There appears to be a link between the age-associated increase in body iron stores and the age-related incidence of Alzheimer’s disease (AD), the most prevalent cause of senile dementia. Body iron stores that increase with age could be pivotal to AD pathogenesis and progression.

Increased stored iron is associated with common medical conditions such as diabetes and vascular disease that increase risk for development of AD.

Increased stored iron could also promote oxidative stress/free radical damage in vulnerable neurons, a critical early change in AD. A ferrocentric model of AD described here forms the basis of a rational, easily testable experimental therapeutic approach for AD, which if successful, would be both widely applicable and inexpensive.

Clinical studies have shown that calibrated phlebotomy is an effective way to reduce stored iron safely and predictably without causing anemia. We hypothesize that reducing stored iron by calibrated phlebotomy to avoid iron deficiency will improve cerebrovascular function, slow neurodegenerative change, and improve cognitive and behavioral functions in AD. The hypothesis is eminently testable as iron reduction therapy is useful for chronic diseases associated with iron excess such as nonalcoholic steatohepatitis (NASH), atherosclerosis, hereditary hemochromatosis and thalassemia.

Testing this hypothesis could provide valuable insight into the causation of Alzheimer’s disease and suggest novel preventive and treatment strategies.

Multiple studies associate disturbances in metal ion homeostasis with AD and suggest a pathogenic role. Iron is the most abundant redox active metal in humans. Dietary iron is actively absorbed but minimally excreted, and there is mounting evidence that body iron stores present in free-living apparently healthy adults, rise with age reaching toxic levels. Sullivan raised two important questions in relation to iron and heart disease: first, are body iron stores excessive, even if they fall within clinically “normal” limits? Second, is stored iron safe? We believe these questions are relevant to AD whose risk increases with age.

Body iron stores increase with age in both men and women. Serum ferritin, which is a useful marker of body iron stores, increases sharply between the teenage years and age 40 in men. A comparable increase in serum ferritin occurs in women after menopause, between 40–49 and 60–69 years of age. Sullivan recognized that the risk of heart disease in men and women paralleled the increases in body iron stores. He formulated the iron hypothesis of coronary artery disease, which suggests that pre-menopausal women are protected from atherosclerosis and atherosclerotic events because of low body iron stores until menopause after which body iron stores rise.

Iron is implicated in the pathogenesis of atherosclerosis, which begins relatively early in life and involves oxidation of low-density lipoprotein by incompletely understood mechanisms. Significantly, the relationship between increased body iron stores and risk of heart disease is observed in men under 50. AD is a disease of aging; its incidence rises dramatically after 60 years of age. However, changes in brain metabolism can precede disease-associated cognitive decline by decades. Thus, it is likely that an age-associated increase in body iron stores will precede or overlap the early cerebral metabolic changes that presage AD in the majority of elderly individuals eventually diagnosed with this disease.

Vasculopathy, cerebral hypoperfusion, and tissue hypoxia biologically link these risk factors, and are implicated in the etiology of Alzheimer’s disease.

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