Hugo Lövheim1, Fredrik Elgh2, Anders Johansson3, Henrik Zetterberg4, Kaj Blennow5, Göran Hallmans6, Sture Eriksson7. 1. Department of Community Medicine and Rehabilitation, Geriatric Medicine, Umeå University, Umeå, Sweden. Electronic address: hugo.lovheim@umu.se. 2. Department of Clinical Microbiology, Virology, Umeå University, Umeå, Sweden. 3. Department of Odontology, Umeå University, Umeå, Sweden; Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden. 4. 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. 5. Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. 6. Department of Public Health and Clinical Medicine, Nutritional Research, Umeå University, Umeå, Sweden; Department of Biobank Research, Umeå University, Umeå, Sweden. 7. 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.
Abstract
INTRODUCTION: 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 Aβ40 and Aβ42. RESULTS: Plasma concentrations of free Aβ40 and Aβ42 did 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. DISCUSSION: 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.
INTRODUCTION: 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 Aβ40 and Aβ42. RESULTS: Plasma concentrations of free Aβ40 and Aβ42 did 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. DISCUSSION: 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.
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