AI Article Synopsis
- Parkinson's disease results from the loss of dopaminergic neurons, leading to various symptoms, and there is currently no treatment to slow its progression.
- This study aimed to evaluate canine adenovirus type 2 (CAV-2) as a gene transfer tool in monkey brains and explore the possibility of creating a large nonhuman primate model for a common genetic mutation linked to Parkinson's.
- The findings show that CAV-2 vectors can effectively target neurons and may be optimized for modeling specific neurodegenerative processes associated with Parkinson's disease using LRRK2 expression in monkeys.
Article Abstract
Parkinson's disease is characterized by motor and nonmotor symptoms that gradually appear as a consequence of the selective loss of dopaminergic neurons in the . Currently, no treatment can slow Parkinson's disease progression. Inasmuch, there is a need to develop animal models that can be used to understand the pathophysiological mechanisms underlying dopaminergic neuron death. The initial goal of this study was to determine if canine adenovirus type 2 (CAV-2) vectors are effective gene transfer tools in the monkey brain. A second objective was to explore the possibility of developing a large nonhuman primate that expresses one of the most common genetic mutations causing Parkinson's disease. Our studies demonstrate the neuronal tropism, retrograde transport, biodistribution, and efficacy of CAV-2 vectors expressing GFP and leucine-rich repeat kinase 2 (LRRK2) in the brain. Our data also suggest that following optimization CAV-2-mediated LRRK2 expression could help us model the neurodegenerative processes of this genetic subtype of Parkinson's disease in monkeys.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7109318 | PMC |
| http://dx.doi.org/10.3389/fnmol.2020.00049 | DOI Listing |
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