While ultimately the interaction of tau and beta-amyloid is additive in promoting the spread of AD pathology, at a given stage during evolution of the disease the proteins might plausibly have mutually reciprocal effects on synaptic function and network connectivity: for example, prior to undergoing pathogenic misfolding tau protein protects against beta-amyloid-induced neuronal dysfunction (Dawson et al., 2010), while tau and beta-amyloid associate with distinct network profiles in the aging brain (Sepulcre et al., 2016). The gene discussed is MAPT; the disease is Alzheimer disease.