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Brain–Barrier Regulation, Metal (Cu, Fe) Dyshomeostasis, and Neurodegenerative Disorders in Man and Animals

Institute of Infection and Global Health, School of Veterinary Science, University of Liverpool, ic2 Science Park, Brownlow Hill, Liverpool L3 5RF, UK
Inorganics 2019, 7(9), 108; https://doi.org/10.3390/inorganics7090108
Received: 16 June 2019 / Revised: 22 August 2019 / Accepted: 24 August 2019 / Published: 28 August 2019
(This article belongs to the Special Issue Metals in Neurodegenerative Diseases)
The neurodegenerative diseases (Alzheimers, Parkinsons, amyotrophic lateral sclerosis, Huntingtons) and the prion disorders, have in common a dysregulation of metalloprotein chemistry involving redox metals (Cu, Fe, Mn). The consequent oxidative stress is associated with protein plaques and neuronal cell death. An equilibrium exists between the functional requirement of the brain for Cu and Fe and their destructive potential with the production of reactive oxygen species. The importance of the brain barrier is highlighted in regulating the import of these metals. Upregulation of key transporters occurs in fetal and neonatal life when brain metal requirement is high, and is downregulated in adult life when need is minimal. North Ronaldsay sheep are introduced as an animal model in which a neonatal mode of CTR1 upregulation persists into adulthood and leads to the premise that metal regulation may return to this default setting in ageing, with implications for the neurodegenerative diseases. View Full-Text
Keywords: blood–brain barrier; copper/iron homeostasis; neurodegenerative (Alzheimers; Parkinsons; prion) disease; North Ronaldsay sheep blood–brain barrier; copper/iron homeostasis; neurodegenerative (Alzheimers; Parkinsons; prion) disease; North Ronaldsay sheep
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Haywood, S. Brain–Barrier Regulation, Metal (Cu, Fe) Dyshomeostasis, and Neurodegenerative Disorders in Man and Animals. Inorganics 2019, 7, 108.

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