Ferrous iron formation following the co-aggregation of ferric iron and the Alzheimer's disease peptide β-amyloid (1–42)

Everett, James; Céspedes, Eva; Shelford, L. R.; Exley, Christopher; Collingwood, Joanna F.; Dobson, Jon; Laan, G. van der; Jenkins, Catherine; Arenholz, Elke; Telling, Neil D.

doi:10.1098/rsif.2014.0165

Cited by 112 publications

(109 citation statements)

References 53 publications

(86 reference statements)

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“…Evidence for this comes from recent work showing that once A␤ forms aggregates they induce iron accumulation [40]. Iron-related therapies could still be relevant for patients who are in the early stages of AD.…”

Section: Discussionmentioning

confidence: 99%

No Genetic Overlap Between Circulating Iron Levels and Alzheimer’s Disease

Lupton

Benyamin

Proitsi

et al. 2017

JAD

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Abstract. Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). Recently, peripheral iron measures have also been shown to be associated with AD status. However, it is not known whether these associations are causal: do elevated or depleted iron levels throughout life have an effect on AD risk? We evaluate the effects of peripheral iron on AD risk using a genetic profile score approach by testing whether variants affecting iron, transferrin, or ferritin levels selected from GWAS meta-analysis of approximately 24,000 individuals are also associated with AD risk in an independent case-control 1 Data used in the preparation of this article were obtained from the Genetic and Environmental Risk for Alzheimer's disease (GERAD1) Consortium. As such, the investigators within the GERAD1 consortia contributed to the design and implementation of GERAD1 and/or provided data but did not participate in analysis or writing of this report (except those who are named authors). Membership of the GERAD1 Consortium is provided in the Acknowledgments section.2 Data used in preparing this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators may be found at: http://adni.loni.usc.edu/wpcontent/uploads/how to apply/ADNI Acknowledgement List.pdf * Correspondence to: Michelle K. Lupton, PhD, QIMR

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Section: Discussionmentioning

confidence: 99%

No Genetic Overlap Between Circulating Iron Levels and Alzheimer’s Disease

Lupton

Benyamin

Proitsi

et al. 2017

JAD

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“…Fe was extracted according to Everett et al (2014) as follows. Dried leaf samples (20-60 mg) were soaked in 1 M HCl overnight at room temperature under gentle shaking; extracted Fe is referred to as available Fe.…”

Section: Determination Of Available Fementioning

confidence: 99%

Enhanced Secondary- and Hormone Metabolism in Leaves of Arbuscular Mycorrhizal Medicago truncatula

et al. 2017

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Arbuscular mycorrhizas (AM) are the most common symbiotic associations between a plant's root compartment and fungi. They provide nutritional benefit (mostly inorganic phosphate [P i ]), leading to improved growth, and nonnutritional benefits, including defense responses to environmental cues throughout the host plant, which, in return, delivers carbohydrates to the symbiont. However, how transcriptional and metabolic changes occurring in leaves of AM plants differ from those induced by P i fertilization is poorly understood. We investigated systemic changes in the leaves of mycorrhized Medicago truncatula in conditions with no improved P i status and compared them with those induced by high-P i treatment in nonmycorrhized plants. Microarray-based genome-wide profiling indicated up-regulation by mycorrhization of genes involved in flavonoid, terpenoid, jasmonic acid (JA), and abscisic acid (ABA) biosynthesis as well as enhanced expression of MYC2, the master regulator of JA-dependent responses. Accordingly, total anthocyanins and flavonoids increased, and most flavonoid species were enriched in AM leaves. Both the AM and P i treatments corepressed iron homeostasis genes, resulting in lower levels of available iron in leaves. In addition, higher levels of cytokinins were found in leaves of AM-and P i -treated plants, whereas the level of ABA was increased specifically in AM leaves. Foliar treatment of nonmycorrhized plants with either ABA or JA induced the up-regulation of MYC2, but only JA also induced the up-regulation of flavonoid and terpenoid biosynthetic genes. Based on these results, we propose that mycorrhization and P i fertilization share cytokinin-mediated improved shoot growth, whereas enhanced ABA biosynthesis and JA-regulated flavonoid and terpenoid biosynthesis in leaves are specific to mycorrhization.

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“…Iron may upregulate amyloid precursor protein expression; it can also bind to amyloid formations and facilitate their fibrillation. On the other hand, Abeta is capable of reducing ferrihydrite to ferrous ion [144,145].…”

Section: Parkinson's and Alzheimer's Diseasesmentioning

confidence: 99%

Iron chelation in the treatment of neurodegenerative diseases

Dušek

Schneider

Aaseth

2016

Journal of Trace Elements in Medicine and Biology

101

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a b s t r a c tDisturbance of cerebral iron regulation is almost universal in neurodegenerative disorders. There is a growing body of evidence that increased iron deposits may contribute to degenerative changes. Thus, the effect of iron chelation therapy has been investigated in many neurological disorders including rare genetic syndromes with neurodegeneration with brain iron accumulation as well as common sporadic disorders such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. This review summarizes recent advances in understanding the role of iron in the etiology of neurodegeneration. Outcomes of studies investigating the effect of iron chelation therapy in neurodegenerative disorders are systematically presented in tables. Iron chelators, particularly the blood brain barrier-crossing compound deferiprone, are capable of decreasing cerebral iron in areas with abnormally high concentrations as documented by MRI. Yet, currently, there is no compelling evidence of the clinical effect of iron removal therapy on any neurological disorder. However, several studies indicate that it may prevent or slow down disease progression of several disorders such as aceruloplasminemia, pantothenate kinase-associated neurodegeneration or Parkinson's disease.

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Ferrous iron formation following the co-aggregation of ferric iron and the Alzheimer's disease peptide β-amyloid (1–42)

Cited by 112 publications

References 53 publications

No Genetic Overlap Between Circulating Iron Levels and Alzheimer’s Disease

No Genetic Overlap Between Circulating Iron Levels and Alzheimer’s Disease

Enhanced Secondary- and Hormone Metabolism in Leaves of Arbuscular Mycorrhizal Medicago truncatula

Iron chelation in the treatment of neurodegenerative diseases

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