Fig. 5
From: Modulating the catalytic activity of AMPK has neuroprotective effects against α-synuclein toxicity
T172Dα1 overexpression decreases the α-syn burden in the striatum. Deposition of human α-syn in dystrophic axons is analyzed at 4 months after vector injection. a Staining for aggregated forms of α-syn (5G4 antibody) in the STR. Note the significantly lower signal in the representative animal that overexpresses T172Dα1 AMPK. Scale bar: 50 μm. b TH-positive dystrophic fibers (arrowheads) in the STR. Note the correlation with the signal for aggregated forms of α-syn. Scale bar: 50 μm. c Dopamine fibers in the STR, positive for phosphorylated form of α-syn (pS129-α-syn). Arrowheads indicate characteristic fibers’ dystrophy. Scale bar: 25 μm. d Representative sections of the medial STR stained for aggregated forms of α-syn (5G4 antibody). Note the lower signal in the animal overexpressing the T172Dα1 subunit. e Optical densitometry for the 5G4 signal, showing a significant reduction of α-syn burden in the STR of rats co-expressing human α-syn and AMPK T172Dα1 in the nigrostrialal system. Statistical analysis: one-way ANOVA with Newman-Keuls post hoc test; for 5G4-OD analysis, n = 8 (control), n = 12 (α1), n = 8 (α2), n = 8 (T172Dα1); *P < 0.05; **P < 0.01; ***P < 0.001