Zinc(II) Induced Alzheimer’s Disease Prevention and Progression With Early, Middle and Lately Stages

Tsuneo Ishida
2-3-6, Saido, Midori-Ku, Saitama-Shi, Saitama-Ken, 〒336-0907, Japan.

Correspondence to: Tsuneo Ishida, 2-3-6, Saido, Midori-Ku, Saitama-Shi, Saitama-Ken, 〒336-0907, Japan.
Received date: June 01, 2024; Accepted date: June 07, 2024; Published date: July 15, 2024
Citation: Ishida T. Zinc(II) Induced Alzheimer’s Disease Prevention and Progression With Early, Middle and Lately Stages. J Med Res Surg. 2024;5(4):80-87. doi: 10.52916/jmrs244142
Copyright: ©2024 Ishida T. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Abstract

Zinc(II) induced Alzheimer’s Disease (AD) prevention and suppressive progression with early, middle, and lately stages are elucidated, and subsequently zinc binding molecular mechanism on each Aβ peptide and Tau protein in progressing stages is clarified. Zinc homeostasis regulates MCI and AD prevention, in which ZnCl₂ could prevent AD pathology by that zinc can reduce β-Amyloid (Aβ) and Tau proteins. Zinc transporters may allow the novel therapies that ZnT-6 functions to a likely site of Aβ generation. At AD progression with early stage, zinc-induced aggregation of Aβ peptides and tau hyperphosphorylation on amyloid and tau aggregation consider the involvement of environmental zinc in Aβ and tau pathology. Zinc can suppress spreading of the Aβ peptide and the Tau protein that elemental zinc 150 mg daily is showed to be evident for an improvement of memory, understanding, communication, and social contact in AD. Zinc induced middle stage AD progression is pathologically characterized by the deposition of Aβ plaques and hyperphosphorylated Tau Proteins (p-tau). Zinc Finger Proteins (ZNFs) regulate the accumulation of tau proteins to affect the Neurofibrillary Tangles (NFTs), resulting in the formation of NFTs, and can inhibit protein phosphatase, promoted abnormal phosphorylation of tau protein. Zinc(II) can prevent heavy stage AD with pathological deposits of Senile Plaques (SPs) and NFTs that the tau-zinc interaction will help understanding the zinc-related tau regulation or aggregation processes in both physiological and pathological conditions. Zinc accelerates the fibrillization of human Tau and thereby increases Tau toxicity in neuronal cells with zinc exacerbated tauopathic deficits.
Zinc induced toxic Reactive Oxygen Species (ROS) generation and hyperphosphorylated tau cause oxidative stress and neurotoxicity, leading to hyperphosphorylated tau damages.
Zinc(II) binding AD molecular mechanism on Aβ and Tau proteins is that Zn²⁺ ions which having Zn²⁺ ions-centered tetrahedral geometric coordination pattern and Zn-CysHis Ligands complexes with tetrahedral geometry formed, bind with Aβ and Tau proteins in each three AD progressing stages, causing Zn²⁺ ions-each stages protein complex formations and oxidative stress to Aβ and Tau protein cells, leading the Zn-CysHis Ligands complexes to molecular and apoptosis activities of synaptic cells.

Keywords:

Zinc(II), Aβ and Tau proteins, SPs and NFTs, Tau hyperphosphorylation, Tau toxicity and tauopathy, ROS and oxidative stress, Zinc-binding molecular mechanism.

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