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/Corpus ); précédent : 000822; suivant : 000824

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

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

Source :

RBID : ISTEX:623F6888A7B960F1E7BF39FC9094613747719D6C

English descriptors

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

Url:
DOI: 10.1002/mds.22522

Links to Exploration step

ISTEX:623F6888A7B960F1E7BF39FC9094613747719D6C

Le document en format XML

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<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>
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<name>Emilia Bescos BS</name>
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<keyword xml:id="kwd1">homocysteine</keyword>
<keyword xml:id="kwd2">Parkinson's disease</keyword>
<keyword xml:id="kwd3">dementia</keyword>
<keyword xml:id="kwd4">mild cognitive impairment</keyword>
<keyword xml:id="kwd5">genetics</keyword>
<keyword xml:id="kwd6">white matter hyperintensities</keyword>
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<fundingNumber>SAF2006‐00724</fundingNumber>
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<p>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 (
<i>MTHFR</i>
,
<i>MTR</i>
,
<i>MTRR</i>
, and
<i>CBS</i>
) and silent cerebrovascular events were analyzed. Plasma levels of Hcy were increased in PD patients (
<i>P</i>
= 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</p>
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<abstract 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</abstract>
<note type="content">*Potential conflict of interest: Nothing to report.</note>
<note type="funding">Government of Navarra - No. 49/2004; </note>
<note type="funding">Novartis Pharma (Basel, Switzerland)</note>
<note type="funding">Ministerio de Educación y Ciencia, Spain - No. SAF2006‐00724; </note>
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<topic>homocysteine</topic>
<topic>Parkinson's disease</topic>
<topic>dementia</topic>
<topic>mild cognitive impairment</topic>
<topic>genetics</topic>
<topic>white matter hyperintensities</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
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