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October 22, 2019; 93 (17) Editorial

Screening with a high-precision blood-based assay for Alzheimer disease

Barbara B. Bendlin, Henrik Zetterberg
First published August 1, 2019, DOI: https://doi.org/10.1212/WNL.0000000000008080
Barbara B. Bendlin
From the Wisconsin Alzheimer's Disease Research Center (B.B.B.), University of Wisconsin School of Medicine and Public Health, University of Wisconsin–Madison; Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry (H.Z.), Sahlgrenska Academy at University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z.), University College London Institute of Neurology; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
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Henrik Zetterberg
From the Wisconsin Alzheimer's Disease Research Center (B.B.B.), University of Wisconsin School of Medicine and Public Health, University of Wisconsin–Madison; Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry (H.Z.), Sahlgrenska Academy at University of Gothenburg; Clinical Neurochemistry Laboratory (H.Z.), Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease (H.Z.), University College London Institute of Neurology; and UK Dementia Research Institute at UCL (H.Z.), London, UK.
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Screening with a high-precision blood-based assay for Alzheimer disease
Barbara B. Bendlin, Henrik Zetterberg
Neurology Oct 2019, 93 (17) 737-738; DOI: 10.1212/WNL.0000000000008080

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The use of biomarkers for defining the pathobiology of Alzheimer disease (AD) has had a transformative effect on the field, facilitating disease detection prior to autopsy, as well as substantially altering clinical trial design.1 In the last 5–10 years, there has been a substantial shift toward using amyloid PET in human research, as well as clinically, to rule out AD (a negative scan meaning little or no plaque is present). Likewise, obtaining a sample of CSF via lumbar puncture provides a plethora of information on amyloid plaque burden, tau pathology, neurodegeneration, and gliosis. While amyloid PET and CSF β-amyloid (Aβ)42/Aβ40 have excellent diagnostic accuracy, and correspond well with plaque burden measured postmortem,2 it is widely recognized that access to a simple blood test for AD would change the field yet again.

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  • Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

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  • © 2019 American Academy of Neurology
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