In vivo, in vitro and pharmacologic models of Parkinson's disease

Abstract

Parkinson's disease (PD), which is the second most common neurodegenerative disorder after Alzheimer's disease, is firstly defined after James Parkinson's report. It carries motor symptoms such as resting tremor, bradykinesia and rigidity of skeletal muscle and freezing of gait. Furthermore, non-motor symptoms such as cognitive and behavioral problems, besides sensory impairments are seen in the patients. However, they may also suffer from sleep disorders or autonomic dysfunction. Although there are some medications in order to symptomatic management, but unfortunately, scientist could not have found exact approaches to cure this disease. Hence, producing a model which can express the most pathophysiologic and behavioral aspects of the disease is a desire. In this paper, we aimed to describe the different models of Parkinson's disease in brief.

An In Vitro Partial Lesion Model of Differentiated Human Mesencephalic Neurons: Effect of Pericyte Secretome on Phenotypic Markers

“…Our data lends support to the hypothesis that brain pericytes may present a new actor in the central nervous system regeneration that is related to their secretory abilities . Several neurotoxins have been utilised to model PD in vitro and in vivo of which MPP + and 6-OHDA are the most widely used ones (Bove and Perier 2012;Presgraves et al 2004;Salari and Bagheri 2019;Zeng et al 2018). MPP + causes the specific degeneration of DA neurons being actively taken up via DAT (Dauer and Przedborski 2003) and inhibits the complex I activity inducing mitochondrial dysfunction.…”

“…Toxins such as 1-methyl-4-phenylpyridinium (MPP + ) and 6-hydroxydopamine (6-OHDA) are widely used to model PD in vivo and in vitro (Bove and Perier 2012;Kowall et al 2000;Presgraves et al 2004;Salari and Bagheri 2019;Zeng et al 2018). MPP + and 6-OHDA induce DA toxicity by increasing oxidation and mitochondrial dysfunction (Blum et al 2001;Richardson et al 2007;Subramaniam and Chesselet 2013).…”

Development of early diagnosis of Parkinson's disease: Illusion or reality?

“…Apparently, this can be done using animal models of PD. 116 According to our hypothesis, only those biomarkers can be considered as preclinical, which were found both in PD patients at the clinical stage and in animal models of the preclinical stage. 95 However, first it is necessary to make sure that the selected model adequately reproduces the PD pathogenesis in certain metabolic pathways, showing the same marker in the blood of patients and animals when modeling the clinical stage of PD.…”

“…[51][52][53][117][118][119][120][121] In this case, PD was reproduced in mice C57BL by systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), converted in the body to 1-methyl-4-phenylpyridinium, a toxin of dopaminergic neurons ( Figure 1C,D). 116,122 Testing of this methodology showed that among 13 Animal models of preclinical PD can be used not only to select preclinical biomarkers among all biomarkers that have already been found in PD patients, but also to searching biomarkers that were not been found in patients. Despite the fact that this idea was expressed several years ago, 21 there is no progress.…”

Neuroprotective Properties of Green Tea (Camellia sinensis) in Parkinson’s Disease: A Review

“…However, loss of dopamine causes an irregular pattern of nerve firing and results in loss of movement control [ 56 ]. The neurotoxins 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA) selectively damages the substantia nigra region of the brain resulting in the dopaminergic neuronal loss and is widely used in identifying the underlying molecular mechanism in the progression of PD [ 57 ].…”