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Homocysteine and cognitive impairment in Parkinson's disease: a biochemical, neuroimaging, and genetic study.
Mov Disord. 2009 Jul 30; 24(10):1437-44.MD

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.

Authors+Show Affiliations

Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain. mcroroz@unav.esNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19452554

Citation

Rodriguez-Oroz, Maria C., et al. "Homocysteine and Cognitive Impairment in Parkinson's Disease: a Biochemical, Neuroimaging, and Genetic Study." Movement Disorders : Official Journal of the Movement Disorder Society, vol. 24, no. 10, 2009, pp. 1437-44.
Rodriguez-Oroz MC, Lage PM, Sanchez-Mut J, et al. Homocysteine and cognitive impairment in Parkinson's disease: a biochemical, neuroimaging, and genetic study. Mov Disord. 2009;24(10):1437-44.
Rodriguez-Oroz, M. C., Lage, P. M., Sanchez-Mut, J., Lamet, I., Pagonabarraga, J., Toledo, J. B., García-Garcia, D., Clavero, P., Samaranch, L., Irurzun, C., Matsubara, J. M., Irigoien, J., Bescos, E., Kulisevsky, J., Pérez-Tur, J., & Obeso, J. A. (2009). Homocysteine and cognitive impairment in Parkinson's disease: a biochemical, neuroimaging, and genetic study. Movement Disorders : Official Journal of the Movement Disorder Society, 24(10), 1437-44. https://doi.org/10.1002/mds.22522
Rodriguez-Oroz MC, et al. Homocysteine and Cognitive Impairment in Parkinson's Disease: a Biochemical, Neuroimaging, and Genetic Study. Mov Disord. 2009 Jul 30;24(10):1437-44. PubMed PMID: 19452554.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Homocysteine and cognitive impairment in Parkinson's disease: a biochemical, neuroimaging, and genetic study. AU - Rodriguez-Oroz,Maria C, AU - Lage,Pablo Martínez, AU - Sanchez-Mut,Jose, AU - Lamet,Isabel, AU - Pagonabarraga,Javier, AU - Toledo,Jon B, AU - García-Garcia,David, AU - Clavero,Pedro, AU - Samaranch,Lluis, AU - Irurzun,Cecilia, AU - Matsubara,Juan M, AU - Irigoien,Jaione, AU - Bescos,Emilia, AU - Kulisevsky,Jaime, AU - Pérez-Tur,Jordi, AU - Obeso,Jose A, PY - 2009/5/20/entrez PY - 2009/5/20/pubmed PY - 2009/10/23/medline SP - 1437 EP - 44 JF - Movement disorders : official journal of the Movement Disorder Society JO - Mov Disord VL - 24 IS - 10 N2 - 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. SN - 1531-8257 UR - https://www.unboundmedicine.com/medline/citation/19452554/Homocysteine_and_cognitive_impairment_in_Parkinson's_disease:_a_biochemical_neuroimaging_and_genetic_study_ L2 - https://doi.org/10.1002/mds.22522 DB - PRIME DP - Unbound Medicine ER -