ArticleInternational journal of molecular sciences2020
Associative Interactions among Zinc, Apolipoprotein E, and Amyloid-β in the Amyloid Pathology.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Serum multi-trace elements and post-stroke cognitive impairment: a prospective observational cohort study.Translational psychiatry · 2025Observational
- Urinary Metal Levels, Cognitive Test Performance, and Dementia in the Multi-Ethnic Study of Atherosclerosis.JAMA network open · 2024Article
- Endothelial Dysfunctions in Blood-Brain Barrier Breakdown in Alzheimer's Disease: From Mechanisms to Potential Therapies.CNS neuroscience & therapeutics · 2024Review
- Metabolic Derangement of Essential Transition Metals and Potential Antioxidant Therapies.International journal of molecular sciences · 2024Review
- Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Effect of metal ions on Alzheimer's disease.Brain and behavior · 2022Review
- Metals toxicity and its correlation with the gene expression in Alzheimer's disease.Molecular biology reports · 2021Article
- Complement Activation in the Central Nervous System: A Biophysical Model for Immune Dysregulation in the Disease State.Frontiers in molecular neuroscience · 2021Article
- RETRACTED: Ameliorative Properties of Boronic Compounds in In Vitro and In Vivo Models of Alzheimer's Disease.International journal of molecular sciences · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Zinc and apolipoprotein E (apoE) are reportedly involved in the pathology of Alzheimer's disease. To investigate the associative interaction among zinc, apoE, and amyloid-β (Aβ) and its role in amyloid pathogenesis, we performed various biochemical and immunoreactive analyses using brain tissues of Tg2576 mice and synthetic Aβ and apoE peptides. On amyloid plaques or in brain lysates of Tg2576 mice, apoE and Aβ immunoreactivities increased after zinc chelation and were restored by its subsequent replacement. Zinc depletion dissociated apoE/Aβ complexes or larger-molecular sizes of Aβ oligomers/aggregates into smaller-molecular sizes of apoE and/or Aβ monomers/complexes. In the presence of zinc, synthetic apoE and/or Aβ peptides aggregated into larger-molecular sizes of oligomers or complexes. Endogenous proteases or plasmin in brain lysates degraded apoE and/or Aβ complexes, and their proteolytic activity increased with zinc depletion. These biochemical findings suggest that zinc associates with apoE and Aβ to encourage the formation of apoE/Aβ complexes or large aggregates, raising the deposition of zinc-rich amyloid plaques. In turn, the presence of abundant zinc around and within apoE/Aβ complexes may block the access or activity of Aβ-degrading antibodies or proteases. These results support the plausibility of chelation strategy aiming at reducing amyloid pathology in Alzheimer's disease.
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