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Geographic isolates of atypical Parkinsonism and tauopathy in the tropics: Possible synergy of neurotoxins

Identifieur interne : 002F33 ( Istex/Corpus ); précédent : 002F32; suivant : 002F34

Geographic isolates of atypical Parkinsonism and tauopathy in the tropics: Possible synergy of neurotoxins

Auteurs : Dominique Caparros-Lefebvre ; John Steele ; Yaichiro Kotake ; Shigeru Ohta

Source :

RBID : ISTEX:120038CF0BBA03A07A0CDAFF4AEFC81FB29C9FDD

English descriptors

Abstract

Over the last 60 years an abnormally high prevalence of atypical Parkinsonism has been reported in 5 different geographic isolates. It was first described on Guam, later in New Guinea and in the Kii peninsula, on Guadeloupe, and in New Caledonia. We investigated the phenotype of atypical Parkinsonism in three of these foci and observed several similarities with dementia in most and amyotrophic lateral sclerosis in some. This disappearance of this disease in two places—Guam and New Guinea—suggested an environmental origin which has not been clarified before the disease ended. The exposure to annonaceae acetogenins and/or rotenone has been documented in four of these places, and experimental studies in animals demonstrated annonaceae acetogenins neurotoxicity, which is similar to rotenone neurotoxicity. Simultaneous exposure to acetogenins and rotenone could produce a synergistic toxicity on neurons. © 2006 Movement Disorder Society

Url:
DOI: 10.1002/mds.21024

Links to Exploration step

ISTEX:120038CF0BBA03A07A0CDAFF4AEFC81FB29C9FDD

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<description>Correspondence: Centre Hospitalier de Valenciennes – Val d'Escaut, Avenue Desandrouin – F59300 Valenciennes, France</description>
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<namePart type="family">Steele</namePart>
<namePart type="termsOfAddress">MD</namePart>
<affiliation>Micronesian Health Study II, Tamuning, Guam, USA</affiliation>
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<name type="personal">
<namePart type="given">Yaichiro</namePart>
<namePart type="family">Kotake</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Department of Xenobiotic Metabolism and Molecular Toxicology, Graduate School of Biomedical Sciences, Hiroshima University, Minami‐ku, Hiroshima, Japan</affiliation>
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<roleTerm type="text">author</roleTerm>
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<name type="personal">
<namePart type="given">Shigeru</namePart>
<namePart type="family">Ohta</namePart>
<namePart type="termsOfAddress">PhD</namePart>
<affiliation>Department of Xenobiotic Metabolism and Molecular Toxicology, Graduate School of Biomedical Sciences, Hiroshima University, Minami‐ku, Hiroshima, Japan</affiliation>
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<dateIssued encoding="w3cdtf">2006-10</dateIssued>
<dateCaptured encoding="w3cdtf">2005-08-03</dateCaptured>
<dateValid encoding="w3cdtf">2005-10-24</dateValid>
<copyrightDate encoding="w3cdtf">2006</copyrightDate>
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<abstract lang="en">Over the last 60 years an abnormally high prevalence of atypical Parkinsonism has been reported in 5 different geographic isolates. It was first described on Guam, later in New Guinea and in the Kii peninsula, on Guadeloupe, and in New Caledonia. We investigated the phenotype of atypical Parkinsonism in three of these foci and observed several similarities with dementia in most and amyotrophic lateral sclerosis in some. This disappearance of this disease in two places—Guam and New Guinea—suggested an environmental origin which has not been clarified before the disease ended. The exposure to annonaceae acetogenins and/or rotenone has been documented in four of these places, and experimental studies in animals demonstrated annonaceae acetogenins neurotoxicity, which is similar to rotenone neurotoxicity. Simultaneous exposure to acetogenins and rotenone could produce a synergistic toxicity on neurons. © 2006 Movement Disorder Society</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>atypical Parkinsonism</topic>
<topic>Guam</topic>
<topic>Guadeloupe</topic>
<topic>annonaceae acetogenins</topic>
<topic>rotenone</topic>
</subject>
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<title>Movement Disorders</title>
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<title>Mov. Disord.</title>
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<genre>article category</genre>
<topic>Brief Report</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2006</date>
<detail type="volume">
<caption>vol.</caption>
<number>21</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>10</number>
</detail>
<extent unit="pages">
<start>1769</start>
<end>1771</end>
<total>3</total>
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</part>
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<identifier type="istex">120038CF0BBA03A07A0CDAFF4AEFC81FB29C9FDD</identifier>
<identifier type="DOI">10.1002/mds.21024</identifier>
<identifier type="ArticleID">MDS21024</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition>
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