Innovations in the Speciation of Organolead Compounds in Water: Towards a More Rational, Rapid, and Simple Analytical Process

Speciation analysis calls for rapid, simple systems for minimizing errors made in the most troublesome of all steps in the analytical process: sample preparation. In this context, continuous-flow systems are of great help. The evolution in the different methodologies enabled solutions to the main shortcomings occurring from the lack of selectivity of using RP–C18 as sorbent material. One solution was a shift to more sensitive and selective, but only partially automated, systems employing C60 fullerene and Grignard’s reagent; another was a shift to completely automated systems employing sodium tetrapropylborate; and a final solution was to employ the simplest possible configuration by removing the reagent stream. The analytical methods developed allowed the identification and quantification of different organolead species at the pg/ml levels in rainwater samples, with precision (RSD) of about 5% and recoveries ranging from 92 to 100%

Longitudinal amyloid and tau accumulation in autosomal dominant Alzheimer's disease: findings from the Colombia-Boston (COLBOS) biomarker study

Background: Neuroimaging studies of autosomal dominant Alzheimer's disease (ADAD) enable characterization of the trajectories of cerebral amyloid-beta (A beta) and tau accumulation in the decades prior to clinical symptom onset. Longitudinal rates of regional tau accumulation measured with positron emission tomography (PET) and their relationship with other biomarker and cognitive changes remain to be fully characterized in ADAD.Methods: Fourteen ADAD mutation carriers (Presenilin-1 E280A) and 15 age-matched non-carriers from the Colombian kindred underwent 2-3 sessions of A beta (11C-Pittsburgh compound B) and tau (18F-flortaucipir) PET, structural magnetic resonance imaging, and neuropsychological evaluation over a 2-4-year follow-up period. Annualized rates of change for imaging and cognitive variables were compared between carriers and non-carriers, and relationships among baseline measurements and rates of change were assessed within carriers.Results: Longitudinal measurements were consistent with a sequence of ADAD-related changes beginning with A beta accumulation (16 years prior to expected symptom onset, EYO), followed by entorhinal cortex (EC) tau (9 EYO), neocortical tau (6 EYO), hippocampal atrophy (6 EYO), and cognitive decline (4 EYO). Rates of tau accumulation among carriers were most rapid in parietal neocortex (similar to 9%/year). EC tau PET signal at baseline was a significant predictor of subsequent neocortical tau accumulation and cognitive decline within carriers.Conclusions: Our results are consistent with the sequence of biological changes in ADAD implied by cross-sectional studies and highlight the importance of EC tau as an early biomarker and a potential link between A beta burden and neocortical tau accumulation in ADAD