamin E. Comment by [email protected]: Bu kısım için referans koymamışsın.birden fazla referans olursa iyi olur. In this study, it was shown that the intake of foods rich in antioxidant vitamin E can have a neuroprotective effect, also known as neuron protection, and thus prevent the development of Parkinson's disease. However, taking high doses of vitamin E has no significant results. Furthermore, synthetic vitamins E have been shown to have greater bioactivity than natural vitamins E. In another study, it was shown that taking vitamin E did not delay the need for levodopa. After these contradictory results, a larger study was needed. No significant results were obtained for vitamin C and carotene intake. In other words, vitamin C and carotene have no significant effects on the diseaseof Parkinson's. It is believed that vitamin C may not have a neuroprotective effect due to its dissolution in water.ConclusionAlthough many studies have been conducted on Parkinson's disease, the results are generally left incomplete. For this reason, despite being the second most common neurodegenerative disease in the world, there is still no clear cure for Parkinson's disease. Many active substances believed to have an effect on Parkinson's disease have been the subject of experimental studies. Unfortunately it was not possible to obtain very significant results. The aim of current treatment of patients with Parkinson's disease is to maintain the patient's living conditions at an optimal level. Pharmacological and physiotherapeutic treatments are applied so that the patient can satisfy their needs. Please note: This is just an example. Get a custom paper from our expert writers now. Get a custom essay In pharmacological studies, it is aimed at minimizing patients' free time and improving motor disorders. However, the difficulty encountered in studies is that the cause of the disease is not known. For this reason, many gene expression analyzes have also been performed to seek answers to the question "is Parkinson's disease genetic?" Studies on this topic have increased in recent years with the increase in technology. References Alastair J. J. Wood, M. (1993, September). Treatment of Parkinson's disease. Retrieved from New England Journal Of Medicine: https://www.nejm.org/doi/full/10.1056/NEJM199309303291408Amar D, SR (2017, May). GSE99039 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99039Beaulieu JM, GR (2011, February 08). The physiology, signaling and pharmacology of dopamine receptors. Retrieved from NCBI: https://www.ncbi.nlm.nih.gov/pubmed/21303898/Bogetofte H, RB-L.-M. (2017, June). GSE99142 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99142Bogetofte H, RB-L.-M. (2017, June). GSE99471 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99471Cowley, S.A. (2017, June). GSE99473 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99473Deane KH, SS (2004, October 18). Catechol-O-methyltransferase inhibitors for levodopa-induced complications in Parkinson's disease. Retrieved from NCBI: https://www.ncbi.nlm.nih.gov/pubmed/15495119Emborgt ME, CM (2007, March). Subthalamic glutamic acid decarboxylase gene therapy: changes in motor function and cortical metabolism. Retrieved from Sage Journals: https://journals.sagepub.com/doi/full/10.1038/sj.jcbfm.9600364Ertan S. (2005, January). Parkinson Hastalığının Klinik Özellikleri. Retrieved from CTF: http://www.ctf.edu.tr/stek/pdfs/42/4221.pdfEtminan M., G.S. (2005, June). Vitamin E, vitamin C, and carotenoid intake and risk of Parkinson's disease: a meta-analysis. Retrieved from Science Direct: https://www.sciencedirect.com/science/article/pii/S1474442205700971Fénelon G, MH (2003, May). Secondary parkinsonian syndromes. Retrieved from NCBI: https://www.ncbi.nlm.nih.gov/pubmed/12773887Fernandes HJ, HE-M. (2013, December). GSE53424 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53424Fernandes HJ, HE-M. (2013, December). GSE53425 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53425Fernandes HJ, HE-M. (2013, December). GSE53426 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE53426Fox SH, KR (2018, March 23). International Parkinson and Movement Disorder Society Review of Evidence-Based Medicine: