Olfactory heterogeneity in LRRK2 related Parkinsonism
Identifieur interne : 000B81 ( Istex/Corpus ); précédent : 000B80; suivant : 000B82Olfactory heterogeneity in LRRK2 related Parkinsonism
Auteurs : Laura Silveira-Moriyama ; Renato Pupi Munhoz ; Margarete De J. Carvalho ; Salmo Raskin ; Ekaterina Rogaeva ; Patricia De C. Aguiar ; Rodrigo A. Bressan ; Andre C. Felicio ; Orlando G. P. Barsottini ; Luiz Augusto F. Andrade ; Hsin F. Chien ; Vincenzo Bonifati ; Egberto R. Barbosa ; Helio A. Teive ; Andrew J. LeesSource :
- Movement Disorders [ 0885-3185 ] ; 2010-12-15.
English descriptors
- KwdEn :
- LRRK2, PARK8, olfaction, parkinsonism, smell.
Abstract
LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (p = 0.007, 95% CI for β = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23325
Links to Exploration step
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<front><div type="abstract" xml:lang="en">LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (p = 0.007, 95% CI for β = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society</div>
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<abstract>LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in LRRK2 was higher than in PD (p > 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (p = 0.007, 95% CI for β = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society</abstract>
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<abstract xml:lang="en"><p>LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (p = 0.007, 95% CI for β = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society</p>
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<titleGroup><title type="main" xml:lang="en">Olfactory heterogeneity in <i>LRRK2</i>
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<supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p>
<supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds23325:MDS_23325_sm_suppinfo"></mediaResource>
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<p><i>LRRK2</i>
mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in <i>LRRK2</i>
are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S <i>LRRK2</i>
mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in <i>LRRK2</i>
was higher than in PD (<i>p</i>
< 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (<i>p</i>
= 0.007, 95% CI for β = +0.6 to +3.6). In the <i>LRRK2</i>
group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in <i>LRRK2</i>
parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society</p>
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<noteGroup><note xml:id="fn3"><p>Potential conflict of interest: The authors do not have any conflict of interest.</p>
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<affiliation>Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, London, United Kingdom</affiliation>
<description>Correspondence: Reta Lila Weston Institute of Neurological Studies, UCL Institute of Neurology, 1 Wakefield St, London, WC1N 1PJ, United Kingdom</description>
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<place><placeTerm type="text">Hoboken</placeTerm>
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<dateIssued encoding="w3cdtf">2010-12-15</dateIssued>
<dateCaptured encoding="w3cdtf">2010-02-24</dateCaptured>
<dateValid encoding="w3cdtf">2010-06-01</dateValid>
<copyrightDate encoding="w3cdtf">2010</copyrightDate>
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<extent unit="figures">1</extent>
<extent unit="tables">1</extent>
<extent unit="references">36</extent>
<extent unit="words">3625</extent>
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<abstract lang="en">LRRK2 mutations can cause familial and sporadic Parkinson's disease (PD) with Lewy‐body pathology at post‐mortem. Studies of olfaction in LRRK2 are sparse and incongruent. We applied a previously validated translation of the 16 item smell identification test from Sniffin' Sticks (SS‐16) to 14 parkinsonian carriers of heterozygous G2019S LRRK2 mutation and compared with 106 PD patients and 118 healthy controls. The mean SS‐16 score in LRRK2 was higher than in PD (p < 0.001, 95% CI for β = −4.7 to −1.7) and lower than in controls (p = 0.007, 95% CI for β = +0.6 to +3.6). In the LRRK2 group, subjects with low scores had significantly more dyskinesia. They also had younger age of onset, longer disease duration, and reported less frequently a family history of PD, but none of these other differences reached significance. Odor identification is diminished in LRRK2 parkinsonism but not to the same extent as in idiopathic PD. © 2010 Movement Disorder Society</abstract>
<note type="content">*Potential conflict of interest: The authors do not have any conflict of interest.</note>
<note type="funding">Reta Lila Weston Trust for Medical Research and Foundation Philantropique Edmond Safra</note>
<subject lang="en"><genre>Keywords</genre>
<topic>olfaction</topic>
<topic>smell</topic>
<topic>LRRK2</topic>
<topic>PARK8</topic>
<topic>parkinsonism</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
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<titleInfo type="abbreviated"><title>Mov. Disord.</title>
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<note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information - </note>
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<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>2010</date>
<detail type="volume"><caption>vol.</caption>
<number>25</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>16</number>
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<extent unit="pages"><start>2879</start>
<end>2883</end>
<total>5</total>
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<identifier type="istex">812BDDD70A7C5A82FA206880E00F606B2AC14CD9</identifier>
<identifier type="DOI">10.1002/mds.23325</identifier>
<identifier type="ArticleID">MDS23325</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition>
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