Molecular targets and therapeutic interventions for iron induced neurodegeneration.
Identifieur interne : 000068 ( Main/Exploration ); précédent : 000067; suivant : 000069Molecular targets and therapeutic interventions for iron induced neurodegeneration.
Auteurs : Siddhi Bagwe-Parab [Inde] ; Ginpreet Kaur [Inde]Source :
- Brain research bulletin [ 1873-2747 ] ; 2020.
Abstract
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.
DOI: 10.1016/j.brainresbull.2019.12.011
PubMed: 31866454
Affiliations:
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Electronic address: Ginpreet.Kaur@nmims.edu.</nlm:affiliation><country xml:lang="fr">Inde</country><wicri:regionArea>Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM's NMIMS, Mumbai-400056, Maharashtra</wicri:regionArea><wicri:noRegion>Maharashtra</wicri:noRegion></affiliation></author></analytic><series><title level="j">Brain research bulletin</title><idno type="eISSN">1873-2747</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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. 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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.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bagwe-Parab</LastName><ForeName>Siddhi</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM's NMIMS, Mumbai-400056, Maharashtra, India.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kaur</LastName><ForeName>Ginpreet</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM's NMIMS, Mumbai-400056, Maharashtra, India. Electronic address: Ginpreet.Kaur@nmims.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>12</Month><Day>19</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Brain Res Bull</MedlineTA><NlmUniqueID>7605818</NlmUniqueID><ISSNLinking>0361-9230</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Alzheimer disease</Keyword><Keyword MajorTopicYN="Y">Cognitive decline</Keyword><Keyword MajorTopicYN="Y">Flavonoids</Keyword><Keyword MajorTopicYN="Y">Iron-Sulfur clusters</Keyword><Keyword MajorTopicYN="Y">Mitochondrial dysfunction</Keyword></KeywordList><CoiStatement>Declaration of Competing Interest The authors declare no conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>08</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>12</Month><Day>14</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>12</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>12</Month><Day>24</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31866454</ArticleId><ArticleId IdType="pii">S0361-9230(19)30651-3</ArticleId><ArticleId IdType="doi">10.1016/j.brainresbull.2019.12.011</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Inde</li></country></list><tree><country name="Inde"><noRegion><name sortKey="Bagwe Parab, Siddhi" sort="Bagwe Parab, Siddhi" uniqKey="Bagwe Parab S" first="Siddhi" last="Bagwe-Parab">Siddhi Bagwe-Parab</name></noRegion><name sortKey="Kaur, Ginpreet" sort="Kaur, Ginpreet" uniqKey="Kaur G" first="Ginpreet" last="Kaur">Ginpreet Kaur</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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