Iron is an essential nutrient for all living organisms, and the pathology involving this biometal is one of humans’ most common nutritional disorders. Senescent cells accumulate iron, withholding it from pathogens and cancer. However, excessive intracellular iron can damage the genome and oxidize the lipid bilayer of plasma and mitochondrial membranes. Ferroptosis is a programmed cell death driven by excessive intracellular iron in deficient glutathione peroxidase 4 (GPX-4). Neurons are susceptible to ferroptosis as they import antioxidants and organelles from astrocytes, including GPX-4 and ferritin, as well as mitochondria and lysosomes. Consequently, dysfunctional astrocytes can trigger neuronal death by either ferroptosis or glial neurotoxicity. In this chapter, we take a closer look at neurocognitive disorders, including schizophrenia, and their association with ferroptosis, glial neurotoxicity, and ferrosenescence, a unique ferroptosis-resistant phenotype. We also discuss potential strategies for rescuing the brain cells from ferroptosis by facilitating the transfer of biomolecules and organelles from the astrocyte to neurons. In this regard, we highlight several ferroptosis-preventing strategies, including natural and synthetic senotherapeutics, aryl hydrocarbon receptor (AhR) antagonists, antioxidant phenothiazines as well as cellular interventions such as membrane lipid replacement (MLR), and mitochondrial transplant.