Mitochondrial iron metabolism and neurodegenerative diseases

Iron is a key element for mitochondrial function and homeostasis, which is also crucial for maintaining the neuronal system, but too much iron promotes oxidative stress. A large body of evidence has indicated that abnormal iron accumulation in the brain is associated with various neurodegenerative diseases such as Huntington's disease, Alzheimer's disease, Parkinson's disease, and Friedreich's ataxia. However, it is still unclear how irregular iron status contributes to the development of neuronal disorders. Hence, the current review provides an update on the causal effects of iron overload in the development and progression of neurodegenerative diseases and discusses important roles of mitochondrial iron homeostasis in these disease conditions. Furthermore, this review discusses potential therapeutic targets for the treatments of iron overload-linked neurodegenerative diseases.

Automated summary

Iron is crucial for mitochondrial function and neuronal homeostasis, but excessive iron can lead to oxidative stress and is associated with various neurodegenerative diseases. The mechanisms through which irregular iron status contributes to the development of neuronal disorders remain unclear. This review discusses the impact of iron overload on neurodegenerative diseases and potential therapeutic targets.