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Figure 6 | Molecular Neurodegeneration

Figure 6

From: Expression of human A53T alpha-synuclein in the rat substantia nigra using a novel AAV1/2 vector produces a rapidly evolving pathology with protein aggregation, dystrophic neurite architecture and nigrostriatal degeneration with potential to model the pathology of Parkinson's disease

Figure 6

Axon morphology in the striatum of AAV1/2 treated rats. Delivery of AAV1/2 human A53T alpha-synuclein to the substantia nigra produces dystrophic and bulging neurites in the striatum 3 weeks later. These changes in axonal morphology do not appear in the AAV1/2 GFP (GFP-immunoreactive [-ir]) or empty vector (represented by tyrosine hydroxylase-immunoreactive [ir]) treated animals. Arrows point to evidence of human alpha-synuclein positive dystrophic neurites; scale bar is 50 μm.

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Molecular Neurodegeneration

ISSN: 1750-1326