EXPERIMENTAL ANIMAL MODELS OF PARKINSON’S DISEASE: AN OVERVIEW

Mohd Imran,Anuradha Mishra,Afreen Usmani,Asif Eqbal

doi:10.22159/ajpcr.2020.v13i11.39131

Mohd Imran, Anuradha Mishra + Show 2 more

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https://doi.org/10.22159/ajpcr.2020.v13i11.39131

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Abstract

Parkinson’s disease (PD) is the 2nd most common neurodegenerative disorder due to gradual loss of dopaminergic nerves in the substantia nigra in the midbrain which leads to motor symptoms: For instance, gait dysfunction, involuntary tremor, rigidity, and progressive postural instability. PD has no cure and available current treatment is only symptomatic. At present, the main treatment of PD relies on Levodopa that slowing down the disease development to some level but can lead to several side effects. The literature confirms the available models of Parkinsonism that is chemical-induced, that is, by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine-induced Parkinsonism furthermore transgenic models linked to monogenic alterations in SNCA, LRRK2, UCH-L1, PRKN, and PINK1 genes. In this review article, we conclude that the presently available neurotoxic models of PD that offer a platform for neuroprotective drug discovery.

Highlights

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that affects 1% of the population over 55 years of age
The pathologic hallmark of the disease is the loss of dopaminergic neurons in the Substantia Nigra pars compacta (SNpc) and the presence of intracytoplasmic inclusions named Lewy bodies, formed mainly by synuclein and ubiquitin
Experimental Parkinsonism was incited in animals through various neurotoxins such as MPTP, 1-methyl-4-phenylpyridinium (MPP+), 6-OHDA, Rotenone, 3-Nitrotyrosine, and Parkin

Summary

INTRODUCTION

Parkinson’s disease (PD) is a progressive neurodegenerative disorder that affects 1% of the population over 55 years of age. The progressive loss of dopaminergic neurons in the basal complexes is the most important pathological finding in the patient’s brain. Destruction of these neurons results in the DA level in this area. The everlasting expression of either the duplicated human or rat DA transporters conferred to SK-N-MC cells exposure to the cytotoxic effects of MPP+ in low concentrations. The extent of this action was depend on the apparent level of the DA transporters and could be exactly antagonized by the catecholamine acceptance inhibitor mazindol. 15–20 mg/kg 0.086–0.430 mg/kg 0.05–0.032 mg/kg 2–3 mg/kg 0.075 mg/kg 0.4 mg/kg 0.1 mg/kg 0.4 mg/kg 2.5 mg/kg

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CONFLICTS OF INTEREST