A review of studies on vascular dementia and iron metabolism

Vascular dementia (VaD) is recognized as the second most prevalent form of dementia after Alzheimer's disease, with its pathogenesis intricately associated with cerebrovascular pathologies, including chronic hypoperfusion, oxidative stress, and neuroinflammation. Recent studies have highlighted dysregulated iron metabolism as a pivotal factor in the pathogenesis of VaD; however, the precise mechanisms and therapeutic implications of this dysregulation remain insufficiently elucidated. In this article, we synthesize clinical and basic research to systematically explore the interaction between iron metabolism and VaD. Aberrant iron metabolism contributes to neuronal damage by exacerbating oxidative stress, lipid peroxidation, and ferroptosis, while cerebrovascular injuries, such as blood-brain barrier disruption and chronic inflammation, further compromise iron metabolism, thereby perpetuating a detrimental cycle. From a diagnostic standpoint, imaging modalities such as susceptibility-weighted imaging, alongside biomarkers like ferritin and soluble transferrin receptors, serve as effective instruments for detecting iron-related pathologies in VaD. At the therapeutic level, the use of chelating agents such as deferoxamine and deferiprone, in combination with antioxidants and innovative nanomaterials, has exhibited neuroprotective effects in animal models by alleviating iron-induced oxidative damage. Nevertheless, further validation is required to establish their clinical efficacy and safety. This is a narrative review. This article investigates the influence and significance of iron metabolism in the pathophysiology of VaD and explores potential therapeutic targets associated with iron metabolism, offering implications for future clinical applications.