The Aging of Iron Man
Azhaar Ashraf,1 Maryam Clark,2 and Po-Wah So1,*
Front Aging Neurosci. 2018; 10: 65.
Published online 2018 Mar 12. doi: 10.3389/fnagi.2018.00065
PMCID: PMC5857593
PMID: 29593525

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5857593/

Abstract
Brain iron is tightly regulated by a multitude of proteins to ensure homeostasis. Iron dyshomeostasis has become a molecular signature associated with aging which is accompanied by progressive decline in cognitive processes. A common theme in
neurodegenerative diseases where age is the major risk factor, iron dyshomeostasis coincides with neuroinflammation, abnormal protein aggregation, neurodegeneration, and neurobehavioral deficits. There is a great need to determine the mechanisms
governing perturbations in iron metabolism, in particular to distinguish between physiological and pathological aging to generate fruitful therapeutic targets for neurodegenerative diseases. The aim of the present review is to focus on the age-related
alterations in brain iron metabolism from a cellular and molecular biology perspective, alongside genetics, and neuroimaging aspects in man and rodent models, with respect to normal aging and neurodegeneration. In particular, the relationship between
iron dyshomeostasis and neuroinflammation will be evaluated, as well as the effects of systemic iron overload on the brain. Based on the evidence discussed here, we suggest a synergistic use of iron-chelators and anti-inflammatories as putative anti-
brain aging therapies to counteract pathological aging in neurodegenerative diseases.

Keywords: brain iron, iron regulation, iron overload, aging, neuroinflammation, neurodegenerative diseases, Alzheimer's disease, Parkinson's disease

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