Objective: The problem for experimental studies of the pathogenesis of Parkinson’s disease is the impossibility of taking material from patients with this pathology, therefore, it is almost completely impossible to observe the processes occurring in living human cells in BP. Models of Parkinson’s disease are known in vivo (on living organisms) and in vitro (“in vitro”). The most approximate to the processes of human cells are models of pathology in vivo in animals, but when using them there are difficulties with the reproducibility of results, the difficulty of keeping pure lines of animals and justifying the use of models in vivo before the ethical committee. At the same time, recently in vitro models have been increasingly used. Thus, cell cultures are a universal method for studying “physiological” and pathological phenomena, clarifying the mechanisms of signal transmission, regulation of gene expression, cell proliferation, as well as the mechanisms of their death. These models do not completely exclude the model in vivo, but are a good addition to them, allowing to study physiological phenomena and pathogenesis mechanisms of diseases.

Background: To find out the mechanisms of signal transmission, regulation of gene expression, cell proliferation and death.

Methods: Among the models of Parkinson’s diseases in vivo are models of genetic (knockout and transgenic models), neurotoxic (systemic administration of neurotoxins) and stereotaxic (stereotaxic administration of rotenone, paraquat, 6-OHDA, MPP +, MPTP, methamphetamine, degeline and other neurotoxins). Models with exogenous applications (rotenone, paraquat and MPTP) and endogenous (6-hydroxydopamine, MPP +, L-DOPA) neurotoxins are mainly used in in vitro models. For the modeling of Parkinson’s disease in vitro, cultures of neurons, astrocytes and microglial cells are used that make up a functional network in the cytoarchitectonics of the brain that contact each other through neuronal-glial interactions and support the brain homeostasis.

Results: In the near future, possible models of Parkinson’s disease in vitro may be models with the reproduction of previously studied pathophysiological mechanisms of BP development in vivo (AFK effect, creation of conditions for reactive astrogliosis and microgliosis, creation of mitochondrial dysfunction) and in vitro observations production of ROS, lipid peroxidation, activation of microglial NADPH oxidase, enhancement of expression of pro-inflammatory cytokines-IL-1β, TNF-α, IL-6 and / or nitric oxide-NO).

Conclusions: To develop new models of Parkinson’s disease in vitro, interesting observations can also be taken into account in other models: according to Imam S.Z. and others, glucose protects dopaminergic neurons in vitro and in vivo from neurotoxin-mediated cytotoxicity. Based on these data, in new models of Parkinson’s disease, glucose deprivation can be used as an additional damaging factor, which is used to create models of cerebral ischemia in vitro.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/models-of-parkinsons-disease-in-vitro/