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- deoxyribos...
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| Veröffentlicht in: | Brain research bulletin 2020-03, Vol.156, p.1-9 |
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| creator | Bagwe-Parab, Siddhi Kaur, Ginpreet |
| description | 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 |
| doi_str_mv | 10.1016/j.brainresbull.2019.12.011 |
| format | Article |
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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 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.</description><identifier>ISSN: 0361-9230</identifier><identifier>EISSN: 1873-2747</identifier><identifier>DOI: 10.1016/j.brainresbull.2019.12.011</identifier><identifier>PMID: 31866454</identifier><language>eng</language><publisher>OXFORD: Elsevier Inc</publisher><subject>Alzheimer disease ; Cognitive decline ; Flavonoids ; Iron-Sulfur clusters ; Life Sciences & Biomedicine ; Mitochondrial dysfunction ; Neurosciences ; Neurosciences & Neurology ; Science & Technology</subject><ispartof>Brain research bulletin, 2020-03, Vol.156, p.1-9</ispartof><rights>2019 Elsevier Inc.</rights><rights>Copyright © 2019 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>20</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000515207600001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c380t-2d5f69ca2fc8684a64fd53b11695543d43bb0523acc5942df36d9d6c5fbae3de3</citedby><cites>FETCH-LOGICAL-c380t-2d5f69ca2fc8684a64fd53b11695543d43bb0523acc5942df36d9d6c5fbae3de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.brainresbull.2019.12.011$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27929,27930,28253,46000</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31866454$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bagwe-Parab, Siddhi</creatorcontrib><creatorcontrib>Kaur, Ginpreet</creatorcontrib><title>Molecular targets and therapeutic interventions for iron induced neurodegeneration</title><title>Brain research bulletin</title><addtitle>BRAIN RES BULL</addtitle><addtitle>Brain Res Bull</addtitle><description>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 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.</description><subject>Alzheimer disease</subject><subject>Cognitive decline</subject><subject>Flavonoids</subject><subject>Iron-Sulfur clusters</subject><subject>Life Sciences & Biomedicine</subject><subject>Mitochondrial dysfunction</subject><subject>Neurosciences</subject><subject>Neurosciences & Neurology</subject><subject>Science & Technology</subject><issn>0361-9230</issn><issn>1873-2747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><recordid>eNqNkMuKFDEUQIMoTjv6C1K4EqTKvKvKnfT4ghFBdB1Syc2Ypjpp8xjx703b7eByVgnhnBvuQegFwQPBRL7eDUvSPiTIS13XgWIyD4QOmJAHaEOmkfV05ONDtMFMkn6mDF-gJznvMMZyEvIxumBkkpILvkFfP8cVTF116opON1Byp4Ptyg9I-gC1eNP5UCDdQig-hty5mDqfYmjPthqwXYCaooUbCE05Mk_RI6fXDM_O5yX6_v7dt-3H_vrLh0_bt9e9YRMuPbXCydlo6swkJ64ld1awhRA5C8GZ5WxZsKBMGyNmTq1j0s5WGuEWDcwCu0QvT3MPKf6skIva-2xgXXWAWLOijLWFMRt5Q9-cUJNizgmcOiS_1-m3Ilgdm6qd-r-pOjZVhKrWtMnPz__UZQ_2Tv0XsQGvTsAvWKLLxkMwcIe16oIIikfZbvg4bro_vfXlb9NtrKE09eqkQst66yGps259AlOUjf4-C_0Byn-x7g</recordid><startdate>202003</startdate><enddate>202003</enddate><creator>Bagwe-Parab, Siddhi</creator><creator>Kaur, Ginpreet</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202003</creationdate><title>Molecular targets and therapeutic interventions for iron induced neurodegeneration</title><author>Bagwe-Parab, Siddhi ; Kaur, Ginpreet</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c380t-2d5f69ca2fc8684a64fd53b11695543d43bb0523acc5942df36d9d6c5fbae3de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alzheimer disease</topic><topic>Cognitive decline</topic><topic>Flavonoids</topic><topic>Iron-Sulfur clusters</topic><topic>Life Sciences & Biomedicine</topic><topic>Mitochondrial dysfunction</topic><topic>Neurosciences</topic><topic>Neurosciences & Neurology</topic><topic>Science & Technology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bagwe-Parab, Siddhi</creatorcontrib><creatorcontrib>Kaur, Ginpreet</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Brain research bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bagwe-Parab, Siddhi</au><au>Kaur, Ginpreet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular targets and therapeutic interventions for iron induced neurodegeneration</atitle><jtitle>Brain research bulletin</jtitle><stitle>BRAIN RES BULL</stitle><addtitle>Brain Res Bull</addtitle><date>2020-03</date><risdate>2020</risdate><volume>156</volume><spage>1</spage><epage>9</epage><pages>1-9</pages><issn>0361-9230</issn><eissn>1873-2747</eissn><abstract>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 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.</abstract><cop>OXFORD</cop><pub>Elsevier Inc</pub><pmid>31866454</pmid><doi>10.1016/j.brainresbull.2019.12.011</doi><tpages>9</tpages></addata></record> |
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| source | ScienceDirect Journals (5 years ago - present); Web of Science - Science Citation Index Expanded - 2020<img src="https://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /> |
| subjects | Alzheimer disease Cognitive decline Flavonoids Iron-Sulfur clusters Life Sciences & Biomedicine Mitochondrial dysfunction Neurosciences Neurosciences & Neurology Science & Technology |
| title | Molecular targets and therapeutic interventions for iron induced neurodegeneration |
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