Molecular targets and therapeutic interventions for iron induced neurodegeneration

Abbreviations: 1. BBB- Blood Brain Barrier 2. C19orf12- Chromosome 19 Open Reading Frame 12 3. COASY- Coenzyme A Synthase protein gene 4. CP- Ceruloplasmin gene 5. CUL4- Cullin 4 gene 6. DCAF17- DDB1 and CUL4 Associated Factor 17 gene 7. DDB1- Damage Specific DNA Binding Protein 1 8. DNA- deoxyribose nucleic acid 9. FA2H- Fatty Acid 2-Hydroxylase protein gene 10. FTL1- Ferritin Light chain 1 gene 11. FXN- Frataxin gene 12. GLRX5- Glutaredoxin-related protein 5 gene 13. GTPB2- GTP-binding proteins 2 gene 14. HSPA9- Heat Shock Protein Family A (Hsp70) Member 9 gene 15. ISCU- Iron-sulfur cluster assembly enzyme gene 16. LYRM4- LYR motif containing 4 protein gene 17. MFRN2- Mitoferrin-2 18. NBIA- Neurodegeneration with brain iron accumulation 19. NFS1- Cysteine desulfurase enzyme gene 20. PANK2- Pantothenate kinase 2 protein gene 21. PLA2G6- Phospholipase A2, Group VI protein gene 22. SCP2- Sterol Carrier protein 2 gene 23. WDR45- WD repeat-containing protein 45 gene [Display omitted] •Manifestations of Iron overload in the Brain.•Intracellular damage by reactive oxygen species due to brain iron overload.•Iron overload induced mitochondrial damage and dysregulation of apoptotic pathway.•Genetic predispositions for iron accumulation in the brain.•Treatment strategies for amelioration of iron overload induced neurodegeneration. 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 a