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      The role of iron in brain ageing and neurodegenerative disorders

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          Abstract

          In the CNS, iron in several proteins is involved in many important processes such as oxygen transportation, oxidative phosphorylation, myelin production, and the synthesis and metabolism of neurotransmitters. Abnormal iron homoeostasis can induce cellular damage through hydroxyl radical production, which can cause the oxidation and modification of lipids, proteins, carbohydrates, and DNA. During ageing, different iron complexes accumulate in brain regions associated with motor and cognitive impairment. In various neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, changes in iron homoeostasis result in altered cellular iron distribution and accumulation. MRI can often identify these changes, thus providing a potential diagnostic biomarker of neurodegenerative diseases. An important avenue to reduce iron accumulation is the use of iron chelators that are able to cross the blood–brain barrier, penetrate cells, and reduce excessive iron accumulation, thereby affording neuroprotection.

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          Author and article information

          Journal
          101139309
          30413
          Lancet Neurol
          Lancet Neurol
          The Lancet. Neurology
          1474-4422
          1474-4465
          30 October 2017
          October 2014
          06 November 2017
          : 13
          : 10
          : 1045-1060
          Affiliations
          Centre for Neuroinflammation and Neurodegeneration, Department of Medicine, Hammersmith Hospital Campus, Imperial College London, London, UK (Prof R J Ward PhD); Faculte de Science, Université Catholique de Louvain, Louvain–la–Neuve, Belgium (Prof R J Ward, Prof R R Crichton PhD) Institute of Biomedical Technologies, National Research Council of Italy, Segrate, Milan, Italy (F A Zucca PhD, L Zecca MD); and Advanced MRI Section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA (J H Duyn PhD)
          Author notes
          Correspondence to: Dr Luigi Zecca, Institute of Biomedical Technologies, National Research Council of Italy, Segrate, MI 20090, Italy, luigi.zecca@ 123456itb.cnr.it
          [*]

          Joint first authors

          Article
          PMC5672917 PMC5672917 5672917 nihpa899692
          10.1016/S1474-4422(14)70117-6
          5672917
          25231526
          e194eadb-7644-4ceb-b4b8-f71bc9ff7898
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