Table of ContentsSummary and AcknowledgmentsIntroductionTypes of Parkinson's DiseaseTreatments for Parkinson's DiseaseConclusionReferencesSummary and AcknowledgmentsIn this project, a literature review of Parkinson's disease studies around the world was included. The aforementioned studies focus on 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 should not be banned”?Get the original essayIntroductionParkinson's disease is a neurodegenerative disease that causes the loss of nerve cells responsible for the production of dopamine (C2H11NO2) in the area called 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, results in resting tremor, 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 the causes of the loss of these nerve cells are still being studied, it is believed to be caused by environmental factors and genetic disorders. Types of Parkinson's Disease There 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 aims to use medications that increase the amount of dopamine in the brain or 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 that helps distinguish secondary Parkinsonism from primary Parkinsonism. The cause of secondary parkinsonism is generally known and does not respond well to dopamine medications. This is an important difference that helps distinguish secondary Parkinsonism from primary Parkinsonism. Drug-induced parkinsonism, vascular parkinsonism, normal pressure hydrocephalus (NSA), corticoscopic degeneration (CBD), progressive supranuclear disease (PSP), and multiple system atrophy (MSA) are the known causes of secondary parkinsonism. (Fénelon G)Treatments for Parkinson's diseaseAlthough there is no clear treatment for Parkinson's disease today, the intended treatment is for the patient to be able to perform personal work independently. The important thing is that these conditions are met and that the symptoms are controlled. For this, medications are used that contribute to dopamine deficiency, a dopamine-like effect, and prevent the breakdown of dopamine in the brain. These medications include levodopa. Levodopa is converted to dopamine in the human body and brain. In addition, physiotherapy practices are important for the well-being of patients and facilitate their adaptation to daily life. Adenosine A2A Antagonist Researchers tested the A2A receptor antagonist KW-6002 for antiparkinsonian activity in primates that received MTPT (the chemical that creates the Parkinson's effect). L-Dopa is a common treatment that leads to complications, including loss of drug effectiveness and the development of dyskinesia. They can increase antiparkinsonian activity when theKW-600 and L-dopa are applied together. This means that KW-600 can reduce the dosage of L-Dopa. Therefore, this study shows that A2A receptor antagonist is an antiparkinsonian agent that does not cause any dyskinesia or complications. Treatment with COMT inhibitors (catechol-O-methyl transferase inhibitors) Treatment with COMT inhibitors 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 investigated. The results showed that entacapone reduced downtime compared to placebo. Tolcapone further reduced downtime and provided more significant results. In addition to positive results, tolcapone diarrhea, entacapone increased constipation and dizziness. Both caused side effects of nausea, vomiting, and dyskinesia. Another negative finding is that tolcapone causes three cases of fatal liver toxicity. The negative results raised concerns about the reliability of tolcapone.PhysiotherapyIn this study, the effect of physiotherapy on Parkinson's disease was investigated. Manual muscle testing (MMT) was applied to patients with Parkinson's disease who continued to take medications. Significant results were obtained regarding the muscle strength of patients who received physiotherapy. These results showed that physiotherapy had a positive effect on Parkinson's disease. Gene therapy Pharmacological treatments are useless in Parkinson's disease in the long term and therefore patients need deep brain stimulation (DBS). Since the underlying pathogenic process cannot be changed after DBS, patients' motor symptoms cannot be fully treated, and patients continue to undergo the medical treatment process. Gene therapy aims to control symptoms or pathogenic corrections. Comment from [email protected]: But what does it mean? Buraya bi başka makleden de alıntı yapıp referansı zenginleştirelim.It is necessary to know the necessary temporal and spatial properties of gene expression and disease pathogenesis. The vectors for this treatment encircle the blood-brain barrier, indicate the anatomical regions to be treated and avoid areas where transgene expression is not required. This study focused on applying gene therapy to the brain region relevant to Parkinson's disease patients. As a result, infiltration into border areas and perivascular spaces was prevented in further studies. Additionally, complete transduction of the targeted structure was performed. 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 investigating the effects of consuming Vitamin C, Vitamin E and Karoten on Parkinson's disease, Vitamin E protects against Parkinson's disease, but Vitamin C and karoten have no effect like vitamin E. Comment from [protected email]: Bu kısım için referans koymamışsın.birden fazla referans olursa iyi olur. In this study, it was shown that consuming foods rich in the antioxidant vitamin E can have a neuroprotective effect, also called neuron protection, and thus prevent the development of Parkinson's disease. However, taking high doses of vitamin E does not lead to any significant results. Additionally, synthetic vitamin E has been shown to have greater bioactivity than vitamin Enatural. In another study, it was shown that vitamin E intake 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 effect on Parkinson's disease. It is considered that vitamin C cannot have a neuroprotective effect due to its dissolution in water.ConclusionEven though many studies have been carried out on Parkinson's disease, the results generally remain incomplete. For this reason, despite being the second most common neurodegenerative disease worldwide, there is still no clear treatment for Parkinson's disease. Many active substances believed to have an effect on Parkinson's disease have been the subject of experimental studies. Unfortunately, no very significant results could be obtained. The goal 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 meet their own needs. Keep in mind: This is just a sample. Get a personalized article from our expert writers now. Get a Personalized Trial In pharmacological studies, the goal is to minimize patient downtime and improve motor disorders. However, the difficulties encountered in studies are that the cause of the disease is not known. For this reason, many gene expression analyzes have also been carried out to search for answers to the question "Is Parkinson's disease genetic?" » Studies on this subject have multiplied in recent years with the evolution of technology. ReferencesAlastair JJ 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 (May 2017). GSE99039 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99039 Beaulieu JM, GR (February 8, 2011). The physiology, signaling and pharmacology of dopamine receptors. Retrieved from NCBI: https://www.ncbi.nlm.nih.gov/pubmed/21303898/Bogetofte H, RB-L.-M. (June 2017). GSE99142 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99142Bogetofte H, RB-L.-M. (June 2017). GSE99471 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99471 Cowley, SA (June 2017). GSE99473 series. Retrieved from Gene Expression Omnibus: https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE99473 Deane KH, SS (October 18, 2004). 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 (March 2007). 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. (January 2005). Parkinson Hastalığının Klinik Özellikleri. Retrieved from CTF: http://www.ctf.edu.tr/stek/pdfs/42/4221.pdfEtminan M., GS (June 2005). 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 (May 2003). Secondary parkinsonian syndromes. Retrieved from NCBI: https://www.ncbi.nlm.nih.gov/pubmed/12773887Fernandes HJ, HE-M. (December 2013). GSE53424 series. Excerpt from Gene Expression Omnibus: