Extent of the Ross Orogen in Antarctica: new data from DSDP 270 and Iselin Bank

The Ross Sea is bordered by the Late Precambrian–Cambrian Ross–Delamerian Orogen of East Antarctica and the more Pacific-ward Ordovician–Silurian Lachlan–Tuhua–Robertson Bay–Swanson Orogen. A calcsilicate gneiss from Deep Sea Drilling Project 270 drill hole in the central Ross Sea, Antarctica, gives a U-Pb titanite age of 437 ± 6 Ma (2σ). This age of high-grade metamorphism is too young for typical Ross Orogen. Based on this age, and on lithology, we propose a provisional correlation with the Early Palaeozoic Lachlan–Tuhua–Robertson Bay–Swanson Orogen, and possibly the Bowers Terrane of northern Victoria Land. A metamorphosed porphyritic rhyolite dredged from the Iselin Bank, northern Ross Sea, gives a U-Pb zircon age of 545 ± 32 Ma (2σ). The U-Pb age, petrochemistry, Ar-Ar K-feldspar dating, and Sr and Nd isotopic ratios indicate a correlation with Late Proterozoic–Cambrian igneous protoliths of the Ross Orogen. If the Iselin Bank rhyolite is not ice-rafted debris, then it represents a further intriguing occurrence of Ross basement found outside the main Ross–Delamerian Orogen

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele