APP and frontotemporal dementia: The resulting phenotypes mimic, at least to some extent, the human disease condition, including learning and memory deficits [127], phosphorylation–dependent tau toxicity [128, 129], correlation between FTD-related mutant forms and enhanced toxicity [130, 131], tangle formation in some [132] but not all cases [see, f.e.  130], synergistic interaction with Abeta leading to Hirano body formation [131], and altered life-span as well as region-specific neurodegeneration in the adult brain [130-132].