This model is attractive because it can help explain the origins of pTau pathology in the LC, ErC L2 and dendritic tips of solitary L5 and L3 neocortical pyramids and the sequential involvement of other neuron populations in successive NFT stages (Fig. 1, Suppl Table 1).(11) The model also provides a straightforward, plausible explanation for the convergence of Aβ with pTau, ApoE, ApoJ and other RAAAD-P-LTP pathway components in NP niche, and mechanistically links the etiology of NPs to NTs, NFTs and GVDs. This evidence concerns the gene CLU and nail-patella syndrome.