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Forskere har lenge debattert om spesifikke endringer i måten genene våre reguleres på, kalt epigenetiske endringer eller "epimutasjoner," kan øke risikoen for kreft. Våre nylige banebrytende undersøkelser har gitt sterke bevis på at epimutasjoner faktisk er en risikofaktor for visse typer kreft.
I en studie av en stor gruppe kvinner fant vi at de som hadde epimutasjoner i BRCA1-genet, hadde mye større risiko for å utvikle trippel-negativ brystkreft og høygradig serøs eggstokkreft senere i livet. Disse epimutasjonene ser ut til å oppstå tidlig under fosterutviklingen, og fører til at det fødte barnet (og senere det voksne individet) har en mosaikk av celler i kroppen, der noen få celler bærer epimutasjonen.
Nå har vi som mål å utvide disse studiene til andre gener og andre former for kreft. For å gjøre dette vil vi analysere blodprøver fra en studie som har rekruttert over 160 000 kvinner i USA.
Hvis denne forskningen lykkes, kan den revolusjonere vår forståelse av hvordan kreft utvikler seg og føre til bedre forebyggende tiltak. Det kan også ha store implikasjoner for kreftscreeningprogrammer og genetisk veiledning for personer med høy risiko for visse typer kreft.
Alt i alt fremhever vår forskning den viktige rollen som epigenetiske endringer kan spille i kreftutvikling og understreker behovet for ytterligere undersøkelser på dette området.

Cancers result from accumulation of genetic and epigenetic alterations. The minority of cancers are due to inherited (germline) alterations that affect all cells in the body. On the other hand, the majority of cancers (>85%; sporadic cancers) are believed to occur due to localised alterations that accumulate after birth as a result of stochastic processes and/or environmental effects. Recently, in a major breakthrough work, we have provided definitive evidence that some sporadic cancers arise in adult life due to mosaic BRCA1 epimutations that occurred during the early embryonic development. BRCA1 epimutations have a surprisingly high population frequency (>5% of adult women) and hazard ratios for breast and ovarian cancer (2.4 and 1.9, respectively). Together with the findings of epimutations in other tumour suppressor genes (MGMT, MLH1, etc) this has led us to hypothesise that a substantial fraction of other sporadic cancers can be attributed to prenatal epimutations in other tumour suppressor genes.

In this project, we will use ultradeep targeted methylation sequencing for quantitative and qualitative analyses of epimutations. Evaluation of cancer risk related to epimutations will be done by studying samples from prospective biobanks (WHI) with samples from healthy women that remained cancer-free or developed different types of incident cancers years/decades after samples were taken. We will also characterise epimutations present in samples of newborn boys and girls, as well as their parents (MoBa biobank). Finally, using cryopreserved blood-derived stem-like cells from young healthy males and female breast cancer patients (in-house biobank), we will assess mutational and epimutational mosaicism at the single-cell level, generating clonal phylogeny for the methylated cells and thus providing insights on early-developmental processes that create epimutations.

Mosaic epimutations: population prevalence, mechanistic origins, and their role in cancer

Dette prosjektet har som mål å undersøke nervedannelse i primær brystkreft og hjernemetastaser fra brystkreft. Vår hypotese er at en undergruppe av aggressive brystkreftsvulster involverer nervestrukturer for å fremme tumorprogresjon, inkludert metastaser til hjernevev, som er den mest nevrogene nisjen i kroppen.

Hos kvinner er brystkreft den hyppigste kreftsykdommen og den ledende årsaken til kreftrelaterte dødsfall verden over. Trippel-negativ eller basaloid brystkreft er de mest utfordrende subgruppene, på grunn av mangel på effektive behandlingsmål. Studier av nervefiber-tetthet i brystkreft har vist at høyt innerverte svulster er mer aggressive, og tilstedeværelse av nerve-elementer er assosiert med økt metastasering og forverret pasientprognose. Våre foreløpige data, fra vevsanalyse av to brystkreftserier, bekrefter disse funnene. Vi anser derfor nerveinvolvering som en ny og lovende biomarkør i vår forståelse av aggressiv brystkreft.

Nerver er små fiber-strukturer i svulster, som nåler i en høystakk, og vanskelig å oppdage ved vanlig mikroskopisk undersøkelse. Derfor eksisterer det ikke automatiserte prosedyrer for deteksjon av slike svulst-nerver, og nervene sin klinisk-patologiske betydning er lite kjent. I dette prosjektet vil vi utvikle mer sensitive metoder for å påvise små nerveelementer i vev fra svulster, ved hjelp av avansert bildeteknologi. Interaksjon mellom kreftceller og nerver vil bli analysert i funksjonelle studier.

Vår hypotese er at aggressive brystkreftceller utrykker hittil ukjente markører som kontrollerer tiltrekning av nerver til primærsvulsten, og at denne tiltrekningen forårsaker endringer i en undergruppe av brystkreftceller som fremmer spredning til hjernen.

Recent data indicate that nerves might play an active role in the initiation and progress of cancer. In the breast, research by us and others has demonstrated that enhanced innervation is associated with more aggressive tumors, such as the triple negative subtype (TNBC) supporting the formation of a neurogenic niche in primary tumors. However, the detailed clinical relevance of this phenomenon, and the mechanisms by which nerves are attracted to breast tumors and how breast cancer-nerve interaction promotes aggressive tumor features, remain unexplored. Moreover, we lack good experimental models for breast cancer innervation in a human setting. 

TNBCs with a basal-like phenotype are also prone to metastasize to the brain, the most neurogenic niche in the body, but the preference for the brain as a metastatic site is not understood, neither are the phenotypic alterations that breast cancer cells undergo in brain tissue. Here, we launch a new concept - epithelial-to-neural transition (ENT) – linking cancer cell plasticity and nerve involvement in primary and brain metastatic breast cancer. We suggest that aggressive breast cancer cells express yet unknown markers that control attraction of nerves at the primary site, and that some breast cancer cells even transform by acquiring neural-like properties and spread to the brain. Epithelial-to-neural transition will be investigated both clinically and experimentally in primary and brain metastatic breast cancer by combining large clinical cohorts, spatial omics technology, and stem cell methods to establish cutting-edge models. 

This project has the potential to change the way we view neural elements in breast cancer and provide the field with new clinical relevance, models and technologies to study them.

When breast cancer hits a nerve
- Neural involvement as a hallmark of tumor progression

Kreftvev inneholder ikke bare kreftceller, men også en rekke forskjellige immunceller. Noen av dem er nyttige, andre bytter side og hjelper nå svulsten. Kunnskapen om fordelingen av immuncelletyper til en pasient er svært viktig. Denne informasjonen er med på å definere den beste personlige behandlingen, gi en klarere overlevelsesprognose eller hjelper å definere nye mulige behandlingsalternativer. 
I tillegg gjennomgår immunceller i tumormikromiljøet flere endringer, noen er nyttige i kampen mot kreft, andre hjelper svulsten til å vokse eller spre seg. Kunnskapen om disse endringene i de ulike immuncelletypene hjelper til med å forklare prosessene i svulsten eller til å oppdage mulige nye biomarkører for behandlingsalternativer. 
I dette prosjektet ønsker vi å ta hensyn til både den romlige fordelingen og endringene av de forskjellige immuncelletypene avhengig av deres lokalisering i forhold til kreftvev. Hvilke endringer kan vi finne? Hvordan påvirker de hverandre og hvordan påvirkes de av svulsten? Vi ønsker å bruke denne kunnskapen til å oppdage nye mulige biomarkører for behandlingsalternativer.

Spatial transcriptomics provides unprecedented details about the molecular mechanisms that take place within and between cells. ST assesses the molecular content of well-defined regions in a tissue which potentially cover contributions from multiple cells. In order to draw correct biological conclusions from ST analysis, spatial distributions of individual cell types are a prerequisite. This generates an urgent need for computational methods addressing this question. However, computational estimates of cellular compositions from ST are complicated by several factors. First, the methods require well curated data which is usually not available; every specimen has its own individual characteristics and so, every tissue type or even every patient, might require a own, comprehensively verified model. Second, data is noisy, making estimates prone to errors. Moreover, even if a computational model is designed for a specific tissue or even patient, it might be miss-specified, leading to additional systematic errors. In this project, we will develop a toolbox called Computational Dissection of Cellular Distributions (CDCD), which directly accounts for these issues. CDCD will advance the state of the art by (1) taking into account a priori unknown, hidden cellular background contributions, (2) taking into account environmental factors (i.e., tissue and patient dependence), and by (3) comprehensive errors estimation. Intriguingly, in contrast to available techniques, CDCD will facilitate estimates of cellular regulation in space! Such gene-regulation gradients will allow us to address questions of how immune cells adapt their molecular phenotype with respect to their environment. Additionally we will verify our algorithms on a conjoint norwegian phase II melanoma case study. CDCD will be made freely available via easy-to-use webpage and software solution, enabling both expert bioinformaticians and wet-lab biologists an efficient use of the to-be-developed methodology.

Computational dissection of cellular distributions and cell-type specific regulation patterns from spatial transcriptomics data

Antimikrobiell resistens (AMR) er en alvorlig trussel mot folkehelsa som er spådd å bli verre i fremtiden. En av de vanligste metodene som bakterier bruker for å kunne stå imot antibiotika, er å skaffe resistensgener. Disse sitter ofte på noen DNA-deler som heter plasmider. Plasmider som bærer resistensgener er vanligere i kliniske miljøer enn samfunnet ellers, og det å forstå hvorfor vi har denne forskjellen er svært viktig for å forstå hvordan resistente bakterier sprer seg. Men plasmider utvikler seg raskt, og kan spre seg mellom forskjellige bakteriestammer. Derfor er det vanskelig for oss å klassifisere og overvåke dem. I PEAK skal vi benytte oss av nye sekvenseringsteknologier og utvikle nye metoder for å forske på hvordan plasmider utvikler seg og sprer seg, med fokus på den viktige sykdomsfremkallende bakterien Klebsiella pneumoniae. Vi skal utvikle nye metoder for å klassifisere plasmider og analysere de genetiske forskjellene mellom plasmidgrupper. Deretter skal vi bruke disse plasmidgruppene til å forske på hvordan plasmider sprer seg mellom forskjellige miljøer og typer Klebsiella. Så skal vi utføre detaljerte analyser av de genetiske endringene som driver utviklingen av plasmider. Målet er å bruke de nye metodene og kunnskapen til å forbedre overvåkning, både av AMR Klebsiella pneumoniae og andre bakteriestammer.

Antimicrobial resistance (AMR) is a global threat to human health which is predicted to increase in the future. One of the most common ways that bacteria evolve resistance to antibiotics is by acquiring AMR genes; these are often carried on small pieces of DNA called plasmids. Understanding the mechanisms and conditions that promote AMR dissemination via plasmids is critical, but several knowledge gaps remain. AMR is unevenly distributed among environments, whilst the highest levels of AMR are typically found in clinical environments, the risk of AMR acquisition from environmental and animal settings remains less clear. Plasmids are important vectors for the transmission of AMR between environments, but plasmid evolution is complex, and lack of appropriate data and methods has to date largely precluded high-resolution study and surveillance of plasmids in most major pathogens.

In PEAK, we will use two newly generated long-read sequencing datasets to study the evolution and transmission of plasmids and AMR genes in Klebsiella. By combining the datasets, consisting of 1594 isolates from diverse one-health sources, we will establish a unique collection of hybrid assemblies, including thousands of complete plasmids. Next, we will develop novel methods to quantify the genetic structure and diversity of plasmids. By combining this information with genetic variation in the isolate chromosomes and metadata, we will then perform phylogenetic and association analyses to disentangle AMR distributions among environments. This will enable us to identify high-risk environments for AMR transmission, followed by detailed evolutionary analyses to gain insight into the tempo and mode of plasmid evolution, and how chromosomes coevolve with plasmids.

The overarching aims of PEAK are to uncover the drivers and mechanisms of the acquisition and maintenance of AMR, with the ultimate goal of enabling use of this knowledge to design interventions to combat the spread of AMR in the future.

PEAK: Plasmid Evolution and Antimicrobial resistance in Klebsiella pneumoniae

Økonomisk ulikhet øker i Norge og andre høyinntektsland, mens innvandring også er med å endre samfunnets demografiske og sosioøkonomiske struktur. I kjølevannet av økende økonomiske og etniske forskjeller, er det bekymringsfullt at ulike dimensjoner av ulikhet blir stadig mer vedvarende på tvers av generasjoner. Å fremskaffe kunnskap om i hvilken grad ulikhet overføres innenfor familier og bredere sosial kontekster, vil kunne si noe om hvilke muligheter man har senere i livet. Til tross for mye forskning på intergenerasjonell mobilitet for utdanning og arbeid, har det vært lite forskning på betydningen av helse i overføringen av sosioøkonomisk status fra foreldre til barn.  
I  HEALTHMOBILITY ønsker vi å studere (1) i hvilken grad helsestatus overføres gjennom generasjoner og sammenhengen mellom helse og sosioøkonomisk mobilitet, (2) den kausale effekten av helseforskjeller tidlig i livet og i ungdomsårene på voksne prestasjoner og sosial ekskludering, (3) i hvilken grad de ovennevnte prosessene varierer mellom barn av innvandrerforeldre og de uten innvandringsbakgrunn, og, (4) hvordan forholdet mellom sosioøkonomisk status og helse har utviklet seg historisk—ved å studere langsiktige trender som strekker seg over mer enn 50 år. Prosjektets bidrag vil være å undersøke betydningen av både foreldre og barns helse som en dimensjon av intergenerasjonell mobilitet, sosial ekskludering, og livsjanser gjennom generasjoner.

Economic inequality is on the rise in Norway and other high-income countries, while large-scale immigration is also changing the demographic and socioeconomic structure of these societies. In the wake of widening economic disparities and ethnic inequality, there is growing concern among social scientists and policy makers that various dimensions of inequality are becoming increasingly persistent across generations. Knowing to what extent inequality is perpetuated within families and within broader social contexts is crucial since most would agree that opportunities in life should not be determined by which family a child is born into. Despite a vast literature on intergenerational mobility and children’s prospects for moving up the socioeconomic ladder, there is little research on the intergenerational transmission of health status and its role in the transmission of socioeconomic status from parents to children. This is unfortunate, as health is increasingly acknowledged as an essential part of individuals’ human capital, with important consequences for individuals outcomes in education and the labor market. 
In HEALTHMOBILITY we aim to study to what extent (1) health status is passed down through generations and its relation to socioeconomic mobility, (2) the causal impact of early-life health disparities on adult attainments, (3) to what extent these processes vary between children of immigrant and native parents, and (4) how the relationship between socioeconomic status and health status have evolved historically. Our aim is to unpack how mechanisms related to intergenerational transmission of health inequality contributes to socioeconomic and ethnic disparities in educational and labor market attainments. We will use Norwegian data from population-wide administrative registers and large-scale surveys, with detailed information on health service use, self-reported measures of health, and key socioeconomic and demographic characteristics to address these issues

Socioeconomic and Ethnic Inequality in Health and Intergenerational Mobility (HEALTHMOBILITY)

Personer med psykoselidelser som schizofreni, har ofte alvorlige tilleggslidelser som hjertesykdom og diabetes, noe som kan være grunnen til at de lever kortere liv. Disse tilstandene opptrer ikke sammen ved en tilfeldighet; de påvirker hverandre på måter som forskerne bare begynner å forstå.

En revolusjonerende metode kalt metabolomikk, som analyserer molekyler i blodet ditt, hjelper oss med å forstå dette samspillet. Takket være store biobanker og nasjonale helseregistre kan vi nå kartlegge biologiske forbindelser mellom kropp og hjerne.

MAGIC er et banebrytende initiativ som kombinerer genetikk, blodanalysee, hjerneavbildning og helseregistre. Prosjektet tar sikte på å avdekke skjulte sammenhenger mellom metabolsk helse og psykoselidelser ved å:

1. Studere koblinger mellom metabolske markører (som fettmolekyler) og psykotiske opplevelser (f.eks. hallusinasjoner), samt vanlige hjerte- og metabolske sykdommer. Vi vil også knytte dette til endringer i hjernestruktur og kroppssammensetning.

2. Analysere genetiske data for å fastslå hvilke gener som bidrar til disse sammenflettede problemene, og bruke dette for å utforske potensielle årsak-virkning-forhold.

3. Undersøke hvilke genetiske faktorer som er felles eller unike for psykose og kardiometabolske sykdommer, avdekke de underliggende molekylære banene og utdype vår forståelse av begge tilstandene.

4. Bruke kraftige maskinlæringsteknikker for å lage 'digitale tvillinger'—virtuelle pasientmodeller som kan forutsi hvordan disse tilstandene vil utvikle seg hos enkeltpersoner. Dette kan gjøre det mulig å skreddersy intervensjonsstrategier til hver persons unike genetiske og metabolske profil.

MAGIC har som mål å avdekke de biologiske hemmelighetene som kobler metabolisme og mental helse. Ved å øke vår forståelse av disse komplekse sammenhengene, er målet å forbedre forebyggingsstrategier og sykdomsutfall. Dette kan føre til en stor endring innen helsevesenet, og gi håp om bedre og mer persontilpasset behandling.

People with psychotic disorders often suffer from cardiometabolic diseases, which are major determinants of clinical outcome. It is therefore imperative that we better understand the pathogenesis of metabolic dysfunction and its contribution to the development of psychosis. Markers of metabolic processes can be reliably measured in blood samples using new high-throughput metabolomics, i.e., the measurement of proteins, amino acids, and other small molecules. Such data is now available through large biobanks coupled to national health records. This provides unprecedented opportunities to uncover the genetic architecture of metabolism and its impact on body and brain measures.
The MAGIC project will enhance our understanding of the role that metabolic dysfunction plays in psychosis, using a unique set of genomics, metabolomics, imaging, and registry data. We will leverage a transcontinental network of deep-phenotyped, population-based prospective cohorts to (1) establish the relationship between metabolic markers and psychotic experiences, as well as comorbid cardiometabolic conditions, and estimate to what extent associations are mediated by brain morphology and body composition; (2) calculate the amount of genetic overlap between the markers, psychotic disorders and cardiometabolic diseases, and leverage genetic variation to determine causal relationships; (3) identify shared and specific genetic determinants of psychotic disorders and cardiometabolic diseases with enhanced statistical power, thereby uncovering the molecular pathways involved; and (4) predict individual clinical trajectories through a ‘digital twin’ approach, using powerful machine learning techniques. 
This project has transformative potential by generating an unprecedented overview of the biological underpinnings of metabolic dysfunction in psychosis, promoting tailored prevention strategies and improved individual outcome prediction.

Metabolomics And Genomics Investigations of Psychosis and Cardiometabolic Comorbidity

Hjernen, et intrikat nettverk av milliarder av nevroner, fungerer som en organismes sentrale knutepunkt for å behandle informasjon og kontrollere komplekse atferder. Vår kunnskap om komplekse hjernefunksjoner er imidlertid betydelig begrenset av at det tidligere ikke har vært mulig å overvåke aktiviteten i store nevrale populasjoner  hos dyr som fritt utfører sin komplekse atferd.
To-foton-mikroskopi (2P) er i dag en av de mest kraftfulle teknikkene for storskala avbildning av nevrale aktiviteter av dyreatferd. En betydelig begrensning ved denne teknologien er at tradisjonelle 2P-mikroskop er store og krever at dyrene må være hodefiksert under objektivet for avbildning, på samme måte som mennesker må immobiliseres under MR- eller CT-skanning. For å overvinne denne begrensningen har forskere utviklet miniatyriserte 2P-mikroskop som kan festes stabilt på hodet til fritt bevegelige dyr, noe som muliggjør studier av nevral aktivitet under naturlig atferd. Til tross for betydelige teknologiske fremskritt gjenstår fortsatt kapasitetsbegrensninger i eksisterende miniatyriserte 2P-mikroskop, der antallet nevroner som kan registreres samtidig fortsatt ligger på hundretallet - bare en liten brøkdel av det totale antallet nevroner i en typisk mikrokrets i hjernen.
Vårt prosjekt tar sikte på å revolusjonere dette feltet ved å utvikle et neste-generasjons miniatyrisert 2P-mikroskop. Dette systemet integrerer flere teknologiske innovasjoner som samlet vil øke mikroskopets kapasitet for nevrale registreringer fra noen hundre nevroner til tusenvis av nevroner - en potensiell ti gangers forbedring sammenlignet med dagens beste teknologi. Dersom prosjektet lykkes, vil det nye mikroskopet muliggjøre en enestående skala av nevrale registreringer hos fritt bevegelige, adferdsutøvende dyr - et gjennombrudd som vil gi transformative innsikter i de grunnleggende nevrale beregningsprinsippene som gir opphav til høyere kognitive funksjoner.

To uncover the neuronal mechanisms underlying complex cognitive functions, neuroscientists need to understand how information is encoded in populations of neurons. This requires measuring large-scale neuronal activity at cellular resolution in animals exhibiting natural behaviors. The current state-of-the-art technologies are silicon probes and miniaturized two-photon microscopes, or 2P miniscopes. 2P miniscopes offer significant benefits over silicon probes in terms of spatial resolution and the ability to record from the same neuronal population over extended periods. However, the recording capacity of 2P miniscopes is currently limited to hundreds of neurons, which falls short of the thousands of neurons needed to decipher the neurocomputational mechanisms within brain microcircuits. To bridge this gap, a pivotal development direction for this technology is to substantially increase the number of neurons that can be simultaneously recorded. In this project, I aim to push these boundaries by creating a new 2P miniscope (MINI10K) by upgrading most core components and introducing new designs to record, simultaneously, thousands of neurons in freely moving mice, increasing the neuron recording capacity by an order of magnitude compared to existing systems. I will demonstrate the MINI10K’s capability by measuring the spatial organization and population dynamics of various spatial cell types in a large anatomical area of the entorhinal cortex which is a critical step toward understanding the mechanism of cognitive map formation in the mammalian brain. The project is transformative in that it will enable us to explore population coding with unprecedented throughput and without behavioral restrictions, paving the way for studying the nseuronal mechanisms of cognitive functions at the network level.

Miniature two-photon microscope for ultra-high-throughput calcium imaging in freely moving animals

Hovedmålet med prosjektet PrecisePrevent er å øke forståelsen av hvordan hjernes aldring kan begrenses gjennom tilgjengelige, kostnadseffektive, ikke-farmakologiske tiltak. Et sentralt spørsmål er hvilke personer som har størst nytte av hvilke tiltak, da det er store individuelle forskjeller i responsen på intervensjoner. Prosjektet vil undersøke sammenhengen mellom livsstilsfaktorer – som ernæring, søvn, fysisk aktivitet og kognitiv aktivitet– og hjernes helse i aldring.

Gjennom en kombinasjon av store, longitudinelle hjernescanningsstudier og en mega-analyse av syv eksperimentelle hjernehelseintervensjoner, har vi som mål å identifisere både generelle og individuelle faktorer som påvirker effekten av intervensjoner. Resultatene vil bli implementert i en digital, personlig tilpasset intervensjon på tvers av fire land, noe som gjør det mulig å teste hvordan livsstilsendringer påvirker hjernes aldring og kognitiv funksjon.

Vi vil utvikle individuelle prediktorer og mål for intervensjonen ved å analysere genetiske og ikke-genetiske faktorer, og anvende en tilnærming som gjør det mulig for deltagerne å velge sine egne mål og vurdere de antatte effektene på hjernehelse. For å møte utfordringen med å opprettholde livsstilsendringer, vil vi utvikle en plattform som optimaliserer kostnads-nytte-effektiviteten ved hjelp av maskinlæring.

Intervensjonsprogrammene vil bli levert gjennom en validert mobil helseplattform. Dette vil gjøre det mulig for oss å sammenligne effekten av personlige versus generelle tilnærminger, og bidra til utviklingen av et skalerbart, lavterskel intervensjonsrammeverk som kan brukes på tvers av Europa. Det overordnede målet er å oppnå samfunnsmessige gevinster gjennom flere mindre individuelle forbedringer i hjernehelse.

The main aim of PrecisePrevent is to contribute knowledge about how brain aging can be 
ameliorated through low-cost, easily accessible non-pharmacological means. There are large 
individual differences in response to interventions, and a crucial question regards who 
benefits the most from what? We will test the associations between lifestyle factors, including 
nutrition, sleep, physical and cognitive activity, and brain health in aging. We will leverage 
retrospective large-scale longitudinal brain imaging studies combined with mega-analysis of 
seven experimental brain health interventions. General and specific factors for individuals 
and interventions will be systematically mapped. The results will be implemented in a digital 
personalized intervention run across four countries. This allows us directly to test how much 
brain aging and cognitive function can be affected by lifestyle changes, and which variables 
that contribute to promote or restrict the effects. We will systematically estimate how much
benefits can be optimized using genetic and non-genetic factors to generate individual-level 
predictors and intervention targets. As lifestyle changes are difficult to sustain, we will, 
working with stakeholders and target-groups, develop a personalized intervention which 
allows participants to select their own targets and evaluate predicted effects on brain health. 
Machine learning will be used to optimize the cost-benefit balance. The personalized 
intervention programs will be delivered and assessed through an interactive mobileHealth 
platform, which we already have preliminary validated. This enables us to determine the 
increase in benefits from personalized vs. general intervention approaches. The aim is to 
develop a framework for a scalable low-threshold intervention feasible at a pan-European 
level. The rationale is that aggregation of modest individual benefits will result in substantial 
societal advantages.

Prevention of brain decline:general and individual factors influencing benefit from nutrition, physical activity and lifestyle interventions

Med økt levealder øker også forkomsten av demens. Tall fra Norge viser at omlag 1% av de under 70 har demens, mens tallet øker til nesten 50% hos de som er over 90år. Det anslås at omlag 40% av all demens kunne vært unngått ved forebygging.  TEIDe-prosjektet har som mål å framskaffe ny kunnskap om demensforebygging ved  følgende tilnærminger I) Prediktiv medisin: Nåværende modeller for å forutsi demensrisiko er vanskelige å bruke i primærhelsetjenesten og har begrensninger som mangel på ekstern validering og spesifisitet. Målet med dette prosjektet er å implementere skalerbare forebyggende screeningmetoder og endre paradigmet i demensomsorgen. II)Presisjonsmedisin: Fysisk inaktivitet er trukket fram som en viktig risikofaktor for å få demens. TEIDe vil identifisere  optimale treningsdosene og type trening  som gir kognitive fordeler basert på individuelle pasientkarakteristikker. Dette vil lette til rette for å kunne foreskrive skreddersydde treningsintervensjoner i primærhelsetjenesten. III) Mekanistisk tilnærming: Kunnskapen om hvordan treningsrelaterte  mekanismene  påvirker hjernens helse i voksen alder,  er begrenst, og dette hindrer utbredt bruk av trening som en terapeutisk eller forebyggende tilnærming for demens. TEIDe vil undersøke hvordan ulike typer trening forbedrer ulike aspekter ved kognitiv funksjon. IV) Klinisk tilnærming: TEIDe vil i gjennomføre en klinisk studie hvor vi skal teste gjennomførbarheten av å screene pasienter med høy risiko for demens, forskrive skreddersydd trening for disse risikopasienter, og implementere personlige treningsintervensjoner.

Dementia is a leading cause of disability globally. TEIDe will combine predictive, precision, mechanistic, and clinical application approaches for the effective prevention of dementia. Predictive medicine; At present models to predict dementia risk are based on factors like sociodemographic, cognitive, imaging, biomedical, and genetic variables. However, many scores are difficult to use in primary healthcare and have limitations such as lack of external validation and specificity.  The goal of this project  is to implement scalable preventive screenings and shift the paradigm in dementia care by (i) identify scores for all-cause and specific types of dementia using accessible data; (ii) validate these scores in different populations; and (iii) assess their feasibility for screening high-risk individuals in primary care. Precision medicine: Up to 40% of dementia cases may be prevented by targeting 12 key risk factors, including physical inactivity. However, research is needed to identify the optimal doses and types of exercise that confer cognitive benefits based on individual patient characteristics, which will facilitate the rapid prescription of tailored exercise interventions in primary healthcare. Mechanistic approach; The limited understanding of the mechanisms by which exercise impacts brain health in late adulthood hinders the widespread use of exercise as a therapeutic or preventive approach for dementia. Thus, research is needed to elucidate the mechanisms by which resistance or aerobic exercise improves cognition.  Clinical approach: There is a need to establish the real-life applications of these potential screening strategies and exercise interventions. TEIDe will test the feasibility of: (i) screening patients at high risk of dementia; (ii) prescribing tailored exercise for at-risk patients; and, (iii) implementing in-person exercise interventions based on defined prescription.

Tailored Exercise Interventions for Dementia Prevention: bridging research evidence and primary care practice.

In response to the urgent need for effective interventions in age-related cognitive dysfunction and dementia, our research proposal addresses the challenge of delayed treatment initiation and the potential of dietary interventions. We aim to prevent pathological brain aging and cognitive disorders by targeting brain metabolism early. Our pilot study adopts a double-blind, placebo-controlled design, focusing on older, frail individuals not yet affected by dementia. Central to our approach is nicotinamide adenine dinucleotide (NAD)-replenishment therapy using nicotinamide riboside (NR), aimed at enhancing neuronal resilience and resistance to cognitive disorder-related stresses.

We will leverage our clinical and translational expertise in trials, nutrition, metabolism, the gut microbiome, and neurodegeneration. Clinical endpoints, imaging, and biological samples will be collected to investigate the interplay between nutrition, the gut microbiome, host metabolism, cognitive function, and NR treatment response.

Our specific aims include assessing NR treatment’s efficacy in reducing physical and cognitive dysfunction in aging-related frailty, its potential to lower the risk of cognitive dysfunction and dementia, and analyzing individual variability in NAD bioavailability and clinical effects post-NR intake. We will also elucidate the gut microbiome’s role in NR and NAD metabolism and its impact on clinical responses, as well as NR treatment’s effects on microbiome composition and metabolism. Additionally, we will explore the relationship between dietary factors and cognitive function in large cohorts of older individuals.

Ultimately, this research promises to transform our approach to dementia and cognitive disorders, offering new pathways for innovative, nutrition-based therapeutic and preventive interventions that could change the landscape of treatment and prevention strategies for these debilitating conditions.

Boosting NAD metabolism to prevent pathological brain aging

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Professor

The project is concerned with the publication of a monograph the manuscript of which was originally a PhD thesis presented in 2010. Heavily revised, the monograph explores the contentious and often violence dynamics between processes of state ordering and  domains that remain external to the state in Mozambique. In this way the monograph maps new terrain theoretically and empirically within research not only on Mozambique but also on colonial and postcolonial Africa.

Given publication support the monograp h will be made available at the cost of around USD 90 and, thus, will in terms of price be made more accessible for prospective individual buyers as well as libraries than without the publication support. Put differently, fulfilling the aim of the applica tion would mean the research results presented in the monograph under contract would be disseminated considerably more effectively than if such support would not be forthcoming.

Publication grant for the monograph 'Violent Becomings. State Formation, Culture and Power in Mozambique'

Smart and CO2 neutral Olefin Production by arTificial Intelligence and MAchine Learning

The proposed project is to develop and maintain long term collaborations between Europe and China towards CO2 neutral Olefin production. We will realize this objective by carrying out joint research in big data and artificial intelligence (AI) for ethylene plants integrated with carbon capture and CO2 utilisation. Specifically this requires a universal set of skills such as pilot scale experimental study, process modelling and analysis, optimisation, catalysis and reaction kinetics that will be strengthened by the individual mobility of researchers between Europe and China.   There are 12 partners involved in OPTIMAL with 3 industrial partners. These partners are world leading in their respective research areas. OPTIMAL is planned to start from Aug. 2021 and will continue for 48 months. There will be 28 experienced and 35 early stage researchers participating in OPTIMAL with exchange visits of 262 person months. The funding of €772,800 will be requested from European Commission to support these planned secondments.  The European beneficiaries are experts at catalysis, CO2 utilisation, intensified carbon capture, reaction mechanism and kinetics & CFD studies, hybrid modelling, molecular simulation and dynamic optimisation, whilst the Chinese partners are experts at exergy analysis, process control and optimisation, solvent-based carbon capture & data-driven model development, deep reinforced learning based model free control, intelligent predictive control, physics-based reduced order model development, soft exergy sensor development and optimisation under uncertainty. Transfer of knowledge will take place through these exchange visits. We will generate at least 25 Journal publications and 25 Conference papers. 2 Special Issues will be established in leading journals such as Applied Energy. 2 Workshops and 2 Special Sessions in major international conferences will also be organised to disseminate project results.

Water Quality in Drinking Water Distribution Systems.

Safe drinking water is paramount for the health and wellbeing of all populations. Unsafe drinking water can contain pathogenic microorganisms and/or chemicals that can make people immediately unwell or can potentially cause serious illness over prolonged exposures. Within the EU, water is extracted from surface and groundwater sources and treated to comply with EU drinking water standards under the Water Framework Directive and Drinking Water Directive. The water is then circulated through the drinking water distribution system (DWDS). During travel within the DWDS, water quality can deteriorate due to microbiological growth, chemical reactions, interactions with ageing and deteriorating infrastructure, and through maintenance and repair activities.    Water utilities within the EU are administered at the local level, i.e. city or county region and while they adhere to the overarching EU directives governing quality, they can choose their own treatment protocols, maintenance procedures and hydraulic operations. Some DWDS actions such as flushing may serve to improve water quality, however, these can also adversely impact the drinking water system and cause instances of poor water quality or disease outbreaks.   We propose to bridge the gap between science and practice, involving water utilities and researchers from multiple locations across Europe along with third-country expertise, to examine DWDS operational practices and use scientific research approaches to better understand the water quality impact of different interventions to develop a suite of best practices which can be shared to ensure that the EU’s water remains clean and safe. We have assembled a multi-disciplinary, cross sectoral consortium to address various aspects of DWDS practices including flushing, chlorination and system maintenance.  

MAKERSPACES IN THE EARLY YEARS: ENHANCING DIGITAL LITERACY AND CREATIVITY  (MakEY) 

This two-year project involves an international and inter-sector research and training network that focuses on the potential of makerspaces, which are specific spaces that enable creative design and the production of both digital and non-digital artefacts, to foster the digital literacy and creative skills of young children. A key aim of the project is to inform educational policy and practice in this area, enabling formal learning institutions (early years settings and primary schools) to learn from practice in non-formal learning spaces, and vice-versa, and also to foster innovation and entrepreneurship in the makerspace sector, enabling SMEs to develop robust business models and appropriate resources for future work in this area. The project involves 16 academic and non-academic beneficiaries and 10 non-academic, non-beneficiary partners across 6 EU countries (Denmark, Finland, Iceland, Norway, Romania, UK), an Associated Country (Colombia) and 4 Third Countries (Australia, Canada, South Africa and USA). This global network of university scholars, cultural industry partners in makerspaces, early years practitioners, museum educators and librarians will engage in a collaborative research and training programme that addresses 4 objectives, which are to: 1. Conduct a comprehensive review of the role of makerspaces in the formal and non-formal educational experiences of children and young people. 2. Undertake empirical research to determine how makerspaces can foster the digital literacy and creativity skills and knowledge of young children. 3. Develop a conceptual framework for analysing young children’s engagement in makerspaces. 4. Make recommendations for policy and practice that will foster innovation and entrepreneurship in SME makerspaces and facilitate the use of makerspaces for enhancing digital literacy in early childhood educational institutions and non-formal learning spaces. 

0 projects

H20-MSCA-Marie Sklodowska-Curie actions

Smart and CO2 neutral Olefin Production by arTificial Intelligence and MAchine Learning

Awarded: NOK 1.1 mill.

Project Period: 2021-2025

Location: Trøndelag - Trööndelage

H20-MSCA-Marie Sklodowska-Curie actions

Water Quality in Drinking Water Distribution Systems.

Awarded: Hidden

Project Period: 2018-2019

Location: Trøndelag - Trööndelage

H20-MSCA-Marie Sklodowska-Curie actions

MAKERSPACES IN THE EARLY YEARS: ENHANCING DIGITAL LITERACY AND CREATIVITY (MakEY)

Awarded: NOK 0.33 mill.

Project Period: 2017-2019

Location: Oslo