Fig. 12.

Current working model for SFPQ and tau-pathological features in rapidly progressive form of AD. The left box of the picture is depicting nuclear-cytoplasmic translocation of SFPQ and p-tau, and their localization in stress granules based on our data from the cellular model of stress. Oxidative stress induced redistribution of SFPQ and p-tau into cytoplasm, and recruitment into SGs. The right box is depicting pathological features of both proteins observed in the post-mortem brains of specifically rpAD cases. The nuclear dislocation of SFPQ was identified in the post-mortem brains of particularly rpAD cases. Further, SFPQ showed colocalization with tau-tangles, tau-oligomers and TIA-1 in the cytoplasm, in the human brain and also in cultures. Nuclear depletion of SFPQ can be toxic for the cells by both loss of function in the nucleus [49] and toxic gain of functions in the cytoplasm