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

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Abstract

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 Aβ 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.

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

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Publication details

The article was received on 09 Oct 2019, accepted on 29 Oct 2019 and first published on 30 Oct 2019


Article type: Communication
DOI: 10.1039/C9MT00252A
Metallomics, 2019, Advance Article

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

    H. Wu and J. Zhao, Metallomics, 2019, Advance Article , DOI: 10.1039/C9MT00252A

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