Figure 3

Zn²⁺ supplementation rescues AD-related mitochondria deficits in 3xTg-AD mice. BN-PAGE was employed to assess the activity of mitochondrial complexes I (a, d and g), II (b, e and h) and IV (c, f and i) in isolated mitochondria obtained from the hippocampus (a–c), cerebral cortex (d–f), or the cerebellum (g–i) of treated and untreated 3xTg-AD, as well as control mice at 2, 6 and 12–14 m.o.a. When compared with age-matched untreated mice, functioning of mitochondrial complexes I and IV appears to be decreased in the hippocampus of untreated 6-month-old 3xTg-AD mice (a and c). The same deficits are found in hippocampal mitochondria of 3xTg-AD mice at 12–14 m.o.a.; however, Zn²⁺ supplementation completely counteracts the development of these deficits (a–c). When comparing complex activities of cortical mitochondria obtained from 6-month-old 3xTg-AD versus age-matched control mice, complexes I and IV are found not compromised (d–f) while a statistically significant deficit is observed in the case of complex II (e). Still in the cortex, complexes I and IV functioning is greatly compromised in untreated 3xTg-AD mice at 12–14 m.o.a. and Zn²⁺ treatment is able to completely rescue the deficits (d–f). No changes are found in the cerebellum of 3xTg-AD mice compared with age-matched controls (g–i). ^*P<0.05; ^**P<0.01. Error bars indicate mean values±S.E.M.