title: Plasma concentrations of free amyloid β cannot predict the development of Alzheimer's disease.
abstract: BACKGROUND
  Biomarkers that identify individuals at risk of Alzheimer's disease (AD) development would be highly valuable. Plasma concentration of amyloid β (Aβ)-central in the pathogenesis of AD-is a logical candidate, but studies to date have produced conflicting results on its utility.
  
  
  METHODS
  Plasma samples from 339 preclinical AD cases (76.4% women, mean age 61.3 years) and 339 age- and sex-matched dementia-free controls, taken an average of 9.4 years before AD diagnosis, were analyzed using Luminex xMAP technology and INNO-BIA plasma Aβ form assays to determine concentrations of free plasma Aβ40and Aβ42.
  
  
  RESULTS
  Plasma concentrations of free Aβ40and Aβ42did not differ between preclinical AD cases and dementia-free controls, in the full sample or in subgroups defined according to sex and age group (<60 and ≥ 60 years). The interval between sampling and AD diagnosis did not affect the results. Aβ concentrations did not change in the years preceding AD diagnosis among individuals for whom longitudinal samples were available.
  
  
  CONCLUSIONS
  Plasma concentrations of free Aβ could not predict the development of clinical AD, and Aβ concentrations did not change in the years preceding AD diagnosis in this sample. These results indicate that free plasma Aβ is not a useful biomarker for the identification of individuals at risk of developing clinical AD.
authors.affiliation: Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, Umeå, Sweden. Electronic address: hugo.lovheim@umu.se.
authors.forename: Hugo
authors.initials: H
authors.lastname: Lövheim
authors.affiliation: Department of Clinical Microbiology, Virology, Umeå University, Umeå, Sweden.
authors.forename: Fredrik
authors.initials: F
authors.lastname: Elgh
authors.affiliation: Department of Odontology, Umeå University, Umeå, Sweden; Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden.
authors.forename: Anders
authors.initials: A
authors.lastname: Johansson
authors.affiliation: Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, UK.
authors.forename: Henrik
authors.initials: H
authors.lastname: Zetterberg
authors.affiliation: Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
authors.forename: Kaj
authors.initials: K
authors.lastname: Blennow
authors.affiliation: Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; Department of Biobank Research, Umeå University, Umeå, Sweden.
authors.forename: Göran
authors.initials: G
authors.lastname: Hallmans
authors.affiliation: Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, Umeå, Sweden; Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden.
authors.forename: Sture
authors.initials: S
authors.lastname: Eriksson
mesh_terms: D000544:Alzheimer Disease / Q000097:blood / Q000175:diagnosis*; D016229:Amyloid beta-Peptides / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood*
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers; D010446:Peptide Fragments
keywords: Alzheimer's disease; Aβ; Biomarker; Dementia; Plasma amyloid β; Preclinical Alzheimer's disease