Publications by authors named "Kimberley Mauroo"
Background: In Alzheimer's disease (AD), plasma amyloid beta (Aβ) and phosphorylated tau (p-tau) predict high amyloid status from Aβ positron emission tomography (PET); however, the extent to which combination of these plasma assays can predict remains unknown.
Methods: Prototype Simoa assays were used to measure plasma samples from participants who were either cognitively normal (CN) or had mild cognitive impairment (MCI)/AD in the Australian Imaging, Biomarkers and Lifestyle (AIBL) study.
Results: The p-tau181/Aβ ratio showed the best prediction of Aβ-PET across all participants (area under the curve [AUC] = 0.
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.
Article Synopsis
- Blood-based amyloid biomarkers offer a promising way to non-invasively detect cerebral amyloidosis in early stages of disease, potentially making testing more accessible and cost-effective.
- A study compared two testing methods, ELISA and SIMOA, in a group of cognitively normal elderly participants, finding that both methods had similar accuracy in detecting cerebral amyloidosis and improved upon basic demographic models.
- While both methods correlated with amyloid imaging results, ELISA showed stronger correlations with cerebrospinal fluid biomarkers, and there were notable differences in the plasma Aβ levels reported by the two methods, with SIMOA consistently underestimating ELISA results.
Background: Blood-based biomarkers for Alzheimer's disease (AD) might facilitate identification of participants for clinical trials targeting amyloid beta (Abeta) accumulation, and aid in AD diagnostics. We examined the potential of plasma markers Abeta, glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) to identify cerebral amyloidosis and/or disease severity.
Methods: We included individuals with a positive (n = 176: 63 ± 7 years, 87 (49%) females) or negative (n = 76: 61 ± 9 years, 27 (36%) females) amyloid PET status, with syndrome diagnosis subjective cognitive decline (18 PET+, 25 PET-), mild cognitive impairment (26 PET+, 24 PET-), or AD-dementia (132 PET+).
Background: The pathophysiology of neurodegeneration is complex. Its diagnosis requires an early identification of sequential changes in several hallmarks in the brains of affected subjects. The presence of brain pathology can be visualized in the cerebrospinal fluid (CSF) by protein profiling.
View Article and Find Full Text PDFBackground: Reduced cerebrospinal fluid (CSF) concentration of amyloid-β1-42 (Aβ1-42) reflects the presence of amyloidopathy in brains of subjects with Alzheimer's disease (AD).
Objective: To qualify the use of Aβ1-42/Aβ1-40 for improvement of standard operating procedures (SOP) for measurement of CSF Aβ with a focus on CSF collection, storage, and analysis.
Methods: Euroimmun ELISAs for CSF Aβ isoforms were used to set up a SOP with respect to recipient properties (low binding, polypropylene), volume of tubes, freeze/thaw cycles, addition of detergents (Triton X-100, Tween-20) in collection or storage tubes or during CSF analysis.