MAPT and Alzheimer disease: However, the description that: (1) synapse loss and microglial activation anteceded NTFs in a mouse model of tauopathy [12], (2) synaptic and memory impairments are not mediated by NFTs [13], and (3) insoluble deposition of tau may be a compensatory protective mechanism [13], compromise the proposal of tauopathy as the main player in AD pathogenesis [13].