In comparison to existing HD CSF proteome literature, we also observed an increase in NEFL with progression, a moderate increase in the cell surface proteoglycan GPC1 that did not meet the threshold (r = −0.512), and a moderate trend toward an increase with progression in C1Qa (−0.4511), a component of the C1Q molecule that has been implicated in HD pathogenesis and for which the associated protein C1Qb has been reported to correlate with disease severity [5,6,54]. This evidence concerns the gene GPC1 and Huntington disease.