title: Plasma homocysteine and risk of coexisting silent brain infarction in Alzheimer's disease.
abstract: BACKGROUND
  Cerebrovascular disease is common in Alzheimer's disease (AD). Elevated plasma homocysteine (pHcy) levels are reported to be associated with an increased risk of poor cognition and dementia.
  
  
  OBJECTIVE
  To determine whether high pHcy levels are associated with an increased risk of coexisting silent brain infarctions (SBIs) in AD.
  
  
  METHODS
  Study population comprising 143 outpatients with clinical diagnosis of probable AD (73.3 +/- 7.0 years) were classified into 2 groups according to the presence or absence of SBIs on magnetic resonance imaging.
  
  
  RESULTS
  SBIs were noted in 32.9% (47/143) of the AD patients. The pHcy levels in the AD with SBIs (14.0 +/- 4.5 micromol/l) were significant ly elevated compared with the AD without SBIs (11.7 +/- 4.7 micromol/l, p = 0.007). After adjusting for age and gender, high pHcy (>12.4 micromol/l), but not hypertension, was associated with an increased risk of developing SBIs in AD (OR = 4.61, 95% CI = 1.74-12.2, p = 0.002). However, age at onset, cognitive function, cerebrospinal tau or amyloid beta-peptide(1-42) levels were not significantly correlated with pHcy levels in AD.
  
  
  CONCLUSIONS
  SBIs commonly coexist with AD, and may be a unique vascular condition in which homocysteine plays an important role. Homocysteine-lowering therapy rather than antihypertensive medication might be an appropriate strategy to prevent stroke associated with AD.
authors.affiliation: Department of Geriatric and Respiratory Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan.
authors.forename: Toshifumi
authors.initials: T
authors.lastname: Matsui
authors.forename: Miyako
authors.initials: M
authors.lastname: Nemoto
authors.forename: Masahiro
authors.initials: M
authors.lastname: Maruyama
authors.forename: Takefumi
authors.initials: T
authors.lastname: Yuzuriha
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Yao
authors.forename: Haruko
authors.initials: H
authors.lastname: Tanji
authors.forename: Mari
authors.initials: M
authors.lastname: Ootsuki
authors.forename: Naoki
authors.initials: N
authors.lastname: Tomita
authors.forename: Sachio
authors.initials: S
authors.lastname: Matsushita
authors.forename: Susumu
authors.initials: S
authors.lastname: Higuchi
authors.forename: Yo-ichi
authors.initials: Y
authors.lastname: Yoshida
authors.forename: Takashi
authors.initials: T
authors.lastname: Seki
authors.forename: Koh
authors.initials: K
authors.lastname: Iwasaki
authors.forename: Katsutoshi
authors.initials: K
authors.lastname: Furukawa
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Arai
mesh_terms: D000368:Aged; D000483:Alleles; D000544:Alzheimer Disease / Q000150:complications* / Q000453:epidemiology*; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid; D001057:Apolipoproteins E / Q000235:genetics; D016923:Cell Death / Q000502:physiology; D002544:Cerebral Infarction / Q000453:epidemiology* / Q000209:etiology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005492:Folic Acid / Q000097:blood; D005838:Genotype; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009474:Neurons; D010446:Peptide Fragments / Q000134:cerebrospinal fluid; D012307:Risk Factors; D014805:Vitamin B 12 / Q000097:blood; D016875:tau Proteins / Q000134:cerebrospinal fluid
chemical_list: D016229:Amyloid beta-Peptides; D001057:Apolipoproteins E; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D016875:tau Proteins; D006710:Homocysteine; D005492:Folic Acid; D014805:Vitamin B 12