Parkinson's disease (PD) is a neurodegenerative disease that develops slowly; however, there is no efficient method of early diagnosis, nor is there a cure. It is characterized by the relatively selective loss of dopaminergic neuronal cells in the substantia nigra pars compacta and the presence of alpha-synuclein aggregation named as Lewy bodies and Lewy neurites in surviving affected neurons. Nigrostriatal dopaminergic neurodegeneration is shared with other parkinsonian disorders, including some genetic forms of parkinsonism, but many of these disorders do not have Lewy bodies. An ideal animal model for PD, therefore, should exhibit age-dependent and progressive dopaminergic neurodegeneration, motor and non-motor dysfunction, and abnormal alpha-synuclein pathology. A wide range of neurotoxic agents are used to induce PD, alterations that are similar with dose observed in human PD. These agents are classified mainly by administration route and the species involved. The toxins that are mainly used in present 6- hydroxydopamine, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, rotenone, paraquat, reserpine, methamphetamine, 3-nitrotyrosine and isoquinoline derivatives (Tieu, 2011; McDowell and Chesselet, 2012; Bezard et al. 2013). In addition, viral mediated expression of human α-synuclein, as well as the inoculation of pathogenic α-synuclein species from Lewy bodies of PD patients, for accurately modelling progressive self-propagating neurodegeneration and genetic LRRK2 models (PARK8 gene mutation) has been used (Jiang and Dickson, 2018). In conclusion, these models are only approximations, each possibly holding a certain degree of relevance. Thus, researchers should select models whose characteristics are most suitable for addressing the experimental question.
Birincil Dil | İngilizce |
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Konular | Klinik Tıp Bilimleri |
Bölüm | Original Articles |
Yazarlar | |
Yayımlanma Tarihi | 18 Ağustos 2018 |
Yayımlandığı Sayı | Yıl 2018 |