ArticleJournal of Alzheimer's disease : JAD2020
Serum Hepcidin Levels in Cognitively Normal Older Adults with High Neocortical Amyloid-β Load.
Article in Journal of Alzheimer's disease : JAD, 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, 12 citations in OpenAlex.
- Associations of Iron Indicators with Cognitive Impairment Risk in Postmenopausal Women: Evidence from a Matched Case-Control Study and Back Propagation Neural Network Model.Molecular neurobiology · 2026Article
- High intestinal iron absorption induced by decreased hepcidin leads to imbalance of iron metabolism in aging mice.Biogerontology · 2025Article
- Slc22a17 governs postnatal neurogenesis by maintaining the iron homeostasis in hippocampus.Nature communications · 2025Article
- Epstein-Barr virus infection and vitamin D deficiency are both "causal" for multiple sclerosis (MS) - could the common denominator be their effects on hepcidin levels?Metabolic brain disease · 2025Review
- Motion correction of simultaneous brain PET/MR images based on tracer uptake characteristics.EJNMMI physics · 2025Article
- Plasma Hepcidin as a potential informative biomarker of Alzheimer disease and vascular dementia.Alzheimer's research & therapy · 2025Article
- Effect of ferric citrate on hippocampal iron accumulation and widespread molecular alterations associated with cognitive disorder in an ovariectomized mice model.CNS neuroscience & therapeutics · 2024Article
- Iron homeostasis and organismal aging.Ageing research reviews · 2021Review
- Regular Physical Exercise Modulates Iron Homeostasis in the 5xFAD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2021Article
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Authors and funding
17 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectiveHepcidin, 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).
methodsSerum 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.
resultsSerum hepcidin was significantly higher in participants with high NAL compared to those with low NAL before and after adjusting for covariates: age, gender, and APOEɛ4 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).
conclusionThe 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.
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