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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: AAV1/2-induced overexpression of A53T-α-synuclein in the substantia nigra results in degeneration of the nigrostriatal system with Lewy-like pathology and motor impairment: a new mouse model for Parkinson’s disease

Fig. 1

AAV1/2-A53T-aSyn SN injection leads to motor deficits and widespread aSyn expression and aggregation. a Unilateral AAV1/2-A53T-aSyn delivery leads to a significant asymmetry of forepaw use with preference of the ipsilateral forepaw relative to the side of injection as compared to AAV1/2-EV control mice. This behavioral deficit was visible at 5 and 9 weeks after AAV1/2 injection (mean ± SEM). b By immunofluorescence staining of mouse midbrain sections, widespread human A53T-aSyn protein (green) could be detected in the ipsilateral SN (il) 10 weeks after AAV1/2-A53T-aSyn injection (cl = contralateral). c Mutated A53T-aSyn protein (green) was found in the ipsilateral striatum (il) 10 weeks after delivery of AAV1/2-A53T-aSyn in the SN thus indicating a transport of this protein along the nigrostriatal tract. d-f Double immunofluorescence staining of AAV1/2-A53T-aSyn treated mouse SN depicting TH+ dopaminergic neurons (red) (d) and A53T-aSyn transgenic protein (green) (e) that co-localize (f). g-i High magnification of a TH+ dopaminergic neuron in the SN (red) (g). The same neuron is stained for mutated A53T-aSyn (green) (h). Aggregates of mutated A53T-aSyn protein can be detected in the cytoplasm of this neuron (arrows) (h, i). j-l) TH+ neurons that were injected with AAV1/2-EV (j) do not express human A53T-aSyn after 10 weeks (k, l). *P < 0.05; ***P < 0.001

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Acta Neuropathologica Communications

ISSN: 2051-5960

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