Fig. 5: Possible mechanism of CT-α-syn involvement in the pathogenesis of PD. | Communications Biology

Fig. 5: Possible mechanism of CT-α-syn involvement in the pathogenesis of PD.

From: C-terminal truncation modulates α-Synuclein’s cytotoxicity and aggregation by promoting the interactions with membrane and chaperone

Fig. 5

The interaction between FL-α-syn and membranes is critical for neurotransmitter release, and fibrillation of FL-α-syn is inhibited by chaperones. When the C-terminus is truncated, the interaction with membranes and chaperones becomes stronger, leading to diminished inhibition of fibrillation and mitochondrial damage that is likely to elicit a truncation cycle contributing to pathogenesis.

Back to article page