In HD patients, selective loss of synaptic connections between the cortex and striatum, observed in postmortem tissue, correlates with increased activation and localization of complement proteins, particularly C3 and C1q.28 Elevated levels of complement proteins, including C3 and C1q, have been detected in the CSF of premanifest HD patients, highlighting the involvement of complement activation in the disease process.28 It is also important to note that the complement factor C1QB did not exhibit significant changes in the CSF of HD patients.72 Here, VTN is linked to Huntington disease.