In two adequately-powered sample sets, we have shown that neither neurogranin, a putative marker of postsynaptic damage, nor TREM2, a putative marker of microglial function, has an altered concentration in CSF in Huntington’s disease, despite each protein having shown alterations in CSF in other neurodegenerative diseases, and each having potential links to HD pathogenesis. The gene discussed is NRGN; the disease is Huntington disease.