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Cellular Senescence and Iron Dyshomeostasis in Alzheimer’s Disease

Melbourne Dementia Research Centre, The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Parkville, VIC 3052, Australia
Author to whom correspondence should be addressed.
Pharmaceuticals 2019, 12(2), 93;
Received: 26 May 2019 / Revised: 14 June 2019 / Accepted: 17 June 2019 / Published: 19 June 2019
(This article belongs to the Special Issue Iron as Therapeutic Targets in Human Diseases)
Iron dyshomeostasis is a feature of Alzheimer’s disease (AD). The impact of iron on AD is attributed to its interactions with the central proteins of AD pathology (amyloid precursor protein and tau) and/or through the iron-mediated generation of prooxidant molecules (e.g., hydroxyl radicals). However, the source of iron accumulation in pathologically relevant regions of the brain and its contribution to AD remains unclear. One likely contributor to iron accumulation is the age-associated increase in tissue-resident senescent cells that drive inflammation and contribute to various pathologies associated with advanced age. Iron accumulation predisposes ageing tissue to oxidative stress that can lead to cellular dysfunction and to iron-dependent cell death modalities (e.g., ferroptosis). Further, elevated brain iron is associated with the progression of AD and cognitive decline. Elevated brain iron presents a feature of AD that may be modified pharmacologically to mitigate the effects of age/senescence-associated iron dyshomeostasis and improve disease outcome. View Full-Text
Keywords: Alzheimer’s disease; iron homeostasis; ferroptosis; senescence; chelators Alzheimer’s disease; iron homeostasis; ferroptosis; senescence; chelators
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Masaldan, S.; Belaidi, A.A.; Ayton, S.; Bush, A.I. Cellular Senescence and Iron Dyshomeostasis in Alzheimer’s Disease. Pharmaceuticals 2019, 12, 93.

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