Imagine that the brain is like a thriving metropolis, bustling with various processes and activities. Among these is the transportation network, which is vital for delivering goods to different areas. However, as we age, excess iron starts accumulating in the brain, much like traffic congestion. A recent hypothesis suggests that this iron buildup could be a key contributor to the development of Alzheimer’s disease (AD), a condition known for its devastating impact on cognition. Scientists have discovered that proteins involved in AD, like APP and tau protein, are closely linked to iron metabolism in the brain. In individuals with AD, abnormal levels of iron-related proteins lead to a vicious cycle: iron deposits contribute to AD progression, while AD-related proteins promote further iron accumulation. This process can ultimately result in neuronal loss through a phenomenon called ferroptosis. Excitingly, researchers have identified potential therapeutic approaches such as iron chelators and antioxidants that show promise in treating AD. These findings highlight the importance of understanding iron dysregulation and its potential role in developing effective drugs for AD treatment. To delve deeper into this fascinating topic, take a look at the research article linked below!

Iron plays a crucial role in many physiological processes of the human body, but iron is continuously deposited in the brain as we age. Early studies found iron overload is directly proportional to cognitive decline in Alzheimer’s disease (AD). Amyloid precursor protein (APP) and tau protein, both of which are related to the AD pathogenesis, are associated with brain iron metabolism. A variety of iron metabolism-related proteins have been found to be abnormally expressed in the brains of AD patients and mouse models, resulting in iron deposition and promoting AD progression. Amyloid β (Aβ) and hyperphosphorylated tau, two pathological hallmarks of AD, can also promote iron deposition in the brain, forming a vicious cycle of AD development-iron deposition. Iron deposition and the subsequent ferroptosis has been found to be a potential mechanism underlying neuronal loss in many neurodegenerative diseases. Iron chelators, antioxidants and hepcidin were found useful for treating AD, which represents an important direction for AD treatment research and drug development in the future. The review explored the deep connection between iron dysregulation and AD pathogenesis, discussed the potential of new hypothesis related to iron dyshomeostasis and ferroptosis, and summarized the therapeutics capable of targeting iron, with the expectation to draw more attention of iron dysregulation and corresponding drug development.

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