title: Homocysteine and cognitive impairment in Parkinson's disease: a biochemical, neuroimaging, and genetic study.
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.affiliation: Department of Neurology, University Clinic and Medical School of Navarra, Pamplona, Spain. mcroroz@unav.es
authors.forename: Maria C
authors.initials: MC
authors.lastname: Rodriguez-Oroz
authors.forename: Pablo Martínez
authors.initials: PM
authors.lastname: Lage
authors.forename: Jose
authors.initials: J
authors.lastname: Sanchez-Mut
authors.forename: Isabel
authors.initials: I
authors.lastname: Lamet
authors.forename: Javier
authors.initials: J
authors.lastname: Pagonabarraga
authors.forename: Jon B
authors.initials: JB
authors.lastname: Toledo
authors.forename: David
authors.initials: D
authors.lastname: García-Garcia
authors.forename: Pedro
authors.initials: P
authors.lastname: Clavero
authors.forename: Lluis
authors.initials: L
authors.lastname: Samaranch
authors.forename: Cecilia
authors.initials: C
authors.lastname: Irurzun
authors.forename: Juan M
authors.initials: JM
authors.lastname: Matsubara
authors.forename: Jaione
authors.initials: J
authors.lastname: Irigoien
authors.forename: Emilia
authors.initials: E
authors.lastname: Bescos
authors.forename: Jaime
authors.initials: J
authors.lastname: Kulisevsky
authors.forename: Jordi
authors.initials: J
authors.lastname: Pérez-Tur
authors.forename: Jose A
authors.initials: JA
authors.lastname: Obeso
mesh_terms: D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase / Q000235:genetics; D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000473:pathology; D019731:Carbon-Nitrogen Ligases / Q000235:genetics; D016022:Case-Control Studies; D003072:Cognition Disorders / Q000097:blood* / Q000209:etiology / Q000235:genetics* / Q000473:pathology*; D003541:Cystathionine beta-Synthase / Q000235:genetics; D003863:Depression / Q000209:etiology; D005260:Female; D005492:Folic Acid / Q000097:blood; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D007118:Immunoassay / Q000379:methods; D016015:Logistic Models; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008609:Mental Status Schedule; D008875:Middle Aged; D009483:Neuropsychological Tests; D010300:Parkinson Disease / Q000097:blood* / Q000150:complications / Q000235:genetics* / Q000473:pathology*; D011110:Polymorphism, Genetic; D012720:Severity of Illness Index; D014805:Vitamin B 12 / Q000097:blood; D025101:Vitamin B 6 / Q000097:blood
chemical_list: D006710:Homocysteine; D025101:Vitamin B 6; D005492:Folic Acid; D013766:5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; D003541:Cystathionine beta-Synthase; D019731:Carbon-Nitrogen Ligases; C021557:5,10-methenyltetrahydrofolate synthetase; D014805:Vitamin B 12