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Keywords {🔍}

iron, brain, mice, levels, ferritin, article, pubmed, protein, liver, app, google, scholar, cas, appko, increase, months, age, fig, aging, ferroportin, expression, disease, alzheimers, control, bush, agedependent, australia, homeostasis, precursor, amyloid, increased, proteins, research, wildtype, cell, pty, content, compared, central, analysis, study, ablation, saturation, tissue, victoria, data, normal, decreased, role, elevation,

Topics {✒️}

ice-cold phosphate-buffered saline alzheimer beta-amyloid pathology beta-amyloid precursor protein full size image disease amyloid-beta opposes age-dependent increases plateaued nitric oxide-induced loss iron-mediated neuronal death 4 ml/min ammonium nitrate ferroportin-supported iron efflux marked age-related sec–icp-ms profiles wild-type mice exhibited major iron-binding fraction impaired app/ferroportin association major iron-binding protein amyloid precursor protein sec–icp-ms profile app-ko mice plateaued 0 ml/min flow rate st martin sm long-term aging study mouse anti-β-actin wild-type control littermates app-ko mice compared blood–brain barrier serves iron-export ferroxidase activity app-ko mice results app-ko brain compared privacy choices/manage cookies individual amyloid plaques aging app-ko compared age-dependent iron elevation age-dependent iron accumulation persistent age-dependent increase low molecular weight ageing caenorhabditis elegans cognitive decline german research foundation island research building iron exporter channel ferrous iron dyshomeostasis icp-ms detector app knockout mice related subjects iron export protein high oxygen consumption cold homogenization buffer constant flow rate profit share interest

Schema {🗺️}

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         headline:Marked Age-Related Changes in Brain Iron Homeostasis in Amyloid Protein Precursor Knockout Mice
         description:Proteolytic cleavage of the amyloid precursor protein (APP) into the Aβ peptide has been an extensively researched mechanism for Alzheimer’s disease, but the normal function of the protein is less understood. APP functions to regulate neuronal iron content by stabilizing the surface presentation of ferroportin—the only iron exporter channel of cells. The present study aims to quantify the contribution of APP to brain and peripheral iron by examining the lifetime impact on brain and liver iron levels in APP knockout mice. Consistent with previous reports, we found that wild-type mice exhibited an age-dependent increase in iron and ferritin in the brain, while no age-dependent changes were observed in the liver. APP ablation resulted in an exaggeration of age-dependent iron accumulation in the brain and liver in mice that was assessed at 8, 12, 18, and 22 months of age. Brain ferroportin levels were decreased in APP knockout mice, consistent with a mechanistic role for APP in stabilizing this iron export protein in the brain. Iron elevation in the brain and liver of APP knockout mice correlated with decreased transferrin receptor 1 and increased ferritin protein levels. However, no age-dependent increase in brain ferritin iron saturation was observed in APP-KO mice despite similar protein expression levels potentially explaining the vulnerability of APP-KO mice to parkinsonism and traumatic brain sequelae. Our results support a crucial role of APP in regulating brain and peripheral iron, and show that APP may act to oppose brain iron elevation during aging.
         datePublished:2018-08-15T00:00:00Z
         dateModified:2018-08-15T00:00:00Z
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      headline:Marked Age-Related Changes in Brain Iron Homeostasis in Amyloid Protein Precursor Knockout Mice
      description:Proteolytic cleavage of the amyloid precursor protein (APP) into the Aβ peptide has been an extensively researched mechanism for Alzheimer’s disease, but the normal function of the protein is less understood. APP functions to regulate neuronal iron content by stabilizing the surface presentation of ferroportin—the only iron exporter channel of cells. The present study aims to quantify the contribution of APP to brain and peripheral iron by examining the lifetime impact on brain and liver iron levels in APP knockout mice. Consistent with previous reports, we found that wild-type mice exhibited an age-dependent increase in iron and ferritin in the brain, while no age-dependent changes were observed in the liver. APP ablation resulted in an exaggeration of age-dependent iron accumulation in the brain and liver in mice that was assessed at 8, 12, 18, and 22 months of age. Brain ferroportin levels were decreased in APP knockout mice, consistent with a mechanistic role for APP in stabilizing this iron export protein in the brain. Iron elevation in the brain and liver of APP knockout mice correlated with decreased transferrin receptor 1 and increased ferritin protein levels. However, no age-dependent increase in brain ferritin iron saturation was observed in APP-KO mice despite similar protein expression levels potentially explaining the vulnerability of APP-KO mice to parkinsonism and traumatic brain sequelae. Our results support a crucial role of APP in regulating brain and peripheral iron, and show that APP may act to oppose brain iron elevation during aging.
      datePublished:2018-08-15T00:00:00Z
      dateModified:2018-08-15T00:00:00Z
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         Amyloid precursor protein
         Iron
         Ferritin
         Brain
         Neurodegeneration
         Neurosciences
         Neurology
         Neurosurgery
         Neurobiology
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      name:Alzheimer’s Research UK Cambridge Drug Discovery Institute, University of Cambridge, Cambridge, UK
      name:Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia
      name:Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia
      name:Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia
      name:Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia
      name:Alzheimer’s Research UK Cambridge Drug Discovery Institute, University of Cambridge, Cambridge, UK
      name:Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, Australia

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