Iron overload due to repeated blood transfusions in β-thalassemia patients or in predisposed diseases like hemochromatosis may prove lethal. Regulation and deposition of iron is a significant process, which is been explored extensively in the past decade. Iron deposition in the body can cause cellular dysregulation, including neuronal damage. Significant research has been conducted in understanding how iron accumulation in the brain leads to neurodegeneration. Iron chelators have been tested pre-clinically and are in clinical trials for determining their potential role in the treatment of neurodegenerative diseases like Alzheimerös (AD) and Parkinsonös (PD). It has been reported that iron chelators show promising effects pre-clinically in the amelioration of neurodegenerative disorders. In the clinical setup, the main challenge for any drug is to penetrate the blood brain barrier (BBB) and to show therapeutic action. Smaller anti-oxidant molecules that cross BBB, can be expended for the treatment of neurodegenerative disorders. This review exclusively presents an assessment of original research articles published from year 2017-2019. It also addresses the mechanism of brain iron accumulation focusing more on AD and PD, their genetic predispositions, the detrimental effects of iron overload leading to neurodegeneration, iron-induced neuronal apoptosis and treatment strategies for the same.
Keywords: Alzheimer disease; Cognitive decline; Flavonoids; Iron-Sulfur clusters; Mitochondrial dysfunction.
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