Ferrosenescence: The iron age of neurodegeneration?

Abstract

Aging has been associated with iron retention in many cell types, including the neurons, promoting neurodegeneration by ferroptosis. Excess intracellular iron accelerates aging by damaging the DNA and blocking genomic repair systems, a process we define as ferrosenescence. Novel neuroimaging and proteomic techniques have pinpointed indicators of both iron retention and ferrosenescence, allowing for their early correction, potentially bringing prevention of neurodegenerative disorders within reach. In this review, we take a closer look at the early markers of iron dyshomeostasis in neurodegenerative disorders, focusing on preventive strategies based on nutritional and microbiome manipulations.

Keywords: Antioxidants; BACE-1; Cancer; Cognitive impairment; DNA damage; Ferroportin; Ferroptosis; Frontotemporal dementia; Gluthatione perocidase; Insulin-like growth factor; Iron; Iron regulatory protein-2; Mitochomdria associated membranes; Mitochondrial DNA; Quantitative susceptibility mapping; Selenium; Transferrin; Transposable elements; p53.