SUSTAIN drilling at Surtsey volcano, Iceland, tracks hydrothermal and microbiological interactions in basalt 50 years after eruption

The 2017 Surtsey Underwater volcanic System for Thermophiles, Alteration processes and INnovative concretes (SUSTAIN) drilling project at Surtsey volcano, sponsored in part by the International Continental Scientific Drilling Program (ICDP), provides precise observations of the hydrothermal, geochemical, geomagnetic, and microbiological changes that have occurred in basaltic tephra and minor intrusions since explosive and effusive eruptions produced the oceanic island in 1963–1967. Two vertically cored boreholes, to 152 and 192 m below the surface, were drilled using filtered, UV-sterilized seawater circulating fluid to minimize microbial contamination. These cores parallel a 181 m core drilled in 1979. Introductory investigations indicate changes in material properties and whole-rock compositions over the past 38 years. A Surtsey subsurface observatory installed to 181 m in one vertical borehole holds incubation experiments that monitor in situ mineralogical and microbial alteration processes at 25–124 ∘C. A third cored borehole, inclined 55∘ in a 264∘ azimuthal direction to 354 m measured depth, provides further insights into eruption processes, including the presence of a diatreme that extends at least 100 m into the seafloor beneath the Surtur crater. The SUSTAIN project provides the first time-lapse drilling record into a very young oceanic basaltic volcano over a range of temperatures, 25–141 ∘C from 1979 to 2017, and subaerial and submarine hydrothermal fluid compositions. Rigorous procedures undertaken during the drilling operation protected the sensitive environment of the Surtsey Natural Preserve

Refertilized mantle keel below the Southern Alps domain (North-East Italy): Evidence from Marosticano refractory mantle peridotites

The Veneto Volcanic Province (VVP), a Cenozoic magmatic province in northeastern Italy, is one of the widest volcanic areas of the Adria plate. It consists of five main magmatic districts, and its most primitive products commonly host mantle xenoliths. In this study, we present a newly discovered xenolith suite from the Marosticano district that contains peridotites with compositional characteristics of mineral assemblages that provide insight into an unexpected nature of the sub-continental lithospheric mantle (SCLM) of the Adria plate. In contrast to xenoliths from other VVP sites previously studied (i.e., Val d’Adige and Lessini Mts.), Marosticano xenoliths exhibit highly refractory compositions typical of on-craton peridotites. High olivine forsteritic contents (Fo: 91-93) indicate high degrees of partial melting (>25%) that should have been associated with the complete consumption of clinopyroxene. Major and trace element compositions further link these peridotite fragments to early Proterozoic cratonic mantle. The occurrence of clinopyroxene within such rocks suggests Marosticano clinopyroxene testify to a metasomatic legacy. The i) LREE-enrichments of Marosticano clinopyroxene and ii) the dissolved CO2 mole fractions (up to 1.0) for the inferred clinopyroxene-forming melt are consistent with carbonatite/CO2-rich silicatic melts as metasomatic agents. The latter could be responsible for the equilibrium temperatures (1033-1117 °C) and oxidizing conditions [logfO2 (FMQ)= -0.6 - +1.1], anomalously high for a cratonic environment but similar to the off-craton VVP xenoliths. The cratonic signature and carbonatite/CO2-rich silicate metasomatism found together in the Marosticano mantle xenoliths reveal that ancient features can be preserved in SCLM in a young, active geodynamic setting such as the Adria plate boundary. In this framework Lessini Mts. and Val d’Adige xenoliths could be interpreted as circumcratonic reminiscent domains affected by refertilization due to infiltration of asthenosphere-derived melts,rather than newly accreted “off-craton” SCLM. These new interpretations could be useful for completing the reconstruction of the Africa/Eurasia interplay during the Alpine collision

Differential deregulation of NGF and BDNF neurotrophins in a transgenic rat model of Alzheimer's disease

Evidence from human neuropathological studies indicates that the levels of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are compromised in Alzheimer's disease. However, the causes and temporal (pathology-dependent) evolution of these alterations are not completely understood. To elucidate these issues, we investigated the McGill-R-Thy1-APP transgenic rat, which exhibits progressive intracellular and extracellular amyloid-beta (Aβ) pathology and ensuing cognitive deficits. Neurochemical analyses revealed a differential dysregulation of NGF and BDNF transcripts and protein expression. While BDNF mRNA levels were significantly reduced at very early stages of amyloid pathology, before plaques appeared, there were no changes in NGF mRNA expression even at advanced stages. Paradoxically, the protein levels of the NGF precursor were increased. These changes in neurotrophin expression are identical to those seen during the progression of Alzheimer's disease. At advanced pathological stages, deficits in the protease cascade controlling the maturation and degradation of NGF were evident in McGill transgenic rats, in line with the paradoxical upregulation of proNGF, as seen in Alzheimer's disease, in the absence of changes in NGF mRNA. The compromise in NGF metabolism and BDNF levels was accompanied by downregulation of cortical cholinergic synapses; strengthening the evidence that neurotrophin dysregulation affects cholinergic synapses and synaptic plasticity. Our findings suggest a differential temporal deregulation of NGF and BDNF neurotrophins, whereby deficits in BDNF mRNA appear at early stages of intraneuronal Aβ pathology, before alterations in NGF metabolism and cholinergic synapse loss manifest.Fil: Iulita, M. Florencia. McGill University; CanadáFil: Bistue Millon, Maria Beatriz. Universidad Católica de Cuyo - Sede San Juan. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Pentz, Rowan. Universidad Católica de Cuyo - Sede San Juan. Facultad de Ciencias Médicas; ArgentinaFil: Aguilar, Lisi Flores. McGill University; CanadáFil: Do Carmo, Sonia. McGill University; CanadáFil: Allard, Simon. McGill University; CanadáFil: Michalski, Bernadeta. Mc Master University; CanadáFil: Wilson, Edward N.. McGill University; CanadáFil: Ducatenzeiler, Adriana. Universidad Católica de Cuyo - Sede San Juan. Facultad de Ciencias Médicas; ArgentinaFil: Bruno, Martin. Universidad Católica de Cuyo - Sede San Juan. Facultad de Ciencias Médicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Fahnestock, Margaret. Mc Master University; CanadáFil: Cuello, A. Claudio. McGill University; Canad

Nerve growth factor metabolic dysfunction in Down’s syndrome brains

Basal forebrain cholinergic neurons play a key role in cognition. This neuronal system is highly dependent on NGF for its synaptic integrity and the phenotypic maintenance of its cell bodies. Basal forebrain cholinergic neurons progressively degenerate in Alzheimer’s disease and Down’s syndrome, and their atrophy contributes to the manifestation of dementia. Paradoxically, in Alzheimer’s disease brains, the synthesis of NGF is not affected and there is abundance of the NGF precursor, proNGF. We have shown that this phenomenon is the result of a deficit in NGF’s extracellular metabolism that compromises proNGF maturation and exacerbates its subsequent degradation. We hypothesized that a similar imbalance should be present in Down’s syndrome. Using a combination of quantitative reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay, western blotting and zymography, we investigated signs of NGF metabolic dysfunction in post-mortem brains from the temporal (n = 14), frontal (n = 34) and parietal (n = 20) cortex obtained from subjects with Down’s syndrome and age-matched controls (age range 31–68 years). We further examined primary cultures of human foetal Down’s syndrome cortex (17–21 gestational age weeks) and brains from Ts65Dn mice (12–22 months), a widely used animal model of Down’s syndrome. We report a significant increase in proNGF levels in human and mouse Down’s syndrome brains, with a concomitant reduction in the levels of plasminogen and tissue plasminogen activator messenger RNA as well as an increment in neuroserpin expression; enzymes that partake in proNGF maturation. Human Down’s syndrome brains also exhibited elevated zymogenic activity of MMP9, the major NGF-degrading protease. Our results indicate a failure in NGF precursor maturation in Down’s syndrome brains and a likely enhanced proteolytic degradation of NGF, changes which can compromise the trophic support of basal forebrain cholinergic neurons. The alterations in proNGF and MMP9 were also present in cultures of Down’s syndrome foetal cortex; suggesting that this trophic compromise may be amenable to rescue, before frank dementia onset. Our study thus provides a novel paradigm for cholinergic neuroprotection in Alzheimer’s disease and Down’s syndrome