While dietary iron is essential for optimal health¹ — being a key part of proteins and enzymes and playing an important role in energy production and the regulation of cell growth and differentiation, among other things — too much iron in your body can have serious ramifications.² One of the most important roles of iron is to provide hemoglobin (the protein in red blood cells) a mechanism through which it can bind to oxygen and carry it throughout your tissues.

Without proper oxygenation, your cells cannot function properly and eventually die. Common symptoms of insufficient iron include fatigue, decreased immunity or iron-deficiency anemia, which can be serious if left untreated. However, your body has a very limited capacity to excrete iron, which means it can build up in your tissues and organs. This is problematic, as iron is a potent oxidizer, capable of damaging tissues, including your vascular system and brain, thereby raising your risk for both heart disease and dementia.

Excess Iron ‘Rusts’ Your Brain

You’re probably familiar with the fact that Alzheimer’s disease is associated with a buildup of amyloid beta plaque in the brain. According to recent research^3,4 from the Netherlands, buildup of iron, causing a rusting effect in the brain, also plays an important role and is common in most Alzheimer’s patients. As noted by the authors:

“In the presence of the pathological hallmarks of [Alzheimer’s disease], iron is accumulated within and around the amyloid-beta plaques and neurofibrillary tangles, mostly as ferrihydrite inside ferritin, hemosiderin and magnetite.

The co-localization of iron with amyloid-beta has been proposed to constitute a major source of toxicity. Indeed, in vitro, amyloid-beta has been shown to convert ferric iron to ferrous iron, which can act as a catalyst for the Fenton reaction to generate toxic free radicals, which in turn result in oxidative stress.”

Addressing excess iron may therefore be an effective treatment option. A primary focus of conventional treatment so far has been to clear amyloid proteins, but while the approach seems logical, such attempts have met with limited success. Now, researchers suggest clearing out excess iron may be a more effective way to reduce damage and slow or prevent the disease process.

Previous Research Supports Rusty Brain Link

This is not the first time scientists have noted a link between excess iron and Alzheimer’s disease (AD). In 2012, animal research⁵suggested a link between abnormal iron metabolism and amyloid beta accumulation. When iron levels in the blood were reduced using an iron chelator, levels of beta-amyloid and phosphorylated tau protein — which disrupt the ability of neurons to conduct electrical signals — both reverted back to normal.

Interestingly, and unfortunately, this still did not reduce the generation of reactive oxygen species. Nor did it actually lower the level of iron in the brain itself. According to the authors:

“These results demonstrate that deferiprone [an iron chelating drug] confers important protection against hypercholesterolemia-induced AD pathology but the mechanism(s) may involve reduction in plasma iron and cholesterol levels rather than chelation of brain iron. We propose that adding an antioxidant therapy to deferiprone may be necessary to fully protect against cholesterol-enriched diet-induced AD-like pathology.”

In 2013, UCLA researchers found that Alzheimer’s patients tend to have iron accumulation in the hippocampus, and that the iron is responsible for the damage seen in that area. The findings were published in the Journal of Alzheimer’s Disease.⁶ According to the researchers, the damage that eventually results in clinical signs of Alzheimer’s really begin with iron’s destruction of myelin — the fatty coating around your brain’s nerve fibers.

This disrupts communication between neurons and promotes the buildup of beta amyloid plaque, which in turn destroys even more myelin. As explained by UCLA:⁷

“Myelin is produced by cells called oligodendrocytes. These cells, along with myelin, have the highest levels of iron of any cells in the brain … and circumstantial evidence has long supported the possibility that brain iron levels might be a risk factor for age-related diseases like Alzheimer’s. Although iron is essential for cell function, too much of it can promote oxidative damage, to which the brain is especially vulnerable.”

A 2015 study⁸ showed that patients with higher iron levels deteriorated earlier and faster than those with low iron. Here, elevated cerebrospinal fluid iron levels were shown to be strongly correlated with the presence of the Alzheimer’s risk allele, APOE-e4. According to the authors, “These findings reveal that elevated brain iron adversely impacts on AD progression, and introduce brain iron elevation as a possible mechanism for APOE-e4 being the major genetic risk factor for AD.”

Research⁹ published last year in the journal JAMA Neurology also identified brain iron load “as a pathogenic mechanism” in Alzheimer’s, and again linked high iron with the presence of the high-risk genetic mutation APOE-e4. As noted by the authors, “The ε4 allele of APOE confers the greatest genetic risk for Alzheimer disease, and recent data implicate brain-iron load as a pathogenic mechanism because ε4 carriage elevates the level of cerebrospinal fluid ferritin.”