Exploring the putative role of kallikrein‐6, calpain‐1 and cathepsin‐D in the proteolytic degradation of α‐synuclein in multiple system atrophy

Abstract

Accumulation of α-syn in MSA is not due to reduced activity of the proteases we have studied. We suggest that their upregulation is likely to be a compensatory response to increased α-syn in MSA.