Abstract
Parkinson's disease (PD) is a common progressive neurodegenerative disorder. The major pathological hallmarks of PD are the selective loss of nigrostriatal dopaminergic neurons and the presence of intraneuronal aggregates termed Lewy bodies (LBs), but the pathophysiological mechanisms are not fully understood. Epidemiologically, environmental neurotoxins such as pesticides are promising candidates for causative factors of PD. Oxidative stress and mitochondrial dysfunction induced by these toxins could contribute to the progression of PD. While most cases of PD are sporadic, specific mutations in genes that cause familial forms of PD have led to provide new insights into its pathogenesis. This paper focuses on animal models of both toxin-induced and genetically determined PD that have provided significant insight for understanding this disease. We also discuss the validity, benefits, and limitations of representative models.
Highlights
Parkinson’s disease (PD) is one of the most common chronic neurodegenerative disorders
PD is characterized by the severe loss of dopaminergic (DAergic) neurons in the pars-compacta nigra and the presence of proteinaceous αsynuclein inclusions, called Lewy bodies (LBs), which are present in neurons of the central nervous system, peripheral autonomic nervous system, enteric nervous system (ENS), and cutaneous nerves [1,2,3]
The loss of DA function can be accelerated by exposure to neurotoxins and by molecular abnormalities, leading to a fast and significant decrease in the number of DA neurons
Summary
Parkinson’s disease (PD) is one of the most common chronic neurodegenerative disorders It is characterized by a variety of motor (bradykinesia, rigidity, tremor, and postural instability) and nonmotor (autonomic disturbances and psychosis) symptoms. It can be diagnosed accurately, no therapeutic strategies can cure or completely block the progression of PD. Animal models of PD, whether induced by environmental risk factors (neurotoxins) or genetic manipulations, should faithfully reproduce the clinical manifestations (behavioral abnormalities), pathological features, and molecular dysfunctions characterizing the disease. Animal models rarely mimic the etiology, progression, and pathology of PD completely, and in most cases, only partial insight can be gained from these studies. We discuss recently developed neurotoxin-induced and genetic model animals of PD
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