Abstract
Parkinson’s Disease (PD) is a common heterogeneous neurodegenerative disorder in which symptoms include bradykinesia, stiffness, tremors, and eventually dementia and speech issues. PD neuropathology is characterized by the progressive neurodegeneration of dopaminergic neurons in the substantia nigra pars compacta and the presence of a-synuclein protein aggregates known as Lewy bodies in affected cells. Whilst what may cause neurodegeneration in PD is still not understood, research using animal models suggest oxidative stress and mitochondrial respiration dysfunction may play important roles.
Animal models are essential in improving our understanding of PD, the most used of which is rodent models due to the behavioural tests available to evaluate motor functionality. Neurotoxin-based approaches apply known toxins such as MPTP and 6-OHDA to model neurodegeneration and motor deficits in mice and rats. Rotenone is another toxin found in pesticides that has been associated with Parkinson's-like pathology, suggesting the role of environmental toxins as a risk factor in PD development . Genetic models create transgenic
and AAV rodents using mutant forms of a-synuclein, such as A53T, A30P, and E45K. These models are important in understanding how Lewy body pathology contributes towards Parkinson’s pathophysiology. Neurotoxin and genetic-based approaches have assisted in the development of therapeutics for PD, including levodopa, rasagiline, and ongoing research into possible AAV-mediated gene therapies. Rodent models have proven themselves highly useful in investigating the complexities of PD, understanding the strengths and limitations of varying types allows optimal application of rodent models in the field of PD research.
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