Zn is an essential element that plays an important role in several biological functions, including the regulation of cell signalling and protection against inflammation and oxidative stress. Its deficiency has been associated with the development of various neurodegenerative pathologies, such as Alzheimer's and Parkinson's diseases. For this reason, Zn supplementation is being studied to slow down or even stop the development of age-related neurodegenerative pathologies.

The metabolism of Zn is closely linked to Cu; in fact, it is known that there is an antagonism between Cu and Zn absorption [1]. Although no serious adverse effects derived from Zn supplementation have been described, there is a clear need to evaluate the long-term effect of Zn supplementation, since an imbalance in Cu metabolism could condition the appearance of certain pathologies.

In this context, using an animal model of Alzheimer's disease, the APP/PS1 double transgenic mice and the control strain, we are carrying out a comprehensive study of the effect of Zn supplementation on liver tissue of the APP/PS1 mouse and the corresponding controls by means of total analysis (Cu, Fe, Zn, Mn, Mg, P, K) by ICP-MS and metalloproteins fractionation studies of Zn an Cu associated species by HPLC-ICP-MS with post-column isotopic dilution analysis. In addition, the effect of Zn supplementation over time has been studied, employing low volumes of serum samples at different ages of mice (1-16 month), through the elemental analysis of Cu, Zn, K, Mg, P and Ca by ICP-MS.

[1] J. Osredkar, N. Sustar. Journal of Clinical Toxicology, 2011, 3 (1), 1-18.

Acknowledgements

This work was financially supported through project PID2022-137319OB-C21 (Ministerio de Ciencia e Inovación, España). M. Marina-Latorre acknowledges a grant from “Severo Ochoa Program” with Ref. PA-23-BP22-183 funded by Principality of Asturias (Spain).