Lack of Benefit of Iron Chelation in Early Parkinson’s Disease

Abstract

There are no treatments that convincingly slow the progression of Parkinson’s disease. One avenue of investigation is based on iron deposition in the brain, which occurs with aging but is also implicated in neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis.¹ Iron levels are regulated by binding to transferrin and ferritin, and intracellular iron is partitioned in neurons to prevent toxic effects. Ferroptosis refers to iron-dependent toxicity that triggers lipid peroxidation and other oxidative stresses that lead to cell death.² Furthermore, cellular iron may exacerbate aggregation of α-synuclein, the neuronal protein that forms Lewy body inclusions . . .