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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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See page 746
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