Disruption of the Golgi apparatus mediates zinc deficiency-induced impairment of cognitive function in mice

Zinc deficiency is reported to be a global problem that affects cognitive function. The mechanism underlying zinc deficiency-induced impairment of cognitive function is still obscure. In this study, we treated KM mice (Kun Ming mice) with zinc chelator TPEN (N,N,N ',N '-tetrakis(2-pyridinylmethyl)-1,2-ethanediamine) by i.p. injection. NOR (New Object Recognition) tests demonstrated that TPEN can impair the cognitive function of KM mice. Disruption of the GRASP55/Golgin45 complex, and even the Golgi apparatus, was also observed in hippocampus cells by TPEN treatment. Further investigation by IHF showed that enrichment of A beta peptides occurs in neurons of the cerebral tissue of mice, suggesting that amyloidosis may mediate TPEN-induced impairment of cognitive function. This research not only clarifies that zinc plays an important role in Golgi organization in vivo, but also gives us a possible novel pathway underlying AD development.