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

Authors

  • Maria C. Rodriguez-Oroz MD, PhD,

    Corresponding author
    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
    2. Neuroscience Center, CIMA, Pamplona, Spain
    3. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
    • Clínica Universitaria Navarra. Av Pio XII 36, Pamplona 31008. Spain
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  • Pablo Martínez Lage MD, PhD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
    Current affiliation:
    1. Fundación ACE, Instituto Catalán de Neurociencias Aplicadas, Barcelona, Spain
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  • Jose Sanchez-Mut PhD,

    1. Unitat de Genética Molecular, Institut de Biomedicina de València-CSIC, Valencia, Spain
    Current affiliation:
    1. Cancer Epigenetics and Biology Program (PEBC), Catalan Institute of Oncology (ICO), Hospital Duran i Reynals, L'Hospitalet de Llobregat (Barcelona) Spain
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  • Isabel Lamet MS,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Javier Pagonabarraga MD,

    1. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
    2. Department of Neurology, Hospital Sant Pau, Barcelona, Spain
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  • Jon B. Toledo MD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • David García-Garcia MS,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
    2. Neuroscience Center, CIMA, Pamplona, Spain
    3. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
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  • Pedro Clavero MD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
    2. Neuroscience Center, CIMA, Pamplona, Spain
    3. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
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  • Lluis Samaranch PhD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Cecilia Irurzun MD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Juan M. Matsubara MD,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Jaione Irigoien BS,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Emilia Bescos BS,

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
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  • Jaime Kulisevsky MD, PhD,

    1. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
    2. Department of Neurology, Hospital Sant Pau, Barcelona, Spain
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  • Jordi Pérez-Tur PhD,

    1. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
    2. Unitat de Genética Molecular, Institut de Biomedicina de València-CSIC, Valencia, Spain
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  • Jose A. Obeso MD, PhD

    1. Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain
    2. Neuroscience Center, CIMA, Pamplona, Spain
    3. Centros de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Spain
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  • Potential conflict of interest: Nothing to report.

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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