The DOI matches its Crossref record; 132 of the 134 references it cites were found in a registry or an index.
The Role of Zinc in Alzheimer′s Disease
Open accessAbstract
Zinc, the most abundant trace metal in the brain, has numerous functions, both in health and in disease. Zinc is released into the synaptic cleft of glutamatergic neurons alongside glutamate from where it interacts and modulates NMDA and AMPA receptors. In addition, zinc has multifactorial functions in Alzheimer′s disease (AD). Zinc is critical in the enzymatic nonamyloidogenic processing of the amyloid precursor protein (APP) and in the enzymatic degradation of the amyloid‐ β (A β ) peptide. Zinc binds to A β promoting its aggregation into neurotoxic species, and disruption of zinc homeostasis in the brain results in synaptic and memory deficits. Thus, zinc dyshomeostasis may have a critical role to play in the pathogenesis of AD, and the chelation of zinc is a potential therapeutic approach.
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“Mechanistically, high concentrations of Zinc released into the synaptic cleft can induce neurotoxicity through NMDAR and AMPAR inhibition [548].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [548]
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“Zinc may aggravate AD pathogenesis, as zinc can bind Aβ and promote Aβ accumulation. In addition, the accumulation of zinc can cause synaptic and memory defects [548].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [548]
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2 retracted
RETRACTED ARTICLE: APP binds DR6 to trigger axon pruning and neuron death via distinct caspases
Nikolaev, A., McLaughlin, T., O’Leary, D. D. M., & Tessier-Lavigne, M. (2009) · Nature · doi:10.1038/nature07767 · Cited by 992
RetractedEndogenous Zinc in Neurological Diseases
Koh, J.-Y. (2005) · Journal of Clinical Neurology · doi:10.3988/jcn.2005.1.2.121 · Cited by 12
RetractedAlzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Copper, iron and zinc in Alzheimer's disease senile plaques
Lovell, M. A., Robertson, J. D., Teesdale, W. J., Campbell, J. L., & Markesbery, W. R. (1998) · Journal of the Neurological Sciences · doi:10.1016/s0022-510x(98)00092-6 · Cited by 2,120
The neurobiology of zinc in health and disease
Frederickson, C. J., Koh, J., & Bush, A. I. (2005) · Nature reviews. Neuroscience · doi:10.1038/nrn1671 · Cited by 1,841
Rapid induction of Alzheimer A beta amyloid formation by zinc
Bush, A., Pettingell, W., Multhaup, G., d Paradis, M., Vonsattel, J., Gusella, J., Beyreuther, K., Masters, C., & Tanzi, R. (1994) · Science · doi:10.1126/science.8073293 · Cited by 1,522
Cherny, R. A., Atwood, C. S., Xilinas, M. E., Gray, D. N., Jones, W. D., McLean, C. A., Barnham, K. J., Volitakis, I., Fraser, F. W., Kim, Y.-S., et al. (2001) · Neuron · doi:10.1016/s0896-6273(01)00317-8 · Cited by 1,447
Iron accumulation in Alzheimer disease is a source of redox-generated free radicals
Smith, M. A., Harris, P. L. R., Sayre, L. M., & Perry, G. L. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.18.9866 · Cited by 1,365
Edwards, D. R., Handsley, M. M., & Pennington, C. (2008) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2008.08.001 · Cited by 1,163
Ritchie, C. W., Bush, A. I., Mackinnon, A., Macfarlane, S., Mastwyk, M., MacGregor, L., Kiers, L., Cherny, R., Li, Q.-X., Tammer, A., et al. (2003) · Archives of Neurology · doi:10.1001/archneur.60.12.1685 · Cited by 988
Research works printed but not linked: 1
- 10.1172/JCI200420864 · DOI · Paper page
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Sorted by citations
Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
Guo, T., Zhang, D., Zeng, Y., Huang, T. Y., Xu, H., & Zhao, Y. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00391-7 · Cited by 994
Bioinorganic Chemistry of Alzheimer’s Disease
Kepp, K. P. (2012) · Chemical Reviews · doi:10.1021/cr300009x · Cited by 683
Copper, zinc and iron in neurodegenerative diseases (Alzheimer's, Parkinson's and prion diseases)
Kozłowski, H., Łuczkowski, M., Remelli, M., & Valensin, D. (2012) · Coordination Chemistry Reviews · doi:10.1016/j.ccr.2012.03.013 · Cited by 446
Ashraf, A., Jeandriens, J., Parkes, H. G., & So, P. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101494 · Cited by 306
Samsel, A., & Seneff, S. (2013) · Entropy · doi:10.3390/e15041416 · Cited by 307
Metadata
- Authors
- Watt, N. T., Whitehouse, I. J., & Hooper, N. M.
- Affiliations
- University of Leeds (GB)
- Corresponding author
- Hooper, Nigel M.
- Venue
- International Journal of Alzheimer’s Disease
- Publisher
- Wiley
- Published
- 2010-12-20
- Volume
- 2011
- Issue
- 1
- Pages
- 971021-971021
- ISSN
- 2090-0252 (ISSN-L)
- 2090-8024
- PMC
- PMC3010690
- OpenAlex
- W2012671084
- Cited by
- 148
- References
- 134
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 12 · 2023: 10 · 2022: 10 · 2021: 12 · 2020: 19 · 2019: 5 · 2018: 8 · 2017: 10 · 2016: 7 · 2015: 8 · 2014: 6 · 2013: 4 · 2012: 11
- FWCI
- 4.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- International Journal of Alzheimer s Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Research Explorer (The University of Manchester) (submittedVersion)
- Funders
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- zinc, Alzheimer's disease, zinc homeostasis, zinc dyshomeostasis, amyloid precursor protein, amyloid-beta, amyloid-beta aggregation, NMDA receptor, AMPA receptors, glutamatergic synapses, synaptic dysfunction, memory impairment, zinc chelation
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