11 research outputs found

    Coral luminescence identifies the Pacific Decadal Oscillation as a primary driver of river runoff variability impacting the southern Great Barrier Reef

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    The Pacific Decadal Oscillation (PDO) is a large-scale climatic phenomenon modulating ocean-atmosphere variability on decadal time scales. While precipitation and river flow variability in the Great Barrier Reef (GBR) catchments are sensitive to PDO phases, the extent to which the PDO influences coral reefs is poorly understood. Here, six Porites coral cores were used to produce a composite record of coral luminescence variability (runoff proxy) and identify drivers of terrestrial influence on the Keppel reefs, southern GBR. We found that coral skeletal luminescence effectively captured seasonal, inter-annual and decadal variability of river discharge and rainfall from the Fitzroy River catchment. Most importantly, although the influence of El Nino-Southern Oscillation (ENSO) events was evident in the luminescence records, the variability in the coral luminescence composite record was significantly explained by the PDO. Negative luminescence anomalies (reduced runoff) were associated with El Nino years during positive PDO phases while positive luminescence anomalies (increased runoff) coincided with strong/moderate La Nino years during negative PDO phases. This study provides clear evidence that not only ENSO but also the PDO have significantly affected runoff regimes at the Keppel reefs for at least a century, and suggests that upcoming hydrological disturbances and ecological responses in the southern GBR region will be mediated by the future evolution of these sources of climate variability

    A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer's disease

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    Development of tau-based therapies for Alzheimer’s disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer’s disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments

    A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer’s disease

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    Development of tau-based therapies for Alzheimer’s disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer’s disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments

    A soluble phosphorylated tau signature links tau, amyloid and the evolution of stages of dominantly inherited Alzheimer's disease

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    Development of tau-based therapies for Alzheimer's disease requires an understanding of the timing of disease-related changes in tau. We quantified the phosphorylation state at multiple sites of the tau protein in cerebrospinal fluid markers across four decades of disease progression in dominantly inherited Alzheimer's disease. We identified a pattern of tau staging where site-specific phosphorylation changes occur at different periods of disease progression and follow distinct trajectories over time. These tau phosphorylation state changes are uniquely associated with structural, metabolic, neurodegenerative and clinical markers of disease, and some (p-tau217 and p-tau181) begin with the initial increases in aggregate amyloid-β as early as two decades before the development of aggregated tau pathology. Others (p-tau205 and t-tau) increase with atrophy and hypometabolism closer to symptom onset. These findings provide insights into the pathways linking tau, amyloid-β and neurodegeneration, and may facilitate clinical trials of tau-based treatments
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