Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice

Even though the idea that amyloid beta peptide accumulation is the primary event in the pathogenesis of Alzheimer's disease has become the leading hypothesis, the causal link between aberrant amyloid precursor protein processing and tau alterations in this type of dementia remains controversial. We further investigated the role of beta-amyloid production/deposition in tau pathology and neuronal cell death in the mouse brain by crossing Tg2576 and VLW lines expressing human mutant amyloid precursor protein and human mutant tau, respectively. The resulting double transgenic mice showed enhanced amyloid deposition accompanied by neurofibrillary degeneration and overt neuronal loss in selectively vulnerable brain limbic areas. These findings challenge the idea that tau pathology in Alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo

Monolithic integration of functional oxides in silicon by chemical solution deposition

6-10 Avril 2015International audienceno abstrac

Monolitic integration of functional oxides on silicon by chemical solution deposition

6-9 April 2015International audienceIn the past years, great efforts have been devoted to combine the functionality of oxides with the performances of semiconductor platforms for the development of novel and more efficient device applications. However, further incorporation of functional oxide nanostructures as active materials in electronics critically depends on the ability to integrate crystalline metal oxides into silicon structures [1]. In this regard, the presented work takes advantage of all the benefits of soft chemistry to overcome the main challenges for the monolithic integration of novel nanostructured functional oxide materials on silicon including (i) epitaxial piezoelectric α-quartz thin films with tunable textures on silicon wafers [2] and (ii) ferromagnetic La0.7Sr0.3MnO3 (LSMO) thin films epitaxially grown on (100)-silicon at low temperature. Importantly, piezoelectric quartz growth mechanism is governed by a thermally activated devitrification of the native amorphous silica surface layer assisted by a heterogeneous catalysis under atmospheric conditions driven by alkaline earth cations present in the precursor solution. Quartz films are made of perfectly oriented individual crystallites epitaxially grown on (100) face of Si substrate with a controlled porosity after using templating agents [3]. Moreover, a quantitative study of the converse piezoelectric effect of quartz thin films through piezoresponse force microscopy shows that the piezoelectric coefficient d33 is between 1.5 and 3.5 pm/V which is in agreement with the 2.3 pm/V of the quartz single crystal d11. Epitaxial LSMO thin films synthesis, involves the use of polymer assisted deposition (PAD) process [4] combined with the controlled epitaxial growth of SrTiO3 buffer layer grown by molecular beam epitaxy (MBE) at the silicon surface, which allowed LSMO thin films to stabilize and crystallize at low temperature. All together, the methodology presented here exhibits a great potential and offers a pathway to design novel oxide compounds on silicon substrates by chemical routes with unique optical, electric, or magnetic properties. [1] A. Carretero-Genevrier et al. Nanoscale, 20, 892-897. (2014). [2] A. Carretero-Genevrier et al. Science, 20, 892-897. (2013). [3] G.L. Drisko et al. Adv.Funct.Mater. 24, 5494–5502 (2014) [4] Q. X. Jia, et al. Nature Materials 3, 529 (2004

Development of Epitaxial Oxide Ceramics Nanomaterials Based on Chemical Strategies on Semiconductor Platforms

International audienc

Microbial Diversity and Processes in Lake Kivu (East Africa)

Lake Kivu is a deep meromictic and oligotrophic tropical African lake with a permanent thermal- and haline stratification with huge accumulations of dissolved CO2 and CH4 (ca. 300 km3 and 60 km3, respectively) in the deep anoxic monimolimnion (from 60 o 480 m depth). Although there are a wealth of information on the ecology of small eukaryotes and their trophic role on Kivu, available information on prokaryotic planktonic assemblages is scarce. Molecular analysis of archaeal and bacterial communities showed a vertical segregation imposed by the permanent redoxcline. In relation to Bacteria, Actinobacteria, Betaproteobacteria, Green Sulfur Bacteria and Bacteroidetes were the most commonly retrieved groups. For Archaea, a marked dominance of Thaumarchaeota and Crenarchaeota (75% of all archaeal OTUs) over Euryarchaeota was observed. In the anoxic hypolimnion, Euryarchaoeta (Methanosarcinales and Methanocellales) lineages together with Miscellaneous Crenarchaeotic Group phylotypes were mainly recovered. In turn, Thaumarchaeota phylotypes were recovered in oxic and suboxic waters. CARDFISH analyses over the first 100 m revealed the dominance of Bacteria (51.4% – 95.7% of DAPI-stained cells), especially Actinobacteria (epilimnion), Betaproteobacteria (oxic-anoxic interface) and Bacteroidetes (upper hypolimnion), over Archaea (1.0% – 4.5%; maximum abundances at the oxic-anoxic interface). In turn, flow cytometry evidenced the dominance of HNA cells in the euphotic layer, whereas the proportion of LNA cells increased with depth. HNA and LNA populations were still observed in the anoxic hypolimnion suggesting facultative or strict anaerobic metabolisms. The detection of distinct depth maxima of nitrate, nitrite, archaeal amoA and Marine Thaumarchaeota 16S gene copy numbers together with regularly detection of deep maxima of 3H-Thymidine uptake, and the presence of low-light adapted GSB species point towards a strong link of N, C, and S cycles in the redoxcline of Lake Kivu

Accelerated amyloid deposition, neurofibrillary degeneration and neuronal loss in double mutant APP/tau transgenic mice

Even though the idea that amyloid beta peptide accumulation is the primary event in the pathogenesis of Alzheimer's disease has become the leading hypothesis, the causal link between aberrant amyloid precursor protein processing and tau alterations in this type of dementia remains controversial. We further investigated the role of beta-amyloid production/deposition in tau pathology and neuronal cell death in the mouse brain by crossing Tg2576 and VLW lines expressing human mutant amyloid precursor protein and human mutant tau, respectively. The resulting double transgenic mice showed enhanced amyloid deposition accompanied by neurofibrillary degeneration and overt neuronal loss in selectively vulnerable brain limbic areas. These findings challenge the idea that tau pathology in Alzheimer's disease is merely a downstream effect of amyloid production/deposition and suggest that reciprocal interactions between beta-amyloid and tau alterations may take place in vivo