Dysregulation of Iron Could Play a Central Role in Development of Early Onset Alzheimer’s

Dysregulation of Iron Could Play a Central Role in Development of Early Onset Alzheimer’s
Iron dysregulation in the brains of patients with early onset of Alzheimer’s disease (EOfAD) plays a central role in disease development and progression, according to a new theory. The study, “Dysregulation of Neuronal Iron Homeostasis as an Alternative Unifying Effect of Mutations Causing Familial Alzheimer’s Disease,” was published in the journal Frontiers in Neuroscience. Iron, the most abundant transition metal in the human body, plays a key role in the production of energy by the mitochondria — the compartment of the cell responsible for meeting all of the cell’s energy needs. A charged version of iron, called Fe2+, is the required form for aerobic respiration (the most efficient way in which the mitochondria produce energy). It is extremely important to manage levels of Fe2+ as imbalances can lead to oxidative stress and development of inflammation. Several lines of evidence suggest that iron levels are imbalanced in patients with Alzheimer’s disease. First, these patients have significantly higher levels of protein aggregates called amyloid-β (Aβ) plaques, which are highly enriched with heme, a component of which is iron. Next, levels of ferritin (the iron storage complex) in cerebrospinal fluid (CSF) is significantly higher in patients who have a particular variant of the gene APOE that is associated with late-onset Alzheimer’s disease (LOsAD). Additionally, ferritin levels in the CSF also are predictive of conversion from mild cognitive impairment (MCI) to Alzheimer's disease. Furthermore, levels of ferritin in plasma (a component of blood) strongly corr
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