Behavioral Tests in Neurotoxin-Induced Animal Models of Parkinson’s Disease

Abstract

Currently, neurodegenerative diseases are a major cause of disability around the world. Parkinson’s disease (PD) is the second-leading cause of neurodegenerative disorder after Alzheimer’s disease. In PD, continuous loss of dopaminergic neurons in the substantia nigra causes dopamine depletion in the striatum, promotes the primary motor symptoms of resting tremor, bradykinesia, muscle rigidity, and postural instability. The risk factors of PD comprise environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular injury, aging, and hereditary defects. The pathologic features of PD include impaired protein homeostasis, mitochondrial dysfunction, nitric oxide, and neuroinflammation, but the interaction of these factors contributing to PD is not fully understood. In neurotoxin-induced PD models, neurotoxins, for instance, 6-hydroxydopamine (6-OHDA), 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-Methyl-4-phenylpyridinium (MPP+), paraquat, rotenone, and permethrin mainly impair the mitochondrial respiratory chain, activate microglia, and generate reactive oxygen species to induce autooxidation and dopaminergic neuronal apoptosis. Since no current treatment can cure PD, using a suitable PD animal model to evaluate PD motor symptoms’ treatment efficacy and identify therapeutic targets and drugs are still needed. Hence, the present review focuses on the latest scientific developments in different neurotoxin-induced PD animal models with their mechanisms of pathogenesis and evaluation methods of PD motor symptoms.

GLP-1 and GIP receptor agonists in the treatment of Parkinson’s disease: Translational systematic review and meta-analysis protocol of clinical and preclinical studies

“…The use of animal models has been crucial to elucidate the pathophysiology behind PD and the development of therapeutic strategies. However, each model has its own particularities and there is still no single model that mimics all the human features of PD [ 70 , 71 ].…”

Humanized Mice for Infectious and Neurodegenerative disorders

“…Third, a clear understanding of the role human immunity plays at the neurobiochemical levels can be uncovered and especially those that predict behavioral insufficiencies and vice versa. Especially in the case of PD where gait and locomotor abnormalities have been well-characterized in prior rodent models these can now be fully explored in the context of human T cell functions and immune tolerance [170,[184][185][186][187]. While motor deficits in the humanized CD34 + mice have been described behavioral comparisons between established rodent models and humanized models await future studies in these exciting models reflective a broad range of human infectious and degenerative diseases [186].…”

Early Detection of External Neurological Symptoms through a Wearable Smart-Glasses Prototype

“…PD is characterized by the loss of nigrostriatal dopaminergic neurons. The damage of dopaminergic neurons causes impaired afferents to the striatum, leads to nerve terminal degeneration in the striatum and causes PD motor symptoms [14]. The three key elements characteristic of motor impairment in PD are bradykinesia, rigidity, and tremor [15].…”