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The molecular determinants of Alzheimer's (AD) disease are still not completely known; however, in the past two decades, a large body of evidence has indicated that an important contributing factor for the disease is the development of an unbalanced homeostasis of two signaling cations: calcium (Ca(2+)) and zinc (Zn(2+)). Both ions serve a critical role in the physiological functioning of the central nervous system, but their brain deregulation promotes amyloid-beta dysmetabolism as well as tau phosphorylation. AD is also characterized by an altered glutamatergic activation, and glutamate can promote both Ca(2+) and Zn(2+) dyshomeostasis. The two cations can operate synergistically to promote the generation of free radicals that further intracellular Ca(2+) and Zn(2+) rises and set the stage for a self-perpetuating harmful loop. These phenomena can be the initial steps in the pathogenic cascade leading to AD, therefore, therapeutic interventions aiming at preventing Ca(2+) and Zn(2+) dyshomeostasis may offer a great opportunity for disease-modifying strategies.

The overall effect of brain zinc (Zn(2+)) in the progression and development of Alzheimer's disease (AD) is still not completely understood. Although an excess of Zn(2+) can exacerbate the pathological features of AD, a deficit of Zn(2+) intake has also been shown to increase the volume of amyloid plaques in AD transgenic mice. In this study, we investigated the effect of dietary Zn(2+) supplementation (30 p.p.m.) in a transgenic mouse model of AD, the 3xTg-AD, that expresses both beta amyloid (A beta)- and tau-dependent pathology. We found that Zn(2+) supplementation greatly delays hippocampal-dependent memory deficits and strongly reduces both A beta and tau pathology in the hippocampus. We also evaluated signs of mitochondrial dysfunction and found that Zn(2+) supplementation prevents the age-dependent respiratory deficits we observed in untreated 3xTg-AD mice. Finally, we found that Zn(2+) supplementation greatly increases the levels of brain-derived neurotrophic factor (BDNF) of treated 3xTg-AD mice. In summary, our data support the idea that controlling the brain Zn(2+) homeostasis may be beneficial in the treatment of AD. Cell Death and Disease (2010) 1, e91; doi: 10.1038/cddis.2010.73; published online 28 October 2010

In the subalpine forest ecosystems of the French Alps, European larch trees (Larix decidua Mill.) are periodically affected by outbreaks of a defoliating insect, the larch budmoth (Zeiraphera griseana (Hubner, 1799); LBM). To assess the long-term dynamics of LBM populations, we propose a spatiotemporal analysis of a long outbreak chronology reconstruction for the entire French Alps covering the period 1414-2009. This chronology was obtained by analyzing tree ring width (TRW) chronologies collected from 44 larch populations. The evidence of a latitudinal gradient in LBM is an original result that we have related to the 'travelling waves' and 'epicenter' theory. Wavelet analyses revealed a strong explicit continuous signal for periodicities of 4, 8, and 16 years throughout the entire 1500-2003 time series, except for a loss of power from 1690 to 1790 and since the early 1980s. We hypothesize that these abrupt changes could reflect a physiological response of LBM to past climatic variations. The spatial and temporal variability of LBM outbreaks and the propagation phenomenon in the French Alps highlighted by this study raises questions regarding its future dynamics in response to the expected climate change. Key words: larch budmoth, insect outbreak, French Alps, spatiotemporal heterogeneity, climate change impact. Dans les ecosystemes forestiers subalpins des Alpes francaises, le meleze (Larix decidua Mill.) subit periodiquement les epidemies d'un insecte defoliateur, la tordeuse du meleze (Zeiraphera griseana (Hubner, 1799); LBM). Afin de mieux comprendre les dynamiques a long terme des populations de tordeuse, nous proposons dans cet article une analyse spatio-temporelle d'une tres longue reconstruction des epidemies pour la periode 1414-2009 sur l'ensemble des Alpes francaises. Cette chronologie a pu etre reconstruite a partir des cernes de croissance de 44 populations de meleze. Les resultats ont permis de mettre en evidence le role d'un gradient latitudinal que nous avons attribue au phenomene theorique des << epicentres >> et << vagues de dissemination >>. D'autre part, les analyses temporelles, realisees a l'aide de la methode des ondelettes, ont revele l'existence d'un fort signal continu pour des frequences periodiques de 4, 8 et 16 ans sur l'ensemble de la chronologie a l'exception d'une perte d'energie entre 1690 et 1790 et depuis le debut des annees 1980. Ces changements pourraient refleter une reponse physiologique de la tordeuse a des variations climatiques passees. La variabilite temporelle et spatiale des epidemies de tordeuse ainsi que le mode de propagation a travers les Alpes francaises nous ont conduits a nous interroger sur les dynamiques futures de l'insecte et de son hote en reponse au rechauffement climatique rapide dans les ecosystemes de haute elevation. Mots-cles: tordeuse des bourgeons du meleze, epidemies d'insecte, Alpes francaises, heterogeneite spatio-temporelle, impact du changement climatique., Introduction Outbreaks of defoliator insects are major disturbance events in forests around the world, especially in high-latitude and high-elevation ecosystems. Depending on their intensity, such outbreaks may lead to complete [...]

There is great interest to understand and reduce the massive carbon footprint of the concrete industry. Recent descriptions of microbes incidentally living inside concrete materials ("concrete endoliths") raised questions about how much carbon is either stored in or released from concrete by these microbes. We generated preliminary global estimates of how much organic carbon is stored within the living biomass of concrete endoliths (biomass-carbon) and much CO2 is released from respiring concrete endoliths. Between 2020–2022, we collected widely varying samples of Portland cement-based concrete from Lubbock, Texas. After quantifying endolith DNA from 25 concrete samples and estimating the current global mass of concrete, we calculated that the global concrete endolith biomass-carbon as low as 5191.9 metric tons (suggesting that endoliths are a negligible part of concrete's carbon profile) or as high as 1141542.3 tons (suggesting that concrete endoliths are a pool of carbon that could equal or offset some smaller sources of concrete-related carbon emissions). Additionally, we incubated concrete samples in air-tight microcosms and measured changes in the CO2 concentrations within those microcosms. Two out of the ten analyzed samples emitted small amounts of CO2 due to the endoliths. Thus, "concrete respiration" is possible, at least from concrete materials with abundant endolithic microbes. However, the remaining samples showed no reliable respiration signals, indicating that concrete structures often do not harbor enough metabolically active endoliths to cause CO2 emissions. These results are preliminary but show that endoliths may alter the carbon dynamics of solid concrete and, thus, the carbon footprint of the concrete industry.