From Zine Balance to Disense Progression: Decoding the Puzzle of Neurodegeneration

Abstract

A vital trace element in the human body, zinc is involved in many physiological functions, including DNA repair,
neurotransmission, oxidative stress, and protein synthesis. Intracellular zinc is exported by members of the zinc
transporters (ZnTs) family, while extracellular zinc is imported by Zrt-and-Irt-like proteins (ZIPs). The preservation of
cellular zinc homeostasis depends on these mechanisms. Neurodegenerative disorders have been associated with
imbalances in zinc metabolism. Through processes like ferroptosis, protein phase separation, oxidative stress,
neuroinflammation, and cell death control, zinc level disruptions may affect the survival and function of neurons and
consequently contribute to the development of neurodegenerative disorders. Our knowledge of the pathophysiology of
these illnesses may thus be improved by doing a thorough analysis of the regulatory network of zinc and looking into
the connection between neurodegenerative disorders and zinc dysmetabolism. Furthermore, it could provide new
perspectives and methods for treating neurodegenerative illnesses.