Accumulation of damaged mitochondria in neuropathic Gaucher disease, the most prevalent risk factor for Parkinson's disease, is due to defective cellular degradation machinery
Laura D. OsellameRahimin Affandi Abdul RahimMatthew E. GeggSimon N. WaddingtonAnthony H.V. SchapiraMichael R. Duchen
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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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Abstract The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of ‘stem’ mitochondria with low metabolic activity and a pool of ‘differentiated’ mitochondria with significantly shorter lifespans and high metabolic activity. We consider synaptic mitochondria as a possible example of ‘differentiated’ mitochondria. They are significantly smaller than mitochondria from the cell body, and they are different in key enzyme activity levels, proteome, and lipidome. Synaptic mitochondria are more sensitive to different damaging factors. It has been established that neurons have a sorting mechanism that sends mitochondria with high membrane potential to presynaptic endings. This review describes the properties of synaptic mitochondria and their role in the regulation of synaptic transmission.
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Objective To observe the protective effect of Xinhani against mitochondria injury induced by exogenous Ca~(2+).Methods Isolated mitochondria was prepared from brain of rats.The concentration of free Ca~(2+) in mitochondria,the activity of mitochondria and MPT were measured respectively in the presence of Ca~(2+) at different concentration without or with Xinhani.The swelling of mitochondria represented by OD values at 540 nm.Results AS compared with that of control group,Ca~(2+) concentration of mitochondria was increased significantly(P0.05 or P0.01) respectively when incubated with CaCl_2,decreased the activity of mitochondria(P0.01),MPT induce swelling of mitochondria and OD values at 540 nm of mitochondria suspension decreased.OD values at 540 nm of mitochondria suspension could manifest the change of swelling of mitochondria(P0.01);Xinhani reduced significantly Mca increase induced by CaCl_2(P0.01),and reduced the activity of mitochondria(P0.05 or P0.01),OD values at 540 nm of mitochondria suspension were increased by Xinhani(P0.05 or P0.01).Conclusion Exogenous Ca~(2+) could increase the concentration free Ca~(2+) in mitochondria,leaded to opening of MPT and decrease the activities of mitochondria.Xinhani could protect mitochondria from damage induced by exogenous Ca~(2+).The protection effect of Xinhani on mitochondria may be one of the important mechanisms of protective effect against cerebral damage caused by ischemia reperfusion.
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