Clinical and Epidemiological Profile of Parkinson's Disease in India
Asha KishoreRupam BorgohainDivya Kalikavil PuthenveeduRoopa RajanPramod Kumar PalRukmini Mridula KandadaiRavi YadavSahil MehtaHrishikesh KumarAnil Kumar SharmaPrashanth Lingappa KukkleSoaham DesaiKuldeep ShettyPettarusp M. WadiaAnnu AggarwalPankaj AgarwalMirza Masoom AbbasSyam KrishnanDivya M. RadhakrishnanGautam WaliAchal Kumar SrivastavaNitish KambleTeresa FerreiraVivek LalAshwin Ashok Kumar SreelathaLuis-Giraldo Gonzalez RicardoManas ChackoManu Sharma
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Parkinson’s disease one of the most complex neurological disorder. The disease risk and progression are due to common genetic variants. Approximately 6.2 million cases are reported each year according to the statistics published in 2015 whereas it is expected that this number will be twice by 2040. There are two types of Parkinson’s disease, familial Parkinson’s disease, and sporadic Parkinson’s disease. The disease is characterized by the presence of Lewy bodies. Adult age increases the risk of Parkinson’s disease. In this review, we provide an overview of the disease pathology of Lewy bodies in the occurrence of Parkinson’s disease, in vitro studies to determine the role of iPSCs in treatment of Parkinson’s disease, in vivo studies to determine the role of animal model in studying disease modeling, and future prospective how single-cell RNA sequencing technology is a major advancement in studying and find the treatment for Parkinson’s disease.
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The current review describes the modem Parkinson's disease models in animals, their advantages, limitations and disadvantages. It was noted that the most widespread up-to-date models based on etiology of the Parkinson's disease. Although toxins mostly produce the Parkinson's disease, a study of involved genes allows investigating not only inherited but also sporadic (not inherited) forms of disease since the same genes are involved in both cases. Mutations of genes lead to formation of mutant toxic proteins, which produce a death of the specialized neurons of the nigrostriatal dopaminergic system and the development of Parkinson's disease. A significant place in the review takes adescription of characteristics of the toxic models produced by 6-OHDA, MPTP and rotenone, their similarities and differences in pathogenetic mechanisms of the Parkinson's disease development. On the basis of the considered experimental models of Parkinson's disease a conclusion has been done that none of these models may in full and adequate scale imitate the entire clinical, pathophysiological, morphological, biochemical and other aspects of the Parkinson's disease development.
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Parkinson's disease is caused by the reduction of dopamine in the brain and related to many genes. In addition, the getting together of the α-Synuclein is the important factor of Parkinson's disease. This research mainly discusses the effect of heavy metals and genetics on the prevalence of Parkinson's disease. The author found 10 articles that investigate the relationship between the heavy metals, genetics and the prevalence of Parkinson's disease. In all these materials, 9 of 10 articles focus on the relationship between the heavy metals and the prevalence of Parkinson's disease, namely, how different heavy metals can cause Parkinson's disease. The last reference article is about the genetics and the prevalence of Parkinson's disease. This article is mainly about which gene is changed and will let people get Parkinson's disease. Iron, copper and lead can contribute to the prevalence of Parkinson's disease, while the manganese does not show much related to the prevalence of Parkinson's disease. Besides, many genes together will contribute to the prevalence of Parkinson's disease. Different genes getting together will cause different Parkinson's disease.
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