D, PhD, Kaj Blennow, MD, PhD, Jonas Jogi, MD, PhD, and Oskar Hansson, MD, PhDNeurology 2018;90:e388-e395. doi:10.1212/WNL.Correspondence Dr. Mattsson [email protected] or Dr. Hansson [email protected] To examine PET imaging of tau pathology with CSF measurements (total tau [t-tau] and phosphorylated tau [p-tau]) in terms of diagnostic overall performance for Alzheimer illness (AD). Approaches We compared t-tau and p-tau and 18F-AV-1451 in 30 controls, 14 sufferers with prodromal AD, and 39 sufferers with Alzheimer dementia, recruited from the Swedish BioFINDER study. All sufferers with AD (prodromal and dementia) have been screened for amyloid positivity employing CSF -amyloid 42. Retention of 18F-AV-1451 was measured inside a priori specified regions, selected for known associations with tau pathology in AD. Benefits Retention of 18F-AV-1451 was markedly elevated in Alzheimer dementia and moderately elevated in prodromal AD. CSF t-tau and p-tau was improved to equivalent levels in both AD dementia and prodromal AD. 18F-AV-1451 had quite good diagnostic efficiency for Alzheimer dementia (location beneath the receiver operating characteristic curve [AUROC] ;1.000), and was significantly much better than t-tau (0.876), p-tau (0.890), hippocampal volume (0.824), and temporal cortical thickness (0.860). For prodromal AD, there had been no considerable AUROC variations in between CSF tau and 18F-AV-1451 measures (0.836.939), but MRI measures had reduced AUROCs (0.652.769). Conclusions CSF tau and 18F-AV-1451 have equal efficiency in early clinical stages of AD, but 18F-AV1451 is superior within the dementia stage, and exhibits close to excellent diagnostic functionality for mild to moderate AD. Classification of proof This study provides Class III evidence that CSF tau and 18F-AV-1451 PET have related performance in identifying early AD, and that 18F-AV-1451 PET is superior to CSF tau in identifying mild to moderate AD.More ONLINEClass of EvidenceCriteria for rating therapeutic and diagnostic Studies NPub.KGF/FGF-7 Protein Source org/coeFrom the Clinical Memory Study Unit (N.M., R.S., O.S., S.P., M.S., P.S.I., O.H.), Faculty of Medicine, Lund University; Memory Clinic (N.M., O.H.) and Departments of Neurology (N.M., R.S., S.P.), Clinical Neurophysiology (D.H.), Radiation Physics (T.O.), and Clinical Physiology and Nuclear Medicine ( J.J.), Sk e University Hospital, Lund; MedTech West and the a Division of Clinical Neuroscience (M.S.), University of Gothenburg, Sweden; Center for Imaging of Neurodegenerative Diseases (P.MIF Protein Source S.PMID:24278086 I.), Division of Veterans Affairs Medical Center, San Francisco; Division of Radiology and Biomedical Imaging (P.S.I.), University of California, San Francisco; Clinical Neurochemistry Laboratory (H.Z., K.B.), Sahlgrenska University Hospital; Institute of Neuroscience and Physiology, Division of Molecular Neuroscience (H.Z., K.B.), the Sahlgrenska Academy at the University of Gothenburg, Molndal, Sweden; and Department of Molecular Neuroscience (H.Z.), UCL Institute of Neurology, Queen Square, London, UK. Visit Neurology.org/N for full disclosures. Funding details and disclosures deemed relevant by the authors, if any, are offered in the end on the report. The Short article Processing Charge was funded by Swedish Research Council. This really is an open access post distributed below the terms of your Inventive Commons Attribution License 4.0 (CC BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is adequately c.