Reprint

Iron Metabolism, Redox Balance and Neurological Diseases

Edited by
November 2023
210 pages
  • ISBN978-3-0365-8844-5 (Hardback)
  • ISBN978-3-0365-8845-2 (PDF)

This book is a reprint of the Special Issue Iron Metabolism, Redox Balance and Neurological Diseases that was published in

Biology & Life Sciences
Summary

With the aging of the population, the incidence rate and number of elderly nervous system diseases have increased sharply. This event has brought huge problems to society. Despite significant efforts being made to explore new treatment options and drugs, the results have been limited. The reason may be due to people's incomplete understanding of the pathogenesis of these age-related diseases. Iron is the most abundant trace element in the human body and is essential for normal life activities. Previous studies have shown that brain iron levels increase with age. The abnormal increase in brain iron levels is closely related to age-related neurological diseases. The disruption of the redox balance may be an important mechanism for the occurrence of neurological diseases caused by brain iron abnormalities. This Special Issue mainly highlights and discusses the latest research progress related to the regulation of brain iron metabolism, redox balance, and the pathogenesis of neurological diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), cerebral ischemia, cancer and maintenance of cellular stemness. The molecular mechanisms of iron-misregulation-induced redox imbalance in disease pathogenesis were analyzed. On this basis, further discussions were conducted on potential therapeutic targets for regulating iron metabolism to achieve effective intervention in elderly neurological diseases.

Format
  • Hardback
License
© 2022 by the authors; CC BY-NC-ND license
Keywords
glioma; ferroptosis; lipid peroxidation; molecular mechanisms; treatment; CHIR99021; glycogen synthesis kinase 3; classical Wnt signaling pathway; ferritin; Neuro-2a; cell stemness; MitoQ; PMMP; autophagy; radioprotection; energy phenotype; coenzyme Q10; tissue concentrations; therapeutics; Alzheimer’s disease; dementia; vascular dementia; Lewy body dementia; IRP2; Hif2 inhibition; Fe-S clusters; ferritinophagy; microcytic anemia; iron homeostasis; iron dysregulation; inflammation; infection; cancer; iron chelation; Alzheimer’s disease; glucose metabolism; NLRP3 inflammasome; insulin resistance; oxidative stress; CY-09; OTUD3; ER stress; IRE1α; XBP1s; Fortilin; intracellular iron homeostasis; neuroinflammation; neurodegenerative diseases; Nrf2; NF-κB; ferroptosis; 4-HNE; oxidative stress; Parkinson’s disease; Alzheimer’s disease; stroke; neurodevelopment; iron chelator; n/a