Submarine groundwater discharge (SGD) is an understudied vector for pollution to the coastal ocean. Earlier work demonstrated that SGD is a major source of nutrients, carbon, and metals to the ocean, but it remains unclear whether SGD is a source or sink of contaminants of emerging concern (CECs) to coastal waters. Many CECs can have negative ecological impacts even in trace quantities. For instance, disruption to invertebrate reproductive health or promotion of antimicrobial resistance have been directly linked to CECs in numerous studies. Before reaching the ocean, SGD travels through the subterranean estuary, a natural biogeochemical hotspot. I recently obtained initial evidence that SGD can release CEC compounds such as pharmaceuticals and industrial chemicals to the coastal ocean, but do not have insight into how microbial processes may alter CECs in subterranean estuaries. I will study CEC behavior in the subterreanean estuary to resolve biogeochemical processing driving CEC release from contrasting coastal aquifer. I will rely on an interdisciplinary combination of field, lab, and modeling experiments to establish the controlling factors governing CEC behavior within subterranean estuaries and their eventual release to the coastal ocean via SGD. Field experiments will be conducted in contrasting silicate and carbonate systems to cover the wide range of conditions existing along the European coastline. Laboratory column experiments and groundwater modeling will provide conceptual insight into drivers of CEC in SGD. I will be based at the University of Gothenburg (UGOT), Sweden with a secondment in Germany and close collaboration with researchers in Spain, France, and Poland. These results will inform future EU initiatives and provide key information for upcoming EU CEC watchlists.
Critical to our understanding of Alzheimer’s disease (AD) and also to finding therapies is determining how key pathological factors interact and relate to neuronal toxicity, symptoms and disease progression. My research has focussed on amyloid beta (Aβ) moities and demonstrated that cerebrospinal fluid (CSF) Aβ42 correlates with cerebral Aβ pathology; that Aβ accumulates in the brain 10-20 years prior to onset of symptoms; and that CSF Aβ abnormalities precede CSF tau changes. However, it is increasingly clear that a simple linear model of AD aetiology and progression is inadequate. This proposal aims at developing and validating new diagnostic and prognostic biomarker tools to examine the AD pathogenesis in humans taking a broad view of AD’s multiple pathophysiological features and their putative biomarkers. The major questions, all relevant to therapeutic research, that will be addressed in my proposal include: (i) how are different forms of Aβ produced and modified; (ii) what is the toxicity of these different forms; (iii) how is this toxicity mediated; and iv) what other pathologies may contribute to or modify AD-like phenotypes? We and others have shown that Aβ monomers are relatively non-toxic. We will address the hypothesis that Aβ starts to accumulate in the brains of certain individuals due to defective clearance of the peptide. Once aggregated, Aβ acquires chemical modifications during brain incubation over years. These modified Aβ forms then induce tau hyperphosphorylation and concomitantly over-activate the immune system, resulting in neurotoxicity. Other pathologies, including α-synuclein and TDP-43, may contribute in this process. In PATHAD, we will develop and validate new diagnostic and prognostic tools using a combination of groundbreaking technologies and unique clinical materials to dissect the underlying molecular pathogenesis of AD in much greater detail than what has been possible before and facilitate the development of effective treatments.
In a globally changing climate, scientists have paid little attention on variability of wind speed. A recent discovery to science is the “global stilling"; a worldwide slowdown of wind speed since the 1980s. This stilling is not fully understood and neither the quantity nor the quality of wind speed observations is adequate to allow a reliable study. The scientific aims of this MSCA to fill this key gap are (i) to rescue the longest wind speed series (starting prior to the 1960s), and (ii) to improve our knowledge on the influence of atmospheric circulation. Given the interdisciplinary impacts of "global stilling" on wind energy, agriculture and hydrology, the socioeconomic-environmental aim is (iii) to look at past wind speed to better assess future wind speed projections needed for climate change adaptation. The innovative approach combines the rescue (ACE framework) and homogenization (SNHT test) of historical wind speed data, providing a unique opportunity to statistically assess trends/cycles and atmospheric causes (SOM/RCPA and weather typing techniques) on long time periods and reliable datasets than previous studies. The applicant will bring his new homogenization protocol, extensive expertise on winds and a novel collaboration topic to UGOT and KNMI. In turn, these Institutions are world authorities on data rescue techniques and attributing causes of climate trends; the applicant will also be trained in leadership, management, funding, supervision and communication skills enhancing his career development. Jointly this team is in a position to push the boundaries of “global stilling” knowledge far ahead, with the ultimate intent to allow the applicant to train through research, establish an independent career, and a research group at the forefront of wind research in Europe. Additionally, this MSCA addresses two of the H2020 Societal Challenges: “Secure, Clean and Efficient Energy”, and “Climate action, Environment, Resource efficiency and Raw materials”.