Movement Disorders (revue)

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Homocysteine and cognitive impairment in Parkinson's disease: A biochemical, neuroimaging, and genetic study

Identifieur interne : 000823 ( Istex/Curation ); précédent : 000822; suivant : 000824

Homocysteine and cognitive impairment in Parkinson's disease: A biochemical, neuroimaging, and genetic study

Auteurs : Maria C. Rodriguez-Oroz [Espagne] ; Pablo Martínez Lage [Espagne] ; Jose Sanchez-Mut [Espagne] ; Isabel Lamet [Espagne] ; Javier Pagonabarraga [Espagne] ; Jon B. Toledo [Espagne] ; David García-Garcia [Espagne] ; Pedro Clavero [Espagne] ; Lluis Samaranch [Espagne] ; Cecilia Irurzun [Espagne] ; Juan M. Matsubara [Espagne] ; Jaione Irigoien [Espagne] ; Emilia Bescos [Espagne] ; Jaime Kulisevsky [Espagne] ; Jordi Pérez-Tur [Espagne] ; Jose A. Obeso [Espagne]

Source :

RBID : ISTEX:623F6888A7B960F1E7BF39FC9094613747719D6C

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Abstract

The role of the plasma level of homocysteine (Hcy), as a primary outcome, and the effect of silent cerebrovascular lesions and genetic variants related to Hcy metabolism, as secondary outcomes, in the cognitive decline and dementia in Parkinson's disease (PD) were studied. This case–control study focused on 89 PD patients of minimum 10 years of evolution and older than 60 years, who were neuropsychologically classified either as cognitively normal (n = 37), having mild cognitive impairment (Petersen criteria) (n = 22), or suffering from dementia (DSM‐IV) (n = 30), compared with cognitively normal age‐matched control subjects (n = 30). Plasma levels of Hcy, vitamins B12 and B6, folic acid, polymorphisms in genes related to Hcy metabolism (MTHFR, MTR, MTRR, and CBS) and silent cerebrovascular events were analyzed. Plasma levels of Hcy were increased in PD patients (P = 0.0001). There were no differences between the groups of patients. The brain vascular burden was similar among PD groups. There was no association between polymorphisms in the studied genes and the Hcy plasma levels or cognitive status in PD patients. We found no evidence for a direct relationship between Hcy plasma levels and cognitive impairment and dementia in PD. No indirect effect through cerebrovascular disease or genetic background was found either. © 2009 Movement Disorder Society

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DOI: 10.1002/mds.22522

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ISTEX:623F6888A7B960F1E7BF39FC9094613747719D6C

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Jose Sanchez-Mut
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Le document en format XML

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<name sortKey="Kulisevsky, Jaime" sort="Kulisevsky, Jaime" uniqKey="Kulisevsky J" first="Jaime" last="Kulisevsky">Jaime Kulisevsky</name>
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<name sortKey="Perez Ur, Jordi" sort="Perez Ur, Jordi" uniqKey="Perez Ur J" first="Jordi" last="Pérez-Tur">Jordi Pérez-Tur</name>
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<title level="a" type="main" xml:lang="en">Homocysteine and cognitive impairment in Parkinson's disease: A biochemical, neuroimaging, and genetic study</title>
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<name sortKey="Rodriguez Roz, Maria C" sort="Rodriguez Roz, Maria C" uniqKey="Rodriguez Roz M" first="Maria C." last="Rodriguez-Oroz">Maria C. Rodriguez-Oroz</name>
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<name sortKey="Clavero, Pedro" sort="Clavero, Pedro" uniqKey="Clavero P" first="Pedro" last="Clavero">Pedro Clavero</name>
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<mods:affiliation>Neuroscience Center, CIMA, Pamplona, Spain</mods:affiliation>
<country xml:lang="fr">Espagne</country>
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<mods:affiliation>Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain</mods:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)</wicri:regionArea>
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<name sortKey="Samaranch, Lluis" sort="Samaranch, Lluis" uniqKey="Samaranch L" first="Lluis" last="Samaranch">Lluis Samaranch</name>
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<name sortKey="Irurzun, Cecilia" sort="Irurzun, Cecilia" uniqKey="Irurzun C" first="Cecilia" last="Irurzun">Cecilia Irurzun</name>
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<country xml:lang="fr">Espagne</country>
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<mods:affiliation>Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain</mods:affiliation>
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<name sortKey="Irigoien, Jaione" sort="Irigoien, Jaione" uniqKey="Irigoien J" first="Jaione" last="Irigoien">Jaione Irigoien</name>
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<author>
<name sortKey="Bescos, Emilia" sort="Bescos, Emilia" uniqKey="Bescos E" first="Emilia" last="Bescos">Emilia Bescos</name>
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<name sortKey="Kulisevsky, Jaime" sort="Kulisevsky, Jaime" uniqKey="Kulisevsky J" first="Jaime" last="Kulisevsky">Jaime Kulisevsky</name>
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<mods:affiliation>Department of Neurology, Hospital Sant Pau, Barcelona, Spain</mods:affiliation>
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<author>
<name sortKey="Perez Ur, Jordi" sort="Perez Ur, Jordi" uniqKey="Perez Ur J" first="Jordi" last="Pérez-Tur">Jordi Pérez-Tur</name>
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<author>
<name sortKey="Obeso, Jose A" sort="Obeso, Jose A" uniqKey="Obeso J" first="Jose A." last="Obeso">Jose A. Obeso</name>
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<wicri:regionArea>Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED)</wicri:regionArea>
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<monogr></monogr>
<series>
<title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2009-07-30">2009-07-30</date>
<biblScope unit="vol">24</biblScope>
<biblScope unit="issue">10</biblScope>
<biblScope unit="page" from="1437">1437</biblScope>
<biblScope unit="page" to="1444">1444</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">623F6888A7B960F1E7BF39FC9094613747719D6C</idno>
<idno type="DOI">10.1002/mds.22522</idno>
<idno type="ArticleID">MDS22522</idno>
</biblStruct>
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<idno type="ISSN">0885-3185</idno>
</seriesStmt>
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<keywords scheme="KwdEn" xml:lang="en">
<term>Parkinson's disease</term>
<term>dementia</term>
<term>genetics</term>
<term>homocysteine</term>
<term>mild cognitive impairment</term>
<term>white matter hyperintensities</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">The role of the plasma level of homocysteine (Hcy), as a primary outcome, and the effect of silent cerebrovascular lesions and genetic variants related to Hcy metabolism, as secondary outcomes, in the cognitive decline and dementia in Parkinson's disease (PD) were studied. This case–control study focused on 89 PD patients of minimum 10 years of evolution and older than 60 years, who were neuropsychologically classified either as cognitively normal (n = 37), having mild cognitive impairment (Petersen criteria) (n = 22), or suffering from dementia (DSM‐IV) (n = 30), compared with cognitively normal age‐matched control subjects (n = 30). Plasma levels of Hcy, vitamins B12 and B6, folic acid, polymorphisms in genes related to Hcy metabolism (MTHFR, MTR, MTRR, and CBS) and silent cerebrovascular events were analyzed. Plasma levels of Hcy were increased in PD patients (P = 0.0001). There were no differences between the groups of patients. The brain vascular burden was similar among PD groups. There was no association between polymorphisms in the studied genes and the Hcy plasma levels or cognitive status in PD patients. We found no evidence for a direct relationship between Hcy plasma levels and cognitive impairment and dementia in PD. No indirect effect through cerebrovascular disease or genetic background was found either. © 2009 Movement Disorder Society</div>
</front>
</TEI>
</record>

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