A multi-decade record of high quality fCO2 data in version 3 of the Surface Ocean CO2 Atlas (SOCAT)

The Surface Ocean CO2 Atlas (SOCAT) is a synthesis of quality-controlled fCO2 (fugacity of carbon dioxide) values for the global surface oceans and coastal seas with regular updates. Version 3 of SOCAT has 14.7 million fCO2 values from 3646 data sets covering the years 1957 to 2014. This latest version has an additional 4.6 million fCO2 values relative to version 2 and extends the record from 2011 to 2014. Version 3 also significantly increases the data availability for 2005 to 2013. SOCAT has an average of approximately 1.2 million surface water fCO2 values per year for the years 2006 to 2012. Quality and documentation of the data has improved. A new feature is the data set quality control (QC) flag of E for data from alternative sensors and platforms. The accuracy of surface water fCO2 has been defined for all data set QC flags. Automated range checking has been carried out for all data sets during their upload into SOCAT. The upgrade of the interactive Data Set Viewer (previously known as the Cruise Data Viewer) allows better interrogation of the SOCAT data collection and rapid creation of high-quality figures for scientific presentations. Automated data upload has been launched for version 4 and will enable more frequent SOCAT releases in the future. High-profile scientific applications of SOCAT include quantification of the ocean sink for atmospheric carbon dioxide and its long-term variation, detection of ocean acidification, as well as evaluation of coupled-climate and ocean-only biogeochemical models. Users of SOCAT data products are urged to acknowledge the contribution of data providers, as stated in the SOCAT Fair Data Use Statement. This ESSD (Earth System Science Data) “living data” publication documents the methods and data sets used for the assembly of this new version of the SOCAT data collection and compares these with those used for earlier versions of the data collection (Pfeil et al., 2013; Sabine et al., 2013; Bakker et al., 2014). Individual data set files, included in the synthesis product, can be downloaded here: doi:10.1594/PANGAEA.849770. The gridded products are available here: doi:10.3334/CDIAC/OTG.SOCAT_V3_GRID

Global carbon budget 2019

Accurate assessment of anthropogenic carbon dioxide (CO2) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere – the “global carbon budget” – is important to better understand the global carbon cycle, support the development of climate policies, and project future climate change. Here we describe data sets and methodology to quantify the five major components of the global carbon budget and their uncertainties. Fossil CO2 emissions (EFF) are based on energy statistics and cement production data, while emissions from land use change (ELUC), mainly deforestation, are based on land use and land use change data and bookkeeping models. Atmospheric CO2 concentration is measured directly and its growth rate (GATM) is computed from the annual changes in concentration. The ocean CO2 sink (SOCEAN) and terrestrial CO2 sink (SLAND) are estimated with global process models constrained by observations. The resulting carbon budget imbalance (BIM), the difference between the estimated total emissions and the estimated changes in the atmosphere, ocean, and terrestrial biosphere, is a measure of imperfect data and understanding of the contemporary carbon cycle. All uncertainties are reported as ±1σ. For the last decade available (2009–2018), EFF was 9.5±0.5 GtC yr−1, ELUC 1.5±0.7 GtC yr−1, GATM 4.9±0.02 GtC yr−1 (2.3±0.01 ppm yr−1), SOCEAN 2.5±0.6 GtC yr−1, and SLAND 3.2±0.6 GtC yr−1, with a budget imbalance BIM of 0.4 GtC yr−1 indicating overestimated emissions and/or underestimated sinks. For the year 2018 alone, the growth in EFF was about 2.1 % and fossil emissions increased to 10.0±0.5 GtC yr−1, reaching 10 GtC yr−1 for the first time in history, ELUC was 1.5±0.7 GtC yr−1, for total anthropogenic CO2 emissions of 11.5±0.9 GtC yr−1 (42.5±3.3 GtCO2). Also for 2018, GATM was 5.1±0.2 GtC yr−1 (2.4±0.1 ppm yr−1), SOCEAN was 2.6±0.6 GtC yr−1, and SLAND was 3.5±0.7 GtC yr−1, with a BIM of 0.3 GtC. The global atmospheric CO2 concentration reached 407.38±0.1 ppm averaged over 2018. For 2019, preliminary data for the first 6–10 months indicate a reduced growth in EFF of +0.6 % (range of −0.2 % to 1.5 %) based on national emissions projections for China, the USA, the EU, and India and projections of gross domestic product corrected for recent changes in the carbon intensity of the economy for the rest of the world. Overall, the mean and trend in the five components of the global carbon budget are consistently estimated over the period 1959–2018, but discrepancies of up to 1 GtC yr−1 persist for the representation of semi-decadal variability in CO2 fluxes. A detailed comparison among individual estimates and the introduction of a broad range of observations shows (1) no consensus in the mean and trend in land use change emissions over the last decade, (2) a persistent low agreement between the different methods on the magnitude of the land CO2 flux in the northern extra-tropics, and (3) an apparent underestimation of the CO2 variability by ocean models outside the tropics. This living data update documents changes in the methods and data sets used in this new global carbon budget and the progress in understanding of the global carbon cycle compared with previous publications of this data set (Le Quéré et al., 2018a, b, 2016, 2015a, b, 2014, 2013). The data generated by this work are available at https://doi.org/10.18160/gcp-2019 (Friedlingstein et al., 2019)

Global Carbon Budget 2022

Accurate assessment of anthropogenic carbon dioxide (CO$_2$) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere in a changing climate is critical to better understand the global carbon cycle, support the development of climate policies, and project future climate change. Here we describe and synthesize data sets and methodologies to quantify the five major components of the global carbon budget and their uncertainties. Fossil CO$_2$ emissions (E$_{FOS}$) are based on energy statistics and cement production data, while emissions from land-use change (E$_{LUC}$), mainly deforestation, are based on land use and land-use change data and bookkeeping models. Atmospheric CO$_2$ concentration is measured directly, and its growth rate (G$_{ATM}$) is computed from the annual changes in concentration. The ocean CO$_2$ sink (S$_{OCEAN}$) is estimated with global ocean biogeochemistry models and observation-based data products. The terrestrial CO$_2$ sink (S$_{LAND}$) is estimated with dynamic global vegetation models. The resulting carbon budget imbalance (B$_{IM}$), the difference between the estimated total emissions and the estimated changes in the atmosphere, ocean, and terrestrial biosphere, is a measure of imperfect data and understanding of the contemporary carbon cycle. All uncertainties are reported as ±1σ. For the year 2021, E$_{FOS}$ increased by 5.1 % relative to 2020, with fossil emissions at 10.1 ± 0.5 GtC yr$^{−1}$ (9.9 ± 0.5 GtC yr$^{−1}$ when the cement carbonation sink is included), and E$_{LUC}$ was 1.1 ± 0.7 GtC yr$^{−1}$, for a total anthropogenic CO$_2$ emission (including the cement carbonation sink) of 10.9 ± 0.8 GtC yr$^{−1}$ (40.0 ± 2.9 GtCO$_2$). Also, for 2021, G$_{ATM}$ was 5.2 ± 0.2 GtC yr$^{−1}$ (2.5 ± 0.1 ppm yr$^{−1}$), S$_{OCEAN}$ was 2.9  ± 0.4 GtC yr$^{−1}$, and S$_{LAND}$ was 3.5 ± 0.9 GtC yr$^{−1}$, with a B$_{IM}$ of −0.6 GtC yr$^{−1}$ (i.e. the total estimated sources were too low or sinks were too high). The global atmospheric CO$_2$ concentration averaged over 2021 reached 414.71 ± 0.1 ppm. Preliminary data for 2022 suggest an increase in E$_{FOS}$ relative to 2021 of +1.0 % (0.1 % to 1.9 %) globally and atmospheric CO$_2$ concentration reaching 417.2 ppm, more than 50 % above pre-industrial levels (around 278 ppm). Overall, the mean and trend in the components of the global carbon budget are consistently estimated over the period 1959–2021, but discrepancies of up to 1 GtC yr$^{−1}$ persist for the representation of annual to semi-decadal variability in CO$_2$ fluxes. Comparison of estimates from multiple approaches and observations shows (1) a persistent large uncertainty in the estimate of land-use change emissions, (2) a low agreement between the different methods on the magnitude of the land CO$_2$ flux in the northern extratropics, and (3) a discrepancy between the different methods on the strength of the ocean sink over the last decade. This living data update documents changes in the methods and data sets used in this new global carbon budget and the progress in understanding of the global carbon cycle compared with previous publications of this data set. The data presented in this work are available at https://doi.org/10.18160/GCP-2022 (Friedlingstein et al., 2022b)

Global Carbon Budget 2023

Accurate assessment of anthropogenic carbon dioxide (CO2) emissions and their redistribution among the atmosphere, ocean, and terrestrial biosphere in a changing climate is critical to better understand the global carbon cycle, support the development of climate policies, and project future climate change. Here we describe and synthesize data sets and methodology to quantify the five major components of the global carbon budget and their uncertainties. Fossil CO2 emissions (EFOS) are based on energy statistics and cement production data, while emissions from land-use change (ELUC), mainly deforestation, are based on land-use and land-use change data and bookkeeping models. Atmospheric CO2 concentration is measured directly, and its growth rate (GATM) is computed from the annual changes in concentration. The ocean CO2 sink (SOCEAN) is estimated with global ocean biogeochemistry models and observation-based f CO2 products. The terrestrial CO2 sink (SLAND) is estimated with dynamic global vegetation models. Additional lines of evidence on land and ocean sinks are provided by atmospheric inversions, atmospheric oxygen measurements, and Earth system models. The resulting carbon budget imbalance (BIM), the difference between the estimated total emissions and the estimated changes in the atmosphere, ocean, and terrestrial biosphere, is a measure of imperfect data and incomplete understanding of the contemporary carbon cycle. All uncertainties are reported as ±1σ. For the year 2022, EFOS increased by 0.9 % relative to 2021, with fossil emissions at 9.9 ± 0.5 Gt C yr−1 (10.2 ± 0.5 Gt C yr−1 when the cement carbonation sink is not included), and ELUC was 1.2 ± 0.7 Gt C yr−1, for a total anthropogenic CO2 emission (including the cement carbonation sink) of 11.1 ± 0.8 Gt C yr−1 (40.7±3.2 Gt CO2 yr−1). Also, for 2022, GATM was 4.6±0.2 Gt C yr−1 (2.18±0.1 ppm yr−1; ppm denotes parts per million), SOCEAN was 2.8 ± 0.4 Gt C yr−1, and SLAND was 3.8 ± 0.8 Gt C yr−1, with a BIM of −0.1 Gt C yr−1 (i.e. total estimated sources marginally too low or sinks marginally too high). The global atmospheric CO2 concentration averaged over 2022 reached 417.1 ± 0.1 ppm. Preliminary data for 2023 suggest an increase in EFOS relative to 2022 of +1.1 % (0.0 % to 2.1 %) globally and atmospheric CO2 concentration reaching 419.3 ppm, 51 % above the pre-industrial level (around 278 ppm in 1750). Overall, the mean of and trend in the components of the global carbon budget are consistently estimated over the period 1959–2022, with a near-zero overall budget imbalance, although discrepancies of up to around 1 Gt C yr−1 persist for the representation of annual to semi-decadal variability in CO2 fluxes. Comparison of estimates from multiple approaches and observations shows the following: (1) a persistent large uncertainty in the estimate of land-use changes emissions, (2) a low agreement between the different methods on the magnitude of the land CO2 flux in the northern extra-tropics, and (3) a discrepancy between the different methods on the strength of the ocean sink over the last decade. This living-data update documents changes in methods and data sets applied to this most recent global carbon budget as well as evolving community understanding of the global carbon cycle. The data presented in this work are available at https://doi.org/10.18160/GCP-2023 (Friedlingstein et al., 2023)

Influences de l'homéostasie calcique neuronale sur le métabolisme des protéines impliquées dans la maladie d'Alzeimer

Alzheimer's disease (AD), the most frequent cause of dementia, is characterized by the presence of two neuropathological lesions: accumulation of b-amyloid (Ab) peptides in extracellular senile plaques and neurofibrillary tangles containing hyperphosphorylated protein tau. Ab is generated by the sequential cleavage of its precursor, the amyloid precursor protein (APP), performed by BACE and the g-secretase complex containing presenilin 1, Nicastrin, PEN-2 and APH-1. Tau is a microtubule-associated protein known as a developmentally regulated neuronal phosphoprotein. Calcium signaling is a central process in brain function and its destabilization seems to be central to the pathogenesis of AD. Disruption of cellular calcium homeostasis is also reported to increase age-associated impairments in learning and memory. During aging, changes observed in neuronal calcium buffering processes and activation of calcium voltage-dependent channels support the calcium hypothesis in the development of AD. To investigate the influence of the imbalance of intracellular calcium homeostasis on the APP metabolism, rat cortical neurons infected with human APP were depolarized in presence of extracellular potassium. We report that an influx of extracellular calcium favors the amyloidogenic processing of human APP by increasing the production of intraneuronal C-terminal fragments produced by the b-cleavage of the protein (CTFb). The increase of intracellular calcium levels triggers the specific accumulation of neurotoxic intraneuronal Ab1-42. These effects were completely reversed by nimodipine, an antagonist of L-type calcium channels. Therefore, the release of calcium-store content in the endoplasmic reticulum is not sufficient to induce the production of intraneuronal Ab, but the capacitive calcium entry mechanism, which is a process for replenishing depleted calcium stores in the endoplasmic reticulum, is needed to trigger its accumulation. APP is known to be phosphorylated in its short intracellular cytoplasmic domain on several sites. Among them, only the threonine 668 (Thr668) residue has received particular attention Indeed, the phosphorylation status of this residue seems to be closely linked with the production of Ab. Moreover, glycogen synthase kinase-3b and cyclin-dependent kinase 5 are known to phosphorylate APP on Thr668 and both are thought to regulate the production of Ab in neural cells. These kinases are not only known to regulate the amyloidogenic pathway of APP, but they also play a role in diverse array of cellular functions including cell adhesion, cell division and tau phosphorylation. Since deregulation of calcium homeostasis induced by neuronal depolarization may play an important role in intraneuronal Ab1-42 production, we have investigated the influence of an extracellular calcium influx on the phosphorylation of human APP and endogenous tau in rat cortical neurons. We have analyzed the time course of APP and tau phosphorylations after disrupting neuronal calcium homeostasis by K+-induced depolarization. We report that high cytosolic calcium concentrations induce a transient increase in both APP and tau phosphorylation. Moreover, the transient phosphorylation of APP on Thr668 induces the progressive accumulation of neurotoxic intraneuronal Ab1-42. For the first time, we report that a disruption of cellular calcium homeostasis, induced by neuronal depolarization, triggers the two major processes responsible of the formation of the two typical pathological lesions found in AD brains. Thus, calcium deregulation is a crucial event of AD pathogenesis, and elicits the characteristic lesions of this disorder, including increased Ab formation, hyperphosphorylation of tau and neuronal cell death.La maladie d'Alzheimer (MA) est une démence dégénérative caractérisée par la présence, dans le cerveau, de deux types de lésions : les dégénérescences neurofibrillaires et les plaques séniles. Les paires hélicoïdales de filaments, retrouvées dans les dégénérescences neurofibrillaires de cerveaux de patients atteints de la MA, sont principalement composées de protéines tau hyperphosphorylées. Les plaques séniles, quant à elles, contiennent un noyau amyloïde dont le composant majeur est le peptide Ab. L'Ab est produit suite au clivage séquentiel de son précurseur, le précurseur du peptide amyloïde (APP). La b-sécrétase (BACE) clive l'APP à l'extrémité N-terminale de la séquence du peptide amyloïde et produit un fragment intracellulaire CTFb. Le complexe g-sécrétase contenant la préséniline 1, la nicastrine, PEN-2 et APH-1, en clivant le fragment CTFb, libère le peptide Ab. La rupture de l'homéostasie calcique semble jouer un rôle central dans le développement de la MA. Une dérégulation de la signalisation calcique est observée au cours du vieillissement cérébral normal. En effet, l'altération des mécanismes intracellulaires assurant la clairance du calcium cytosolique, de même que l'activation des canaux calciques membranaires dépendants du voltage, contribuerait à l'altération des processus de mémorisation. Ainsi est née l' « hypothèse calcique » selon laquelle la rupture de l'homéostasie calcique jouerait un rôle majeur dans le développement de la MA. Afin d'étudier l'influence d'une perte de l'homéostasie du calcium sur le métabolisme de l'APP, des neurones corticaux de rat en culture ont été dépolarisés en présence de potassium extracellulaire. L'influx de calcium extracellulaire semble favoriser la voie de maturation amyloïdogène de l'APP en augmentant la production des fragments C-terminaux b-clivés. L'augmentation des taux de calcium intracellulaire induit la production spécifique du peptide Ab1-42 intraneuronal neurotoxique. Ces effets sont totalement inhibés par la nimodipine, un inhibiteur spécifique des canaux calciques de type-L. Enfin, la libération du calcium à partir des stocks calciques intracellulaires du réticulum endoplasmique ne permet pas la production du peptide Ab. Seul l'influx de calcium extracellulaire, au travers d'un mécanisme capacitatif impliqué dans le remplissage des stocks de calcium du réticulum, permet l'accumulation d'Ab1-42 intraneuronal. L'APP est phosphorylé dans son court domaine cytoplasmique intracellulaire sur des sites spécifiques. Parmi ces sites, seul le résidu thréonine 668 (Thr668) a attiré notre attention. En effet, l'état de phosphorylation de ce résidu semble être étroitement lié à la production du peptide Ab. De plus, la glycogène synthase kinase-3b et la cycline-dépendante kinase 5 sont des protéines kinases connues pour phosphoryler l'APP en Thr668 et réguler la production d'Ab dans les cellules neuronales. Ces kinases régulent non seulement le métabolisme amyloïdogène de l'APP, mais elles jouent aussi un rôle important dans la régulation de nombreux autres mécanismes, parmi lesquels l'adhésion cellulaire, la division cellulaire et la phosphorylation de la protéine tau. Puisqu'une dérégulation de l'homéostasie du calcium induite par la dépolarisation neuronale semble jouer un rôle important dans la production d'Ab1-42 intraneuronal, nous avons étudié l'influence de l'influx de calcium extracellulaire sur la phosphorylation de l'APP humain et sur celle de la protéine tau endogène dans des neurones corticaux de rat. Nous avons analysé la cinétique de phosphorylation de l'APP et de tau après rupture de l'homéostasie du calcium induite par une dépolarisation neuronale au potassium. Nous montrons que l'augmentation de la concentration en calcium cytosolique induit, à la fois, une augmentation transitoire de la phosphorylation de l'APP et de tau. De plus, la phosphorylation transitoire de l'APP en Thr668 induit l'accumulation progressive d'Ab1-42 intraneuronal neurotoxique. Nous montrons, pour la première fois, que l'augmentation de la concentration en calcium intracellulaire modifie à la fois l'état de phosphorylation des protéines tau et APP. La perte de l'homéostasie calcique, en augmentant la production du peptide Ab et en hyperphosphorylant la protéine tau, jouerait un rôle majeur dans le développement de la MA. Ainsi, la perte de l'homéostasie calcique est capable, au travers d'un même mécanisme cellulaire, de modifier le métabolisme des protéines associées aux lésions caractéristiques de la MA.Thèse de doctorat en sciences médicales (orientation : neurosciences) (MED 3)--UCL, 200

Processing of amyloid precursor protein and amyloid Peptide neurotoxicity.

Alzheimer's disease is characterized by the presence of two types of lesions in brain: neurofibrillary tangles and senile plaques. Intraneuronal neurofibrillary tangles are made of paired helical filaments containing hyperphosphorylated microtubule associated protein tau. Extracellular senile plaques contain a core of beta-amyloid peptide (Abeta), which is produced by cleavage of the Amyloid Precursor Protein (APP). Among the two catabolic pathways of APP, the amyloidogenic pathway producing Abeta peptides was intensively studied in different cellular models expressing human APP. Differences in APP processing and in toxicity resulting from Abeta accumulation can be observed from one cell type to another. In particular, primary cultures of neurons process APP differently compared with other cultured cells including neuronal cell lines. Neurons accumulate intraneuronal Abeta, which is neurotoxic, and in these cells, APP can be phosphorylated at specific residues. Recent studies suggest that APP phosphorylation can play an important role in its amyloidogenic processing. In addition, protein kinases that phosphorylate APP are also able to phosphorylate the neuronal protein tau. Biochemical analysis of these two proteins in primary cultures of neurons show that phosphorylation of both APP and tau can be a factor linking the two characteristic lesions of Alzheimer's disease