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

A P KielyJames S MinersR CourtneyC StrandS LoveJ L Holton
Published in: Neuropathology and applied neurobiology (2018)
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.
Keyphrases
  • poor prognosis
  • cell proliferation
  • signaling pathway
  • long non coding rna