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Figure 4 | Molecular Neurodegeneration

Figure 4

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 4

Tyrosine hydroxylase and NeuN cell counting in the substantia nigra. Three weeks following delivery of AAV1/2 to the substantia nigra there is significant reductions in the number of TH-immunoreactive neurons and NeuN-immunoreactive neurons for both alpha-synuclein and GFP treated animals compared to empty vector controls. AAV1/2 A53T alpha-synuclein produced significantly greater TH and NeuN cell loss compared to the GFP group. *P < 0.05 cf. empty vector; ** P < 0.01 cf. empty vector;*** P < 0.001 cf. empty vector; ## P < 0.01 cf. GFP; scale bar is 1000 μm.

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Molecular Neurodegeneration

ISSN: 1750-1326