Although the group sizes are small (with only five participants per group), these findings confirm that not all patients with neuroimaging evidence of CAA are PET positive (in keeping with previous reports; a recent meta-analysis found that amyloid-PET sensitivity in CAA ranged from 60% to 91%) [43], and suggest that there is a sub-group with an AD-like profile—lower CSF Aβ42, higher CSF t-tau, phospho-tau, NFL, and neurogranin—who have evidence of additional fibrillary amyloid deposition. The gene discussed is NRGN; the disease is Alzheimer disease.