Journal article
Serum hepcidin levels in cognitively normal older adults with high neocortical Amyloid-β load
Journal of Alzheimer's disease : JAD, Vol.76(1), pp.291-301
2020
Abstract
Background/Objective:
Hepcidin, an iron-regulating hormone, suppresses the release of iron by binding to the iron exporter protein, ferroportin, resulting in intracellular iron accumulation. Given that iron dyshomeostasis has been observed in Alzheimer’s disease (AD) together with elevated serum hepcidin levels, the current study examined whether elevated serum hepcidin levels are an early event in AD pathogenesis by measuring the hormone in cognitively normal older adults at risk of AD, based on high neocortical amyloid-β load (NAL).
Methods:
Serum hepcidin levels in cognitively normal participants (n = 100) aged between 65–90 years were measured using ELISA. To evaluate NAL, all participants underwent 18F-florbetaben positron emission tomography. A standard uptake value ratio (SUVR)<1.35 was classified as low NAL (n = 65) and ≥1.35 (n = 35) was classified as high NAL.
Results:
Serum hepcidin was significantly higher in participants with high NAL compared to those with low NAL before and after adjusting for covariates: age, gender, and APOE ɛ4 carriage (p < 0.05). A receiver operating characteristic curve based on a logistic regression of the same covariates, the base model, distinguished high from low NAL (area under the curve, AUC = 0.766), but was outperformed when serum hepcidin was added to the base model (AUC = 0.794) and further improved with plasma Aβ42/40 ratio (AUC = 0.829).
Conclusion:
The present findings indicate that serum hepcidin is increased in individuals at risk for AD and contribute to the body of evidence supporting iron dyshomeostasis as an early event of AD. Further, hepcidin may add value to a panel of markers that contribute toward identifying individuals at risk of AD; however, further validation studies are required.
Details
- Title
- Serum hepcidin levels in cognitively normal older adults with high neocortical Amyloid-β load
- Authors/Creators
- P. Chatterjee (Author/Creator) - Macquarie UniversityM. Mohammadi (Author/Creator) - Macquarie UniversityK. Goozee (Author/Creator) - Macquarie UniversityT.M. Shah (Author/Creator) - Macquarie UniversityH.R. Sohrabi (Author/Creator) - Macquarie UniversityC.B. Dias (Author/Creator) - Macquarie UniversityK. Shen (Author/Creator) - Australian eHealth Research Centre, CSIRO, Floreat, WA, Australia.P.R. Asih (Author/Creator) - Macquarie UniversityP. Dave (Author/Creator) - Macquarie UniversityS. Pedrini (Author/Creator) - Edith Cowan UniversityN. J. Ashton (Author/Creator) - University of GothenburgA. Hye (Author/Creator) - King's College LondonK. Taddei (Author/Creator) - Edith Cowan UniversityD.B. Lovejoy (Author/Creator) - Macquarie UniversityH. Zetterberg (Author/Creator) - University of GothenburgK. Blennow (Author/Creator) - Sahlgrenska University HospitalR.N. Martins (Author/Creator) - Macquarie University
- Publication Details
- Journal of Alzheimer's disease : JAD, Vol.76(1), pp.291-301
- Publisher
- IOS Press
- Identifiers
- 991005544182507891
- Copyright
- © 2020 – IOS Press and the authors.
- Murdoch Affiliation
- School of Psychology and Exercise Science
- Language
- English
- Resource Type
- Journal article
UN Sustainable Development Goals (SDGs)
This output has contributed to the advancement of the following goals:
Source: InCites
Metrics
24 File views/ downloads
35 Record Views
InCites Highlights
These are selected metrics from InCites Benchmarking & Analytics tool, related to this output
- Collaboration types
- Domestic collaboration
- International collaboration
- Citation topics
- 1 Clinical & Life Sciences
- 1.184 Physiology & Metals
- 1.184.573 Iron Metabolism
- Web Of Science research areas
- Neurosciences
- ESI research areas
- Neuroscience & Behavior