Incidentally, although levels of 17β-HSD10–Aβ complexes are not significantly increased in mitochondria of McGill-R-Thy1-APP rats (Fig. 5ii), the balance between 17β-HSD10–cypD and 17β-HSD10–Aβ complexes seems to be moderately deflected in AD after all towards 17β-HSD10 bounded to Aβ. The gene discussed is THY1; the disease is Alzheimer disease.