Historical and morphological evidence for multi-stage growth of El Volcancito, Volcán de Colima

We present a multidisciplinary study of an important 1869 eruption of Volcán de Colima, Mexico. This eruption created a parasitic cone, known as El Volcancito, which has traditionally been attributed to a small flank eruption. However, new analysis of historical records suggests that the size, explosivity, and duration of this eruption have been seriously underestimated. While previous reports suggest that activity ceased after ~3 years, our evidence shows that the eruption was highly energetic and constituted multiple eruptive phases over an 8-year period. There was a substantial emission of volcanic material into the atmosphere and the event directly affected communities up to 150 km from the volcano. A new estimate of the volume of material emitted (0.8 km3) is almost four times higher than the previous estimate (0.21 km3), and represents the largest historical andesite lava deposit at Volcán de Colima. At least 10 large explosions with eruptive columns of >6 km occurred. The eruption differed significantly to activity from the central summit cone in terms of eruption dynamics, evolution of activity over time, and petrology; as such, it cannot be explained using the widely accepted eruptive scheme for this volcano. Based on seismic and petrological evidence, we suggest that the highly energetic behavior can be explained by changes in the local stress field following two large regional earthquakes (M > 8.0) and subsequent magma-groundwater interaction. This study challenges the common assumption that most monogenetic cone-building flank eruptions at andesitic volcanoes are low energy compared with edifice-building summit activity, which has important implications for risk analysis at similar volcanoes worldwide

Brain iron is associated with accelerated cognitive decline in people with Alzheimer pathology

Cortical iron has been shown to be elevated in Alzheimer's disease (AD), but the impact of the directly measured iron on the clinical syndrome has not been assessed. We investigated the association between post-mortem iron levels with the clinical and pathological diagnosis of AD, its severity, and the rate of cognitive decline in the 12 years prior to death in subjects from the Memory and Aging Project (n = 209). Iron was elevated (β [SE] = 9.7 [2.6]; P = 3.0 × 10-4) in the inferior temporal cortex only in subjects who were diagnosed with clinical AD during life and had a diagnosis of AD confirmed post-mortem by standardized criteria. Although iron was weakly associated with the extent of proteinopathy in tissue with AD neuropathology, it was strongly associated with the rate of cognitive decline (e.g., global cognition: β [SE] = -0.040 [0.005], P = 1.6 × 10-14). Thus, cortical iron might act to propel cognitive deterioration upon the underlying proteinopathy of AD, possibly by inducing oxidative stress or ferroptotic cell death, or may be related to an inflammatory response