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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Ablation of tau causes an olfactory deficit in a murine model of Parkinson’s disease

Fig. 3

Tau−/− primary cortical neurons display autophagic impairment and have an increase in the release of α-synuclein enriched exosomes. a Quantification of western blot densitometry presented as ratio of LC3-II/I of tau−/− primary cortical neurons (n = 5) and WT primary cortical neurons (n = 5). b Representative images of tau−/− and WT primary cortical neurons immunostained for LC3B and post-stained with DiO and Hoechst 33,342 after incubation with either culture medium (untreated) or 1 μM Wortmannin for 8 h, scale bars: 10 μm. c Quantification of the number of LCB3 positive autophagosomes per 100 μm3 of DiO stained cytosol, in untreated and Wortmannin treated WT (n = 5) and tau−/− (n = 5) primary cortical neurons. d Representative electron micrograph images of tau−/− (n = 3) and WT (n = 3) exosome enriched cell culture media (scale bars: 200 μm) with quantitation of number of exosomes per 10 μM2. e Quantification of western blot densitometry from exosomes isolated from tau−/− (n = 2) and WT (n = 2) primary cortical neurons, presented as % of α-syn relative to WT control and representative western blot. Cell lysate for western blots normalised to automated total protein measurement via ChemiDoc stain-free detection software. Immunocytochemistry data analysed by one-way ANOVA. Western blot analysed by unpaired two-sided t test from 3 independent repeats, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns: not significant. Full western blot images presented in Additional file 1: Figure S5

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