Manganese Neurotoxicity: behavioral disorders associated with dysfunctions in the basal ganglia and neurochemical transmission.
Identifieur interne : 000256 ( PubMed/Corpus ); précédent : 000255; suivant : 000257Manganese Neurotoxicity: behavioral disorders associated with dysfunctions in the basal ganglia and neurochemical transmission.
Auteurs : Safa Bouabid ; Anass Tinakoua ; Nouria Lakhdar-Ghazal ; Abdelhamid BenazzouzSource :
- Journal of neurochemistry [ 1471-4159 ] ; 2015.
Abstract
Manganese (Mn) is an essential element required for many physiological functions. While it is essential at physiological levels, excessive accumulation of Mn in the brain causes severe dysfunctions in the central nervous system known as manganism. Manganism is an extrapyramidal disorder characterized by motor disturbances associated with neuropsychiatric and cognitive disabilities similar to Parkinsonism. As the primary brain regions targeted by Mn are the basal ganglia, known to be involved in the pathophysiology of extrapyramidal disorders, this review will examine the impact of Mn exposure on the basal ganglia circuitry and neurotransmitters in relation to motor and non-motor disorders. The collected data from recent available studies in humans and experimental animal models provide new information about the mechanisms by which Mn affects behavior, neurotransmitters and basal ganglia function observed in manganism. The effects of the alterations of metals on basal ganglia and neurochemical functioning are critical in order to develop effective modalities not only for the treatment of vulnerable populations (e.g., Mn-exposed workers), but also for understanding the etiology of neurodegenerative diseases where brain metal imbalances are involved, such as Parkinson's disease. This article is protected by copyright. All rights reserved.
DOI: 10.1111/jnc.13442
PubMed: 26608821
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While it is essential at physiological levels, excessive accumulation of Mn in the brain causes severe dysfunctions in the central nervous system known as manganism. Manganism is an extrapyramidal disorder characterized by motor disturbances associated with neuropsychiatric and cognitive disabilities similar to Parkinsonism. As the primary brain regions targeted by Mn are the basal ganglia, known to be involved in the pathophysiology of extrapyramidal disorders, this review will examine the impact of Mn exposure on the basal ganglia circuitry and neurotransmitters in relation to motor and non-motor disorders. The collected data from recent available studies in humans and experimental animal models provide new information about the mechanisms by which Mn affects behavior, neurotransmitters and basal ganglia function observed in manganism. The effects of the alterations of metals on basal ganglia and neurochemical functioning are critical in order to develop effective modalities not only for the treatment of vulnerable populations (e.g., Mn-exposed workers), but also for understanding the etiology of neurodegenerative diseases where brain metal imbalances are involved, such as Parkinson's disease. This article is protected by copyright. All rights reserved.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">26608821</PMID><DateCreated><Year>2015</Year><Month>11</Month><Day>26</Day></DateCreated><DateRevised><Year>2015</Year><Month>11</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4159</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2015</Year><Month>Nov</Month><Day>26</Day></PubDate></JournalIssue><Title>Journal of neurochemistry</Title><ISOAbbreviation>J. Neurochem.</ISOAbbreviation></Journal><ArticleTitle>Manganese Neurotoxicity: behavioral disorders associated with dysfunctions in the basal ganglia and neurochemical transmission.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1111/jnc.13442</ELocationID><Abstract><AbstractText NlmCategory="UNASSIGNED">Manganese (Mn) is an essential element required for many physiological functions. While it is essential at physiological levels, excessive accumulation of Mn in the brain causes severe dysfunctions in the central nervous system known as manganism. Manganism is an extrapyramidal disorder characterized by motor disturbances associated with neuropsychiatric and cognitive disabilities similar to Parkinsonism. As the primary brain regions targeted by Mn are the basal ganglia, known to be involved in the pathophysiology of extrapyramidal disorders, this review will examine the impact of Mn exposure on the basal ganglia circuitry and neurotransmitters in relation to motor and non-motor disorders. The collected data from recent available studies in humans and experimental animal models provide new information about the mechanisms by which Mn affects behavior, neurotransmitters and basal ganglia function observed in manganism. The effects of the alterations of metals on basal ganglia and neurochemical functioning are critical in order to develop effective modalities not only for the treatment of vulnerable populations (e.g., Mn-exposed workers), but also for understanding the etiology of neurodegenerative diseases where brain metal imbalances are involved, such as Parkinson's disease. This article is protected by copyright. All rights reserved.</AbstractText><CopyrightInformation>This article is protected by copyright. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bouabid</LastName><ForeName>Safa</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Mohammed V, Faculté des Sciences, Equipe Rythmes Biologiques, Neurosciences et Environnement, Rabat, Morocco.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tinakoua</LastName><ForeName>Anass</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Mohammed V, Faculté des Sciences, Equipe Rythmes Biologiques, Neurosciences et Environnement, Rabat, Morocco.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lakhdar-Ghazal</LastName><ForeName>Nouria</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Université Mohammed V, Faculté des Sciences, Equipe Rythmes Biologiques, Neurosciences et Environnement, Rabat, Morocco.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Benazzouz</LastName><ForeName>Abdelhamid</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33000, Bordeaux, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="">Review</PublicationType><PublicationType UI="">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>11</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Neurochem</MedlineTA><NlmUniqueID>2985190R</NlmUniqueID><ISSNLinking>0022-3042</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Basal ganglia functions</Keyword><Keyword MajorTopicYN="N">Manganese neurotoxicity</Keyword><Keyword MajorTopicYN="N">Monoamine neurotransmission</Keyword><Keyword MajorTopicYN="N">Motor deficits</Keyword><Keyword MajorTopicYN="N">Non-motor disorders</Keyword><Keyword MajorTopicYN="N">Parkinson's disease</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2015</Year><Month>09</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2015</Year><Month>10</Month><Day>24</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2015</Year><Month>11</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2015</Year><Month>11</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2015</Year><Month>11</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>11</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">26608821</ArticleId><ArticleId IdType="doi">10.1111/jnc.13442</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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