Christoffer Rosén1, Bahman Farahmand2, Tobias Skillbäck3, Katarina Nägga4, Niklas Mattsson5, Lena Kilander6, Dorota Religa7, Anders Wimo8, Kaj Blennow3, Bengt Winblad7, Henrik Zetterberg9, Maria Eriksdotter2. 1. Clinical Neurochemistry Laboratory, Department of Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. Electronic address: christoffer.rosen@neuro.gu.se. 2. Center for Alzheimer Research, Division of Clinical Geriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institutet, Stockholm, Sweden; Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, Sweden. 3. Clinical Neurochemistry Laboratory, Department of Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. 4. Clinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden. 5. Clinical Neurochemistry Laboratory, Department of Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, University of California San Francisco, San Francisco, CA, USA. 6. Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden. 7. Department of Geriatric Medicine, Karolinska University Hospital, Huddinge, Sweden; Center for Alzheimer Research, Division for Neurogeriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institutet, Huddinge, Sweden. 8. Center for Alzheimer Research, Division for Neurogeriatrics, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institutet, Huddinge, Sweden. 9. Clinical Neurochemistry Laboratory, Department of Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Abstract
INTRODUCTION: New research guidelines for the diagnosis of Alzheimer's disease (AD) include biomarker evidence of amyloid-β (Aβ) and tau pathology. The aim of this study was to investigate what proportion of AD patients diagnosed in clinical routine in Sweden that had an AD-indicative cerebrospinal fluid (CSF) biomarker profile. METHODS: By cross-referencing a laboratory database with the Swedish Dementia Registry (SveDem), 2357 patients with data on CSF Aβ and tau biomarkers and a clinical diagnosis of AD with dementia were acquired. RESULTS: Altogether, 77.2% had pathologic Aβ42 and total tau or phosphorylated tau in CSF. These results were stable across age groups. Female sex and low mini-mental state examination score increased the likelihood of pathologic biomarkers. DISCUSSION: About a quarter of clinically diagnosed AD patients did not have an AD-indicative CSF biomarker profile. This discrepancy may partly reflect incorrect (false positive) clinical diagnosis or a lack in sensitivity of the biomarker assays.
INTRODUCTION: New research guidelines for the diagnosis of Alzheimer's disease (AD) include biomarker evidence of amyloid-β (Aβ) and tau pathology. The aim of this study was to investigate what proportion of ADpatients diagnosed in clinical routine in Sweden that had an AD-indicative cerebrospinal fluid (CSF) biomarker profile. METHODS: By cross-referencing a laboratory database with the Swedish Dementia Registry (SveDem), 2357 patients with data on CSF Aβ and tau biomarkers and a clinical diagnosis of AD with dementia were acquired. RESULTS: Altogether, 77.2% had pathologic Aβ42 and total tau or phosphorylated tau in CSF. These results were stable across age groups. Female sex and low mini-mental state examination score increased the likelihood of pathologic biomarkers. DISCUSSION: About a quarter of clinically diagnosed ADpatients did not have an AD-indicative CSF biomarker profile. This discrepancy may partly reflect incorrect (false positive) clinical diagnosis or a lack in sensitivity of the biomarker assays.
Authors: A Leuzy; N J Ashton; N Mattsson-Carlgren; A Dodich; M Boccardi; J Corre; A Drzezga; A Nordberg; R Ossenkoppele; H Zetterberg; K Blennow; G B Frisoni; V Garibotto; O Hansson Journal: Eur J Nucl Med Mol Imaging Date: 2021-03-05 Impact factor: 9.236
Authors: Nicoleta Stoicea; Amy Du; D Christie Lakis; Courtney Tipton; Carlos E Arias-Morales; Sergio D Bergese Journal: Front Genet Date: 2016-02-09 Impact factor: 4.599