Relationship of Iron Metabolism and Short-Term Cuprizone Treatment of C57BL/6 Mice

Cuprizone Administration Alters the Iron Metabolism in the Mouse Model of Multiple Sclerosis

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Ineffective Erythropoiesis: Anemia and Iron Overload

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The Role of Astrocytes in Multiple Sclerosis

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Mitochondrial Impairment in Oligodendroglial Cells Induces Cytokine Expression and Signaling

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Unraveling the Role of Heme in Neurodegeneration

(2018) Deborah Chiabrando et al.   Frontiers in Neuroscience

The Dual Role of Hepcidin in Brain Iron Load and Inflammation

(2018) Driton Vela   Frontiers in Neuroscience

Iron–sulfur cluster biogenesis and trafficking in mitochondria

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(2016) Hans Lassmann et al.   BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Molecular, Cellular and Clinical Aspects of Intracerebral Hemorrhage: Are the Enemies Within?

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A mouse model for testing remyelinating therapies

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Neogenin Facilitates the Induction of Hepcidin Expression by Hemojuvelin in the Liver

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(2015) Paula G. Franco et al.   FEBS LETTERS

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Mitochondrial iron homeostasis and its dysfunctions in neurodegenerative disorders

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Altered transition metal homeostasis in the cuprizone model of demyelination

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The role of immune cells, glia and neurons in white and gray matter pathology in multiple sclerosis

(2015) Giulia Mallucci et al.   PROGRESS IN NEUROBIOLOGY

Hypoxia induced downregulation of hepcidin is mediated by platelet derived growth factor BB

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(2014) Roberta J Ward et al.   LANCET NEUROLOGY

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Cellular and molecular neuropathology of the cuprizone mouse model: Clinical relevance for multiple sclerosis

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The extrahepatic role of TFR2 in iron homeostasis

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Neurodegeneration with brain iron accumulation: update on pathogenic mechanisms

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Iron and neurodegeneration in the multiple sclerosis brain

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Short-Term Cuprizone Feeding Induces Selective Amino Acid Deprivation with Concomitant Activation of an Integrated Stress Response in Oligodendrocytes

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Cuprizone short-term exposure: Astrocytic IL-6 activation and behavioral changes relevant to psychosis

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Cuprizone [Bis(Cyclohexylidenehydrazide)] is Selectively Toxic for Mature Oligodendrocytes

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The effect of glia-glia interactions on oligodendrocyte precursor cell biology during development and in demyelinating diseases

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Abbreviated exposure to cuprizone is sufficient to induce demyelination and oligodendrocyte loss

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Impairment of heme synthesis in myelin as potential trigger of multiple sclerosis

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Cuprizone neurotoxicity, copper deficiency and neurodegeneration

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The cuprizone animal model: new insights into an old story

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α-1 Antitrypsin binds preprohepcidin intracellularly and prohepcidin in the serum

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In toxic demyelination oligodendroglial cell death occurs early and is FAS independent

(2009) Amke Hesse et al.   NEUROBIOLOGY OF DISEASE

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Fine Tuning of Hepcidin Expression by Positive and Negative Regulators

(2008) Martina U. Muckenthaler   Cell Metabolism

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Pro-hepcidin is unable to degrade the iron exporter ferroportin unless maturated by a furin-dependent process

(2008) Bruno Gagliardo et al.   JOURNAL OF HEPATOLOGY

Tim-2 is the receptor for H-ferritin on oligodendrocytes

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Multiple sclerosis

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