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Alzheimer’s disease (AD) is a common neurodegenerative disorder, but the initiating molecular processes contributing to neuronal death are not well understood. AD is associated with elevated soluble and aggregated forms of amyloid beta (Aβ) and with oxidative stress. Furthermore, there is increasing evidence for a detrimental role of iron in the pathogenic process. In this context, iron chelation by compounds such as 3‐hydroxypyridin‐4‐one, deferiprone (Ferriprox™) may have potential neuroprotective effects. We have evaluated the possible neuroprotective actions of deferiprone against a range of AD‐relevant insults including ferric iron, H₂O₂ and Aβ in primary mouse cortical neurones. We have investigated the possible neuroprotective actions of deferiprone (1, 3, 10, 30 or 100 μM) in primary neuronal cultures following exposure to ferric iron [ferric nitrilotriacetate (FeNTA); 3 and 10 μM], H₂O₂ (100 μM) or …