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. 2023 Jun 26;4(4):e298. doi: 10.1002/mco2.298

FIGURE 4.

FIGURE 4

A generalization of the pathogenesis of brain iron accumulation in ischemic stroke, hemorrhagic stroke, Alzheimer's disease, and Parkinson's disease. Stroke greatly increases the import of brain iron, resulting in iron accumulation. In contrast, the progression of neurodegeneration and iron accumulation are mutually reinforcing. Mass labile iron, as a central link in stroke and neurodegenerative diseases, involves in the Fenton reaction and triggers the imbalance between the oxidation reaction and the antioxidant system in the neurological system, which leads to ferroptosis and then poor outcomes for patients. Tf, transferrin; TfR, transferrin receptor; NTBI, nontransferrin‐bound iron; Fpn, ferroportin; Cp, ceruloplasmin; FtMt, mitochondrial ferritin; MHC‐I, major histocompatibility complex class I; APP, amyloid precursor protein; ARF6, ADP ribosylation factor 6; p‐tau, phosphorylated tau; BBB, the blood–brain barrier; AQP4, aquaporin‐4. Note: "+ in the red cycle” means to promote.