Tectonic deformation of the Andes and the configuration of the subducted slab in central Peru: Results from a micro-seismic experiment

The vast majority of the microearthquakes recorded occurred to the east: on the Huaytapallana fault in the Eastern Cordillera or in the western margin of the sub-Andes. The sub-Andes appear to be the physiographic province subjected to the most intense seismic deformation. Focal depths for the crustal events here are as deep as 50 km, and the fault plane solutions, show thrust faulting on steep planes oriented roughly north-south. The Huaytapallana fault in the Cordillera Oriental also shows relatively high seismicity along a northeast-southwest trend that agrees with the fault scarp and the east dipping nodal plane of two large earthquakes that occurred on this fault in 1969. The recorded microearthquakes of intermediate depth show a flat seismic zone about 25 km thick at a depth of about 100 km. This agrees with the suggestion that beneath Peru the slab first dips at an angle of 30 deg to a depth of 100 km and then flattens following a quasi-horizontal trajectory. Fault plane solutions of intermediate depth microearthquakes have horizontal T axes oriented east-west

βAPP Processing Drives Gradual Tau Pathology in an Age-Dependent Amyloid Rat Model of Alzheimer's Disease.

The treatment of Alzheimer's disease (AD) remains challenging and requires a better in depth understanding of AD progression. Particularly, the link between amyloid protein precursor (APP) processing and Tau pathology development remains poorly understood. Growing evidences suggest that APP processing and amyloid-β (Aβ) release are upstream of Tau pathology but the lack of animal models mimicking the slow progression of human AD raised questions around this mechanism. Here, we described that an AD-like βAPP processing in adults wild-type rats, yielding to human APP, βCTF and Aβ levels similar to those observed in AD patients, is sufficient to trigger gradual Tauopathy. The Tau hyperphosphorylation begins several months before the formation of both amyloid plaques and tangle-like aggregates in aged rats and without associated inflammation. Based on a longitudinal characterization over 30 months, we showed that extrasynaptic and emotional impairments appear before long-term potentiation deficits and memory decline and so before Aβ and Tau aggregations. These compelling data allowed us to (1) experimentally confirm the causal relationship between βAPP processing and Tau pathology in vivo and without Tau transgene overexpression, (2) support the amyloidogenic cascade and (3) propose a 4-step hypothesis of prodromal AD progression