Hake, Ann MarieTrzepacz, Paula T.Wang, ShufangYu, PengCase, MichaelHochstetler, HelenWitte, Michael M.Degenhardt, Elisabeth K.Dean, Robert A.2017-05-242017-05-242015-08Hake, A., Trzepacz, P. T., Wang, S., Yu, P., Case, M., Hochstetler, H., … Dean, R. A. (2015). Florbetapir positron emission tomography and cerebrospinal fluid biomarkers. Alzheimer’s & Dementia : The Journal of the Alzheimer’s Association, 11(8), 986–993. http://doi.org/10.1016/j.jalz.2015.03.002https://hdl.handle.net/1805/12723BACKGROUND: We evaluated the relationship between florbetapir-F18 positron emission tomography (FBP PET) and cerebrospinal fluid (CSF) biomarkers. METHODS: Alzheimer's Disease Neuroimaging Initiative-Grand Opportunity and Alzheimer's Disease Neuroimaging Initiative 2 (GO/2) healthy control (HC), mild cognitive impairment (MCI), and Alzheimer's disease (AD) dementia subjects with clinical measures and CSF collected ±90 days of FBP PET data were analyzed using correlation and logistic regression. RESULTS: In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios. Using logistic regression, Aβ1-42, total tau (t-tau), phosphorylated tau181P (p-tau), and FBP PET composite each differentiated HC versus AD. Aβ1-42 and t-tau distinguished MCI versus AD, without additional contribution by FBP PET. Total tau and p-tau added discriminative power to FBP PET when classifying HC versus AD. CONCLUSION: Based on cross-sectional diagnostic groups, both amyloid and tau measures distinguish healthy from demented subjects. Longitudinal analyses are needed.en-USPublisher PolicyAlzheimer’s diseaseFlorbetapir positron emission tomographyCerebrospinal fluidMild cognitive impairment (MCI)Alzheimer’s Disease Neuroimaging InitiativeBiomarkersArticle