title: Effect of genetic risk factors and disease progression on the cerebrospinal fluid tau levels in Alzheimer's disease.
abstract: OBJECTIVE
  This study was undertaken to gain insights into the clinical utility of measuring cerebrospinal fluid tau protein (CSF-tau) to aid in the diagnosis of Alzheimer's disease (AD).
  
  
  METHODS
  AD patients from Tohoku University Hospital, Sendai Japan were sampled.
  
  
  METHODS
  CSF-tau levels were examined by sandwich enzyme-linked immunosorbent assay in a total of 62 patients carrying different alpha 1-antichymotrypsin (ACT) and presenilin-1 (PS-1) polymorphic alleles. Further, the CSF-tau levels were followed up on two occasions during the progression of the disease in 17 AD patients.
  
  
  RESULTS
  There was no evident gradient for tau protein in CSF. Neither the ACT/A allele nor the PS-1/1 allele affected the CSF-tau levels. Although CSF-tau levels changed to a variable extent over time, the CSF-tau levels were significantly increased (P < .01) during the follow-up period. Three of the AD patients demonstrated decreasing values, whereas 14 patients showed increasing values. Finally, these temporal changes in CSF-tau levels were not influenced by the apolipoprotein E epsilon 4, ACT/A or PS-1/1 alleles during the progression of AD.
  
  
  CONCLUSIONS
  Regardless of the mechanisms leading to the degeneration of neurons in AD, our findings provide further evidences that monitoring CSF-tau levels may provide useful information about AD irrespective of the background of genetic risks and disease progression.
authors.affiliation: Department of Geriatric Medicine, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Arai
authors.forename: M
authors.initials: M
authors.lastname: Terajima
authors.forename: M
authors.initials: M
authors.lastname: Miura
authors.forename: S
authors.initials: S
authors.lastname: Higuchi
authors.forename: T
authors.initials: T
authors.lastname: Muramatsu
authors.forename: S
authors.initials: S
authors.lastname: Matsushita
authors.forename: N
authors.initials: N
authors.lastname: Machida
authors.forename: T
authors.initials: T
authors.lastname: Nakagawa
authors.forename: V M
authors.initials: VM
authors.lastname: Lee
authors.forename: J Q
authors.initials: JQ
authors.lastname: Trojanowski
authors.forename: H
authors.initials: H
authors.lastname: Sasaki
mesh_terms: D017668:Age of Onset; D000368:Aged; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid* / Q000175:diagnosis / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics; D015415:Biomarkers / Q000134:cerebrospinal fluid; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D005838:Genotype; D006801:Humans; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D008875:Middle Aged; D053764:Presenilin-1; D012307:Risk Factors; D013997:Time Factors; D000514:alpha 1-Antichymotrypsin / Q000235:genetics; D016875:tau Proteins / Q000134:cerebrospinal fluid*
chemical_list: D001057:Apolipoproteins E; D015415:Biomarkers; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1; D000514:alpha 1-Antichymotrypsin; D016875:tau Proteins