A Preliminary Study of Cu Exposure Effects upon Alzheimer’s Amyloid Pathology

Pilozzi, Alexander; Yu, Zhanyang; Carreras, Isabel; Cormier, Kerry; Hartley, Dean M.; Rogers, Jack T.; Dedeoglu, Alpaslan; Huang, Xudong

doi:10.3390/biom10030408

Cited by 6 publications

(2 citation statements)

References 105 publications

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“…In our own studies, we have further validated the exacerbation of Aβ oligomerization due to Cu 2+ /Aβ/H 2 O 2 redox interactions in vitro. We have also reported that dietary Cu exposure enhanced APP translations via its 5 untranslated region (5 UTR) of mRNA in human SH-SY5Y cells, increased Aβ amyloidosis, and heightened levels of associated pro-inflammatory cytokines such as MCP-5 in APP/PS1 AD transgenic mice [65]. In summary, it remains to be further determined whether cuproptosis also plays a contributing role in AD neurodegeneration.…”

Section: Cuproptosis and Alzheimer's Diseasementioning

confidence: 95%

A Concise Review on Oxidative Stress-Mediated Ferroptosis and Cuproptosis in Alzheimer’s Disease

Huang

2023

Cells

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Alzheimer’s disease (AD), which was first identified more than a century ago, has become a pandemic that exacts enormous social burden and economic tolls as no measure of combating devastated AD is currently available. Growing etiopathological, genetic, and biochemical data indicate that AD is a heterogeneous, polygenic, multifactorial, and complex disease. However, its exact etiopathology remains to be determined. Numerous experimental data show that cerebral iron and copper dyshomeostasis contribute to Aβ amyloidosis and tauopathy, two neuropathological hallmarks of AD. Moreover, increasing experimental evidence suggests ferroptosis, an iron-dependent and nonapoptotic form of cell death, may be involved in the neurodegenerative process in the AD brain. Thus, the anti-ferroptosis approach may be an efficacious therapeutic strategy for AD patients. Furthermore, it remains to be further determined whether cuproptosis, a copper-dependent and distinct form of regulated cell death, also plays a contributing role in AD neurodegeneration. We hope this concise review of recent experimental studies of oxidative stress-mediated ferroptosis and cuproptosis in AD may spur further investigations on this timely and essential line of research.

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Section: Cuproptosis and Alzheimer's Diseasementioning

confidence: 95%

A Concise Review on Oxidative Stress-Mediated Ferroptosis and Cuproptosis in Alzheimer’s Disease

Huang

2023

Cells

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“…In transgenic animals, copper is reported to either protect against (Bayer et al., 2003; Phinney et al., 2003; Schäfer et al., 2007) or contribute to (Sparks and Schreurs, 2003; Sparks et al., 2006; Sparks, 2007; Quinn et al., 2010; Bourassa et al., 2013; Singh et al., 2013; Harris et al., 2014; Lim et al., 2020; Pilozzi et al., 2020) amyloid plaque formation. Some evidence suggests that copper deposition in Aβ aggregates was the cause rather than the consequence of aggregation (Atwood et al., 1998; Cherny et al., 1999; Atwood et al., 2000; Cherny et al., 2001).…”

Section: Appendix B – Human Studies Considered In the Assessmentmentioning

confidence: 99%

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

More¹,

Bampidis²,

Benford³

et al. 2023

EFS2

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Copper is an essential micronutrient and also a regulated product used in organic and in conventional farming pest management. Both deficiency and excessive exposure to copper can have adverse health effects. In this Scientific Opinion, the EFSA 2021 harmonised approach for establishing health‐based guidance values (HBGVs) for substances that are regulated products and also nutrients was used to resolve the divergent existing HBGVs for copper. The tightly regulated homeostasis prevents toxicity manifestation in the short term, but the development of chronic copper toxicity is dependent on copper homeostasis and its tissue retention. Evidence from Wilson disease suggests that hepatic retention is indicative of potential future and possibly sudden onset of copper toxicity under conditions of continuous intake. Hence, emphasis was placed on copper retention as an early marker of potential adverse effects. The relationships between (a) chronic copper exposure and its retention in the body, particularly the liver, and (b) hepatic copper concentrations and evidence of toxicity were examined. The Scientific Committee (SC) concludes that no retention of copper is expected to occur with intake of 5 mg/day and established an Acceptable Daily Intake (ADI) of 0.07 mg/kg bw. A refined dietary exposure assessment was performed, assessing contribution from dietary and non‐dietary sources. Background copper levels are a significant source of copper. The contribution of copper from its use as plant protection product (PPP), food and feed additives or fertilisers is negligible. The use of copper in fertilisers or PPPs contributes to copper accumulation in soil. Infant formula and follow‐on formula are important contributors to dietary exposure of copper in infants and toddlers. Contribution from non‐oral sources is negligible. Dietary exposure to total copper does not exceed the HBGV in adolescents, adults, elderly and the very elderly. Neither hepatic copper retention nor adverse effects are expected to occur from the estimated copper exposure in children due to higher nutrient requirements related to growth.

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Are high copper levels related to Alzheimer’s and Parkinson’s diseases? A systematic review and meta-analysis of articles published between 2011 and 2022

Scolari Grotto,

Glaser

2023

Biometals

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A Preliminary Study of Cu Exposure Effects upon Alzheimer’s Amyloid Pathology

Cited by 6 publications

References 105 publications

A Concise Review on Oxidative Stress-Mediated Ferroptosis and Cuproptosis in Alzheimer’s Disease

A Concise Review on Oxidative Stress-Mediated Ferroptosis and Cuproptosis in Alzheimer’s Disease

Re‐evaluation of the existing health‐based guidance values for copper and exposure assessment from all sources

Are high copper levels related to Alzheimer’s and Parkinson’s diseases? A systematic review and meta-analysis of articles published between 2011 and 2022

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