There was, however, no clear increase of SHIP2-immunolabelling in the absence of amyloid pathology such as DLBD without AD pathologies, FTD with TDP-43 positive inclusions (Fig. 4e–f) or primary tauopathies such as PSP, CBD, PiD or FTD-tau with MAPT mutation at P301L [81], L266V [50] or G335A [5] (Fig. 4j–l). This evidence concerns the gene INPPL1 and tauopathy.