Browsing by Author "Pesini, Pedro"

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    Detecting amyloid positivity in early Alzheimer’s disease using combinations of plasma Aβ42/Aβ40 and p-tau
    (Wiley, 2022-02) Janelidze, Shorena; Palmqvist, Sebastian; Leuzy, Antoine; Stomrud, Erik; Verberk, Inge M.W.; Zetterberg, Henrik; Ashton, Nicholas J.; Pesini, Pedro; Sarasa, Leticia; Allué, José Antonio; Teunissen, Charlotte E.; Dage, Jeffrey L.; Blennow, Kaj; Mattsson-Carlgren, Niklas; Hansson, Oskar; Neurology, School of Medicine
    Introduction: We studied usefulness of combining blood amyloid beta (Aβ)42/Aβ40, phosphorylated tau (p-tau)217, and neurofilament light (NfL) to detect abnormal brain Aβ deposition in different stages of early Alzheimer's disease (AD). Methods: Plasma biomarkers were measured using mass spectrometry (Aβ42/Aβ40) and immunoassays (p-tau217 and NfL) in cognitively unimpaired individuals (CU, N = 591) and patients with mild cognitive impairment (MCI, N = 304) from two independent cohorts (BioFINDER-1, BioFINDER-2). Results: In CU, a combination of plasma Aβ42/Aβ40 and p-tau217 detected abnormal brain Aβ status with area under the curve (AUC) of 0.83 to 0.86. In MCI, the models including p-tau217 alone or Aβ42/Aβ40 and p-tau217 had similar AUCs (0.86-0.88); however, the latter showed improved model fit. The models were implemented in an online application providing individualized risk assessments (https://brainapps.shinyapps.io/PredictABplasma/). Discussion: A combination of plasma Aβ42/Aβ40 and p-tau217 discriminated Aβ status with relatively high accuracy, whereas p-tau217 showed strongest associations with Aβ pathology in MCI but not in CU.
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    Plasma amyloid beta levels are associated with cerebral amyloid and tau deposition
    (Elsevier, 2019-07-26) Risacher, Shannon L.; Fandos, Noelia; Romero, Judith; Sherriff, Ian; Pesini, Pedro; Saykin, Andrew J.; Apostolova, Liana G.; Radiology and Imaging Sciences, School of Medicine
    Introduction: We investigated the relationship of plasma amyloid beta (Aβ) with cerebral deposition of Aβ and tau on positron emission tomography (PET). Methods: Forty-four participants (18 cognitively normal older adults [CN], 10 mild cognitive impairment, 16 Alzheimer's disease [AD]) underwent amyloid PET and a blood draw. Free and total plasma Aβ40 and Aβ42 were assessed using a validated assay. Thirty-seven participants (17 CN, 8 mild cognitive impairment, 12 AD) also underwent a [18F]flortaucipir scan. Scans were preprocessed by standard techniques, and mean global and regional amyloid and tau values were extracted. Free Aβ42/Aβ40 (Aβ F42:F40) and total Aβ42/Aβ40 (Aβ T42:T40) were evaluated for differences by diagnosis and relation to PET Aβ positivity. Relationships between these measures and cerebral Aβ and tau on both regional and voxel-wise basis were also evaluated. Results: Lower Aβ T42:T40 was associated with diagnosis and PET Aβ positivity. Lower plasma Aβ T42:T40 ratios predicted cerebral Aβ positivity, both across the full sample and in CN only. Finally, lower plasma Aβ T42:T40 ratios were associated with increased cortical Aβ and tau in AD-related regions on both regional and voxel-wise analyses. Discussion: Plasma Aβ measures may be useful biomarkers for predicting cerebral Aβ and tau. Additional studies in larger samples are warranted.
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    The global Alzheimer's Association round robin study on plasma amyloid β methods
    (Wiley, 2021-10-14) Pannee, Josef; Shaw, Leslie M.; Korecka, Magdalena; Waligorska, Teresa; Teunissen, Charlotte E.; Stoops, Erik; Vanderstichele, Hugo M. J.; Mauroo, Kimberley; Verberk, Inge M. W.; Keshavan, Ashvini; Pesini, Pedro; Sarasa, Leticia; Pascual-Lucas, Maria; Fandos, Noelia; Allué, José-Antonio; Portelius, Erik; Andreasson, Ulf; Yoda, Ritsuko; Nakamura, Akinori; Kaneko, Naoki; Yang, Shieh-Yueh; Liu, Huei-Chun; Palme, Stefan; Bittner, Tobias; Mawuenyega, Kwasi G.; Ovod, Vitaliy; Bollinger, James; Bateman, Randall J.; Li, Yan; Dage, Jeffrey L.; Stomrud, Erik; Hansson, Oskar; Schott, Jonathan M.; Blennow, Kaj; Zetterberg, Henrik; Neurology, School of Medicine
    Introduction: Blood-based assays to measure brain amyloid beta (Aβ) deposition are an attractive alternative to the cerebrospinal fluid (CSF)-based assays currently used in clinical settings. In this study, we examined different blood-based assays to measure Aβ and how they compare among centers and assays. Methods: Aliquots from 81 plasma samples were distributed to 10 participating centers. Seven immunological assays and four mass-spectrometric methods were used to measure plasma Aβ concentrations. Results: Correlations were weak for Aβ42 while Aβ40 correlations were stronger. The ratio Aβ42/Aβ40 did not improve the correlations and showed weak correlations. Discussion: The poor correlations for Aβ42 in plasma might have several potential explanations, such as the high levels of plasma proteins (compared to CSF), sensitivity to pre-analytical sample handling and specificity, and cross-reactivity of different antibodies. Different methods might also measure different pools of plasma Aβ42. We, however, hypothesize that greater correlations might be seen in future studies because many of the methods have been refined during completion of this study.