Could conservative iron chelation lead to neuroprotection in amyotrophic lateral sclerosis?
Moreau C1, Danel V2, Devedjian JC3, Grolez G4, Timmerman K5, Laloux C6, Petrault M7, Gouel F8, Jonneaux A9, Dutheil M10, Lachaud C11, Lopes R12, Kuchinski G13, Auger F14, Kyheng M15, Duhamel A16, Perez T17, Pradat PF18, Blasco H19, Veyrat-Durebex C20,
Corcia P21, Oeckl P22, Otto M23, Dupuis L24, Garçon G25, Defebvre L26, Cabantchik IZ27, Duce J28, Bordet R29, Devos D30.
Antioxid Redox Signal. 2017 Dec 29. doi: 10.1089/ars.2017.7493.
Abstract
Iron accumulation has been observed in mouse models and both sporadic and familial forms of Amyotrophic lateral sclerosis. Iron chelation could reduce iron accumulation and the related excess of oxidative stress in the motor pathways. However, classical
iron chelation would induce systemic iron depletion. We assess the safety and efficacy of conservative iron chelation (i.e. chelation with low risk of iron depletion) in a murine preclinical model and pilot clinical trial. In Sod1G86R mice, deferiprone
increased the mean life span as compared with placebo. The safety was good, without anemia after 12 months of deferiprone in the 23 ALS patients enrolled in the clinical trial. The decreases in the ALS Functional Rating Scale and the body mass index (BMI)
were significantly smaller for the first 3 months of deferiprone treatment (30 mg/kg/day) than for the first treatment-free period. Iron levels in the cervical spinal cord, medulla oblongata and motor cortex (according to MRI), as well as cerebrospinal
fluid levels of oxidative stress and neurofilament light chains were lower after deferiprone treatment. Our observation leads to the hypothesis that moderate iron chelation regimen that avoids changes in systemic iron levels may constitute a novel
therapeutic modality of neuroprotection for ALS.

PMID: 29287521 DOI: 10.1089/ars.2017.7493

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