While we see significant α‐2,6 N‐sialylation in AD independent of tau pathology, α‐2,6 N‐sialylation is apparent in other tauopathies: chronic traumatic encephalopathy (CTE), corticobasal degeneration (CBD), and Pick's disease (PiD) all have α‐2,6 sialylated microglia (Figure 5V–Y). This evidence concerns the gene MAPT and Alzheimer disease.