Alpha-Synuclein defects autophagy by impairing SNAP29-mediated autophagosome-lysosome fusion.

When we correlated the abundance of α-Syn with SNAP29 in post-mortem brain tissue, we found a highly significant negative correlation of the two proteins (slope = −0.1838 ± 0.03046; R 2 = 0.1013; P < 0.0001), suggesting that α-Syn exerts a dose-dependent effect on SNAP29 in the human SNc (Fig. 7e ).

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Interestingly, SNAP29 co-expression likewise tended to normalize the α-Syn-mediated increase of in Alix/AIP1, Flotillin-1, and CD81 in EV-enriched medium pellets (although this effect did not reach statistical significance for Alix/AIP1 and CD81; Fig. 5e, f ) and restored the number of EVs in the culture medium (Fig. 5g ).

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