title: Increasing CSF phospho-tau levels during cognitive decline and progression to dementia.
abstract: BACKGROUND
  Little is known about longitudinal changes of cerebrospinal fluid (CSF) biomarkers during cognitive decline in neurodegenerative disease progression.
  
  
  OBJECTIVE
  To investigate longitudinal changes in CSF biomarkers--total-tau (T-tau), phospho-tau (P-tau) and beta-amyloid (Abeta42)--during cognitive decline.
  
  
  METHODS
  Forty memory clinic patients (47.5% females), aged 61.3+/-7.6 (S.D.) years, non-demented at baseline, underwent lumbar puncture and neuropsychological testing at two occasions. Baseline mean MMSE-score was 28.3+/-1.8. Patients were divided into three groups based on baseline memory functioning; severely impaired (SIM), moderately impaired (MIM) and no impairment (NIM).
  
  
  RESULTS
  There was a significant increase in P-tau in the SIM-group during follow-up, while P-tau in MIM and NIM did not change. Eighty-three percent of the SIM-patients converted to dementia (80% AD), while most MIM- and NIM-patients remained non-demented. T-tau- and Abeta42-levels did not change in any of the memory groups during follow-up.
  
  
  CONCLUSIONS
  Increasing P-tau levels during cognitive decline and conversion to dementia suggest that P-tau may be useful as a longitudinal marker of the neurodegenerative process.
authors.affiliation: Department of Neurobiology, Caring Sciences and Society, Karolinska Institutet, NOVUM Karolinska University Hospital Huddinge, S-141 86 Stockholm, Sweden. christin.andersson@ki.se
authors.forename: Christin
authors.initials: C
authors.lastname: Andersson
authors.forename: Kaj
authors.initials: K
authors.lastname: Blennow
authors.forename: Ove
authors.initials: O
authors.lastname: Almkvist
authors.forename: Niels
authors.initials: N
authors.lastname: Andreasen
authors.forename: Peter
authors.initials: P
authors.lastname: Engfeldt
authors.forename: Sven-Erik
authors.initials: SE
authors.lastname: Johansson
authors.forename: Maria
authors.initials: M
authors.lastname: Lindau
authors.forename: Maria
authors.initials: M
authors.lastname: Eriksdotter-Jönhagen
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid / Q000473:pathology / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis / Q000134:cerebrospinal fluid; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use; D003072:Cognition Disorders / Q000134:cerebrospinal fluid* / Q000473:pathology / Q000503:physiopathology; D003704:Dementia / Q000134:cerebrospinal fluid* / Q000473:pathology / Q000503:physiopathology; D018450:Disease Progression; D004569:Electroencephalography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration / Q000134:cerebrospinal fluid* / Q000473:pathology / Q000503:physiopathology; D009483:Neuropsychological Tests; D010766:Phosphorylation; D015854:Up-Regulation / Q000502:physiology; D016875:tau Proteins / Q000032:analysis / Q000134:cerebrospinal fluid*
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D002800:Cholinesterase Inhibitors; C054369:MAPT protein, human; D016875:tau Proteins