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Limb wounds in horses are common, however healing is exceedingly slow and fraught with complications. Contrary to body wounds, limb wounds demonstrate only a small amount of wound contraction. The specialist procedure of applying split-thickness skin grafts to limb wounds stimulates wound contraction by unknown mechanisms. The objective of this project is to identify those mechanisms to develop a treatment strategy for equine limb wounds for use in general  practice. Limb wounds are severely impacting animal welfare due to an extended healing/treatment duration, and the risk of euthanasia due to a poor functional outcome. By stimulating wound contraction, healing time will be reduced, and the functional outcome improved, directly benefitting the welfare of wounded horse and reducing treatment cost for the owner. Aim: To identify dermal components stimulating wound contraction, and to develop this knowledge into future state-of-the-art treatment of equine limb wounds for use in general practice. Hypotheses: i) Application of dermal fractions to collagen gels seeded with equine fibroblasts will increase gel contraction in vitro; ii) Application of dermal fractions to experimental limb wounds in vivo, will increase wound contraction resulting in a faster healing time versus wounds treated by conventional methods. Methods: i) The contractile effect of different dermal components will be assessed in a collagen gel/ fibroblast model; ii) Identified dermal components will be tested in a standardized experimental limb wound model in vivo (n=5). Ultimately, results from this project are expected to improve wound treatment in horses, directly impacting animal welfare by reducing healing time and improving the functional outcome of wounded horses. This will also directly benefit horse owners and caretakers and making veterinarians able to offer better treatment solutions.

HESTEFORSK - Raskere og bedre sårheling hos hest med autologe hudkomponenter

The goal of the Bilingual Experiences, Cognitive Ageing and underlying Mechanisms (BECAME) project is to examine the functional neuroplastic mechanisms underlying mitigatory effects of bilingual experience on age-related cognitive decline. While evidence is available for structural brain changes supporting bilingualism-induced effects on cognitive aging (CA), functional mechanisms underlying such effects are not yet well understood. BECAME aims to fill this gap by investigating the trajectory of bilingualism-induced functional neuroplasticity across the adult lifespan (ages 18-85), crucially adopting an individual differences approach related to measurable degree of bilingual engagement. Importantly, although such benefits are thought to be rooted early in the lifespan, evidence for the timeframe and conditions of their early emergence is scarce. The choice of including the whole adult lifespan allows us to investigate these mechanisms and their emergence more directly from a lifespan perspective. I combine behavioral testing with brain recordings via electroencephalography (EEG). EEG is widely used in cognitive neuroscience to assess brain activity and the degree of communication between brain regions (functional connectivity) in response to stimuli and at rest. Combining behavioral and EEG modalities will allow me to test bilingualism’s effect on functional connectivity, as well as its consequences for functional efficiency, the minimum required neural activation to successfully perform a task. This will enable a detailed, evidence-based account of the protective effects observed in older-aged bilinguals, and how they are built from earlier life stages. By illuminating the relationship between multilingualism and resulting neurocognitive adaptations, BECAME will enable to capitalize on it as a health initiative, with manifold societal implications and the potential to be translated into actionable policies exploiting multilingualism to ameliorate effects of CA.

Bilingual Experiences, Cognitive Ageing and underlying Mechanisms

Hovedmålet med kreftbehandling er å eliminere kreftceller og dette er tradisjonelt oppnådd ved kirurgi, bruk av giftige medikamenter (cellegift) og stråling. En ny og betydningsfull tilnærming til kreftbehandling kalt immunterapi, har derimot fått mye oppmerksomhet det siste tiåret; Her forsøker leger og forskere å utnytte immunsystemet vårt for å målrettet  ødelegge kreftceller. En nøkkelaktør i denne banebrytende tilnærmingen er en gruppe «drapsmenn» i immunsystemet kjent som cytotoxiske T-lymfocytter (CTL-er). Disse cellene har en bemerkelsesverdig evne til å oppdage kreftceller ved å gjenkjenne unormale molekyler på overflaten av kreftcellene - molekyler som friske celler ikke har. Når CTL-er gjenkjenner kreftcellene ødelegger de dem ved å frigjøre giftige molekyler som initierer kreftcellenes selvdestruksjon. 
 
Selv om betydelige innsats har blitt dedikert til å forstå hvordan CTL-er aktiveres og hvordan de gjenkjenner kreftceller, vet vi mindre om de påfølgende hendelsene inne i kreftcellene som fører til deres død. Fra før vet vi at CTL-er kan initiere to forskjellige typer celledød i kreft: den første, kalt apoptose, er en stille og ordnet prosess der kreftcellene krymper og brytes opp uten å varsle immunsystemet; den andre, kalt pyroptose, er en mer dramatisk prosess som involverer dannelse av åpninger i cellemembranen, noe som fører til at cellene svulmer opp og sprekker. Under denne cellebristen blir innholdet inne i cellene frigitt i omgivelsene, og dette kan fungere som 'faretegn' som kan stimulere en sterkere immunrespons mot kreftcellene. Betydningen av denne cellebristen for å forsterke anti-tumorresponsene vil bli undersøkt i dette prosjektet. 
 
Videre er vi fascinert av muligheten for å avdekke ytterligere, ennå ukjente, former for celledød indusert av CTL-er. Utforsking av disse dødsrelaterte prosessene i kreftcellene kan potensielt øke effektiviteten av immunterapi og bidra betydelig i den pågående kampen mot kreft.

The primary goal of most cancer therapies is to induce cancer cell death. Immunotherapy relies on the cytotoxic activity of lymphocytes such as natural killer cells (NKs) and cytotoxic T lymphocytes (CTLs) to achieve this. While a significant amount of research in immunotherapy focuses on the events within cytotoxic lymphocytes or at the interface between cytotoxic lymphocytes and cancer cells, less is known about the molecular mechanisms that orchestrate cancer cell death, particularly in the case of CTL-mediated death.
CTLs are known to induce two types of cell death in cancer: non-inflammatory apoptosis and proinflammatory pyroptosis. Pyroptotic cancer cells release proinflammatory signals that attract immune cells to the tumor site, thereby enhancing the anti-tumor response. Cell lysis is a common outcome of pyroptotic cell death. It is unclear whether lysis can be decoupled from pyroptosis in cancer cells and whether the proinflammatory properties of pyroptotic cancer cell death depend on lysis. Moreover, it remains unknown whether CTLs can induce other forms of cell death in cancer, apart from apoptosis and pyroptosis.
Studying the mechanisms of CTL-mediated cancer cell death is challenging because CTLs selectively target cells expressing specific antigens. However, given the critical role of CTLs in immunotherapy, it is essential to deepen our understanding of CTL-induced cancer cell death.
This project aims to develop novel methodologies to investigate the death mechanisms that are initiated by CTLs. In addition, we will identify new pathways and mediators involved in CTL-induced cancer cell death. Furthermore, we will assess the contribution of proinflammatory cell death and lysis in promoting anti-tumor responses in vivo. Overall, this research will improve our knowledge of the molecular mechanisms of CTL-mediated cancer cell death and potentially reveal novel targets to enhance the efficacy of cancer immunotherapy.

T-cell-mediated proinflammatory cell death and lysis in cancer

En av de vanligste, men minst studerte, utfordringene med å bli eldre er problemer med å kommunisere. Mange eldre sliter spesielt med pragmatiske ferdigheter, som å forstå undertekst, eller tilpasse det de sier til personen de snakker med. 

La oss si at en lege må gi en alvorlig beskjed til en pasient. For å gjøre det litt lettere å takle, bruker legen vagere språk, som "kanskje" i stedet for "sannsynligvis". Mens yngre voksne ofte tar hensyn til høflighetsstrategier i måten de tolker det som blir sagt på, har eldre ofte vanskelig for å forstå når noen snakker indirekte. Mange eldre voksne har vanskelig for å forstå ikke-bokstavelig språk og kan misforstå alvorlighetsgraden av diagnosen. Dette kan påvirke beslutningen deres om behandling, noe som kan føre til utilsiktede konsekvenser. 

Siden god kommunikasjon er viktig både i viktige medisinske samtaler og i hverdagen, er det viktig at vi finner ut hva som gjør at eldre kan ha vansker med å forstå og bli forstått. RESILIENCE skal hjelpe til med denne utfordringen ved å samle data om praktiske, kognitive og språklige ferdigheter hos voksne i alderen 18-90 år over tid. Dette vil gi oss en stor mengde data om pragmatiske, kognitive og språk ferdigheter og gjøre det tilgjengelig for forskning. Med denne dataen som grunnlag har vi følgende mål: 

• Forstå hvordan praktiske evner endrer seg generelt gjennom voksenlivet. 
• Finne ut hvilke mekanismer som påvirker pragmatiske evner på forskjellige tidspunkter i livet.
 • Utvikle en teoretisk modell som forklarer hvordan pragmatiske ferdigheter endrer seg med alderen.
 • Lage algoritmer som kan forutsi hvordan pragmatiske evner vil utvikle seg for enkeltpersoner i årene som kommer. 
• Utvikle og teste et verktøy som kan måle pragmatisk helse (både pragmatiske ferdigheter og deres underliggende mekanismer), noe som kan åpne  for å iverksette tiltak. 

Dette vil gi oss muligheten til å forstå bedre hvordan folk kan utvikle pragmatisk resiliens gjennom livsløpet.

A cornerstone of human communication is our reliance on pragmatic skills to guide linguistic interactions (e.g., reasoning about others' mental states to bridge the gap between what is said and intended in conversation). However these skills are highly sensitive to age-related decline, leading to miscommunication and uninformed decision making in the older adult population. This raises an important question, one which has puzzled linguistics and psychologists for decades: if pragmatic competence is fundamental to communication, why do individuals vary so much in this capacity? 

Traditionally, psychologists have approached pragmatic competence from a cognitive angle, reasoning that individual differences in executive functions (i.e., the cognitive skills associated with goal-directed actions) are what underlie effective pragmatic behavior. In a similar vein, language scientists have taken a linguistic approach, reasoning that one’s language background (e.g., the frequency with which individuals shift between languages) shapes pragmatic skills by enhancing sensitivity to the communicative context. This focus on either cognitive or linguistic influences has resulted in two expansive yet disparate areas of research.

RESILIENCE will unite these disciplines to pursue a longstanding debate on what underlies pragmatic resilience and decline using a large-scale, interdisciplinary and longitudinal approach. By gathering data on adults' (ages 18-90) pragmatic, cognitive and language skills over multiple time points, we will develop a comprehensive theoretical model that explains how cognitive and linguistic systems interact to shape pragmatic competence as we age, and create algorithms that predict the trajectory of an individual’s pragmatic abilities in upcoming years. Based on these results we will design a multidimensional tool that detects the earliest signs of pragmatic deficits, leading to future interventions, allowing us to uncover the paths to pragmatic resilience.

Uncovering the paths to pragmatic resilience

Sink er et essensielt mikronæringsstoff som kreves for funksjonen til hundrevis av proteiner involvert i et bredt spekter av biologiske prosesser. Etter inntak av sink fra kosten reguleres nivåene i kroppen nøye gjennom absorpsjon, sekresjon og ekskresjon via spesialiserte proteiner, såkalte sinktransportører, i tarmen. Enhver ubalanse er skadelig for menneskers helse, spesielt er tarmen følsom for sinkfluktuasjoner, hvilket påvirker tarmbarrieren og kan føre til inflammatoriske sykdommer og kreft i tarmen. 
På molekylært nivå er de presise mekanismene som styrer funksjonen til de ulike sinktransportørene fortsatt uklare. Hos mennesker finnes det over tjue slike proteiner, og de fleste inneholder områder rike på aminosyren histidin. Disse histidinene mistenkes å spille en avgjørende rolle i å binde sink. Nylig oppdaget vi et enzym som modifiserer disse områdene ved å sette metylgrupper på histidin, og viste at metylerte histidiner har en lavere affinitet for sink. Dette prosjektet har som mål å identifisere nye mekanismer som regulerer sinknivåer gjennom histidinmetylering av sinktransportører, å utvikle forskningsverktøy for effektiv studie av histidinmetylering, og å legge grunnlaget for nye behandlinger av tarmsykdommer.

The delicate balance of zinc levels in the body is essential for human health. Zinc is absorbed and excreted via intestinal zinc transporter proteins, and perturbations of this process are associated with pathologies, including inflammatory diseases and cancers of the bowel. The precise molecular mechanisms regulating zinc transport, however, remain a major knowledge gap. Based on the recent discovery of an enzyme methylating histidine residues in zinc transporters, and drawing on preliminary findings which demonstrate reduced affinity of methylated histidines to zinc, this project aims to identify novel mechanisms regulating zinc homeostasis through histidine methylation. We will examine the regulation and effect of histidine methylation on zinc transport in intestinal cell culture and organoids, and examine how knockout of the methylhistidine-generating enzyme affects the integrity and pathology of the intestinal tract in mouse models. In addition, we will identify reader proteins specifically recognizing methylhistidines and develop anti-methylhistidine antibodies and inhibitors to use as tools for detection, enrichment, and inhibition of histidine methylation. Such tools are urgently needed by the international research community, as none are currently available commercially. Overall, this project will lead to great advances in the field of protein regulation, and may uncover novel mechanisms in intestinal zinc transport and pathology.

Zinc transport regulation through histidine methylation

Noen av oss tåler stressende livshendelser godt. Andre derimot utvikler vedvarende fysiske og psykiske plager som følger av stress. Hvor godt vi håndterer stress avhenger av et komplekst samspill mellom miljøfaktorer, sosiale forhold, biologisk sårbarhet og indre motstandskraft. Forskning på stressreaksjonene til dyr og pasientgrupper som til vanlig lever under mye stress viser at en gruppe signalstoffer i kroppen som aktiverer det samme hjernesystemet som cannabis – endocannabinoidene – kan begrense styrken på stressreaksjoner og bidra til at man raskere kommer seg til hektene. I dette prosjektet skal vi undersøke hvordan mestring av stress på kort og lang sikt henger sammen med nivåer av endocannabinoider i kroppen for å forstå hvorfor noen personer er mer motstandsdyktige mot stress enn andre. I den ene studien følger vi pasienter som skal gjennomgå en stressende, men veldig vanlig, situasjon: kirurgi. Her måler vi pasientenes opplevelse av stress, samt mentale og fysiske helse, fra tiden før til to år etter operasjonen og undersøker hvordan dette henger sammen med nivåene deres av endocannabinoider og andre stresshormoner. I den andre studien bruker vi data fra et eksperiment hvor deltakerne har blitt utsatt for psykososialt stress til å undersøke om endocannabinoidnivået deres påvirker hvordan de reagerer på stress, og om stresset i seg selv kan påvirke kroppens produksjon av endocannabinoider. Til syvende og sist er målet med studien å vurdere hvorvidt målinger av endocannabinoidnivåer kan brukes til å forebygge helseplager og til å evaluere behovet for økt oppfølging etter alvorlig stressende påkjenninger i livet.

In the face of major life stressors, some individuals cope well whereas others develop ill health and long-term adverse outcomes. Predicting who needs additional support in response to major life stressors is essential for targeted prevention and more efficient allocation of resources. The endocannabinoid system is emerging as a promising target for understanding vulnerability and resilience to stress. This system appears to buffer stress in two ways: by limiting the magnitude of the stress response, and by facilitating recovery after a stressful event. While the early findings are intriguing, they mainly stem from studies in rodents and small clinical groups with high stress burden. What role endocannabinoids have more globally for human resilience, health and well-being remains elusive. 

In this project we address this gap by leveraging comprehensive experimental and clinical data on two potent stress models: psychosocial stress and surgery. Drawing on these unique datasets, which combine experimental control with ecological validity, we will decipher how endocannabinoid levels influence people’s stress response and recovery across minutes, days, weeks and years. The project represents a novel directional shift for endocannabinoid research and will (i) determine the value of endocannabinoid levels as a biomarker to predict outcomes after surgery, (ii) quantify sex differences, (iii) assess endocannabinoid interplay with opioid analgesics, sex hormones and other stress markers (iv) spearhead open and reproducible science practices in endocannabinoid research, and (v) make this fine-grained and novel data available through an interactive web application. 

This project represents an ambitious effort to understand endocannabinoids’ role in stress resilience and will determine the value of endocannabinoids as a predictive biomarker and potential target for individualized treatment.

Deciphering endocannabinoid stress buffering in humans: 
Mechanistic and clinical investigations

WHeelchair Activity Monitoring project (WHAM)

Wheelchair users (WCU) are three to five times more inactive than the general population, leading to a high risk of developing preventable secondary conditions. Although physical activity (PA) guidelines have been specifically developed for WCU, we lack systematic approaches to implement them in practice, as well as valid algorithms to monitor PA change in WCU through sensor-based solutions. Accordingly, the overall scientific aim of the WHeelchair Activity Monitoring project (WHAM) is to advance PA research and practice in WCU by developing valid digital markers for monitoring of and providing feedback on PA, paving the way for implementation and intervention. I will accomplish this through combining the complementary research fields of 1) behavioural intervention studies focusing on increasing PA in WCU (core competence University of British Columbia, UBC; outgoing phase) and 2) sensor-based PA monitoring (core competence Norwegian University of Science and Technology, NTNU; returning phase – consolidated by non-academic placement at Maastricht Instruments, which develop research prototypes including PA monitors). WHAM’s scientific aim is achieved through three objectives: 1) Measure the effect of a pragmatic exercise intervention trial on self-reported physical activity levels and cardio-respiratory fitness, 2) Develop valid algorithms for tracking PA markers in WCU, and 3) Co-create a framework that outlines how PA can be conjointly monitored and provided feedback on in WCU. This fellowship will enable me to become established as an internationally recognized researcher in the field of “physical activity and disability”, while bringing together ongoing national disjointed research activities in this field. Altogether, my overall ambition is to contribute to reducing inequalities in daily-life participation among WCU compared to the rest of the population.

BOLD MINDS aspires to enhance the understanding of vulnerability factors underlying the emergence of borderline personality disorder (BPD), with an ultimate aim of increasing the potential for young individuals to receive early, evidence-based help when their mental health is at risk. BOLD MINDS will achieve this by investigating whether disruptions in two aspects of autobiographical memory (AM), narrative identity (NI) and involuntary AM (IAM), are associated with BPD features and problem behaviours in adolescents concurrently and over time. In doing so, BOLD MINDS will strengthen the understanding of mechanisms underlying the emergence of BPD in adolescence and lay a groundwork for developing evidence-based early interventions for BPD. While currently limited, the study of AM in this field is essential for two reasons. Firstly, because the aspects of AM under investigation, NI and IAM, are known to be involved in identity formation and emotion regulation which represent two key psychological processes that are disrupted in adults with BPD and are linked to problem behaviours such as self-harm and suicidality. Secondly, because promising research is emerging on the use of AM targets in the treatment of emotional disorder in adults, and provides a strong model for future treatment development with vulnerable adolescents. In addition, this timely research program aligns with calls from international organizations to prioritize early interventions to promote adolescent mental health. BOLD MINDS will adopt and adapt state-of-the-art ecological momentary assessment and analytical techniques and work at the crossroads of clinical and cognitive psychological perspectives, allowing for a multidimensional approach to understanding BPD vulnerability. Training-through-research and formalized training of the experienced researcher will prepare her for a permanent academic position and the founding of her own research lab specializing in AM and early interventions for BPD.

Borderline Personality Disorder: Memory and Identity in Adolescence

Per- og polyfluorerte stoffer (PFAS) er en stor gruppe menneskeskapte kjemikalier med høyt fluorinnhold som antas å ha negative helseeffekter. Kilder til PFAS kan være produksjon av vann-, varme- og flekkbestandige produkter og disse kjemikaliene er en del av hverdagen vår. PFAS påvirkning av biologiske systemer er ikke fullstendig forstått. Noen PFAS er antatt å øke risikoen for å utvikling av ikke-alkoholisk fettleversykdom (NAFLD) og øke risikoen for diabetes. 

For å forstå hvordan PFAS påvirker organene våre ønsker vi å bruke små laboratoriedyrkede organmodeller, kalt organoider. Disse miniatyrorganene kan dyrkes fra menneskelige stamceller og tilbyr et kontrollert miljø for å studere hvordan PFAS påvirker f.eks lever og bukspyttkjertelen vår, uten bruk av dyreforsøk.

For å studere helseeffekter må vi kunne måle nivået av biomolekyler som fettstoffer i leveren og hormoner i bukspyttkjertelen. Til dette trenger vi å utvikle analytiske verktøy for å måle effektene. Først vil vi bekrefte at når leverorganoidene eksponeres for enkelte PFAS-forbindelser utvikles det NAFLD-lignende sykdom ved å sammenligne den biokjemiske profilen (proteiner og metabolitter) til organoider av lever med PFAS-eksponerte organoider. Deretter vil vi utvide den analytiske verktøykassen for å undersøke hvilke metabolske veier som påvirkes, og om effekten er den samme i NAFLD-induserte og PFAS-eksponerte organoider. Vi vil også eksponere insulinproduserende bukspyttkjertelorganoider for PFAS for å undersøke effekten av PFAS på hormonproduksjon. Når effektene av PFAS-eksponering på lever- og bukspyttkjertel-organoider er etablert, vil organoidene bli samkultivert i en chip, og effektene av PFAS-eksponering vil bli undersøkt og sammenlignet med individuelle organoider.

Persistent organic pollutants (POPs) are believed to contribute to metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD) and type 1 diabetes. HE-POP aims to investigate the effects of per- and polyfluoroalkyl compounds (PFAS), a type of POPs), on organ function in a controlled environment.

Organoids are multicellular laboratory-grown miniature organs, that are grown from stem cells. HE-POP will use organoids to examine how PFAS affects our organs and develop cutting-edge bioanalytical tools and methodology to measure these effects using liquid chromatography-mass spectrometry. HE-POP hypothesizes that PFAS negatively affects organ function, as evidenced by changes in hormone and lipid levels characteristic of NAFLD and type 1 diabetes. 

Organoids offer a controlled environment to study the effects of PFAS on the liver and pancreas, without the use of animal models. HE-POP aims to gain evidence of the negative effects of PFAS on organ function through controlled experiments on organoids and aid in understanding the biological mechanisms underlying NAFLD and type 1 diabetes.

HE-POP has fundaments in UN sustainable development goals, specifically #3, #12, and #14/15, seeking an understanding of diseases with worldwide prevalence, and understanding how POPs affect our life and surroundings and help enable the right regulatory actions and replacement chemicals.

HE-POP: Studying the Health Effects of Persistent Organic Pollutants, Using Mass Spectrometry, Organoids, and Organ-On-A-Chip

Dette prosjektet, kalt Hukommelse for musikk, fokuserer på det økende antallet mennesker over hele verden som lever med demens, spesielt Alzheimer's sykdom (AD). AD starter typisk med hukommelsesproblemer og påvirker etter hvert daglige aktiviteter. Aktive musikkintervensjoner, spesielt sang, har vist positive effekter på humør, atferd og livskvalitet for personer med demens, men deres innvirkning på kognisjon er ikke godt forstått. Prosjektet har som mål å fylle dette kunnskapsgapet ved å studere effektene av å lære nye sanger på kognitiv, atferdsmessig og hjernemessig funksjon.

Studien vil omfatte hjemmeboende voksne over 65 år med AD fra Argentina, Østerrike og Norge. Deltakerne vil gjennomgå 5 måneder med intensiv musikalsk opplæring (to ganger i uken) og 5 måneder med minimal opplæring (en gang i måneden) i tilfeldig rekkefølge, med en to måneders pause imellom. Intervensjonene inkluderer å lære nye sanger med en personlig musikklærer. Generell kognisjon vil bli målt ved bruk av Alzheimer's Disease Assessment Scale - Cognitive (ADAS-cog), og hukommelse for musikk vil bli vurdert gjennom ulike metoder, inkludert atferdsoppgaver og hjerneaktivitet (EEG). Humør vil også bli evaluert i hver økt.

Målet er å inkludere 113 deltakere for å sikre pålitelig påvisning av meningsfulle effekter. Studien vil utforske hvordan humør og hukommelse for musikk bidrar til endringer i kognitive evner, og om disse effektene varierer basert på faktorer som kjønn, alder, AD-stadium, eller tidligere musikalsk opplæring og generell utdanning. Prosjektet vektlegger samarbeid mellom forskere, tjenesteytere og brukere for å sikre studiens relevans og anvendelighet.

The number of people living with dementia is increasing and is high in low, middle, and high-income countries. Alzheimer’s disease (AD), the most common type of dementia, manifests itself initially with cognitive impairment in memory domains, and later affects all activities of daily living. Active music interventions, particularly singing, can help to improve mood, behaviour problems, and quality of life. Too little is known about their effects on cognition, although some promising studies exist. The M4M project aims to fill this gap by measuring effects of learning new songs on clinical, behavioural and brain functioning. Specifically, M4M aims to examine changes in general cognitive functioning and memory for music in non-musician adults with AD undergoing intensive individual musical training based on singing novel songs, compared to minimal training.
        Home-dwelling adults with AD, 65 years or older, in 3 countries (Argentina, Austria, Norway), will receive 5 months of intensive intervention (2x/week) and 5 months of minimal intervention (1x/month), in random order, with a 2-month break in between. Interventions will entail learning new songs with an individual music teacher. At the end of each intervention period, general cognition will be measured with the Alzheimer's Disease Assessment Scale – Cognitive (ADAS-cog) by a person who is unaware of the intervention received. Memory for music will be tested with observations, behavioural tasks, and brain responses (EEG). Mood will be assessed in each session. We aim to include 113 participants; this will help us to reliably detect clinically meaningful effects. We will also examine how mood and memory for music lead to changes in cognitive abilities, and whether effects depend on sex, age, AD stage, or previous musical training or general education. M4M will be conducted in close collaboration between academic researchers, service providers, and service users to ensure relevance and applicability.

Memory for Music: Effects of individual intensive musical training based on singing in non-musicians with Alzheimer’s disease

Midlene fra FUNN-3-Tilskudd til ulønnet FoU-innsats fordelt på år

Midlene fra FUNN-3-Tilskudd til ulønnet FoU-innsats fordelt på fylker

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Daglig leder

28977 Utvikle parykkbunn

Despite impressive advances in almost every field of neuroscience, our understanding of brain function remains largely confined to its building blocks at the microscopic level, and to phenomenological descriptions at the macroscopic level. Transgenic mice  have provided neuroscience with countless correlations between microscopic and macroscopic levels, but because most gene knockouts have lacked regional and temporal specificity, insights into computational mechanisms remain scarce. Understanding how comp lex mental functions originate from electrical and chemical processes in brain cells requires an integrated systems-biological analysis focused on the intermediate level of neuronal microcircuits, where myriads of intricately connected neurons with differ ent properties act together. The greatest challenge for an intermediate-level analysis is the need to restrict genetic interventions in freely moving animals to particular brain regions and cell-types. Technologies for this purpose have been developed onl y recently. The aim of the present project is to exploit and improve these recent developments to understand computation in a prototype non-sensory cortex. Using the rat spatial representation system as an experimental model, we shall introduce molecular markers into specific cell types of the hippocampus and entorhinal cortex by stereotaxic injection of viral vectors. Viral vectors shall also be used to introduce transgenes that silence, activate or modify the target cells by interfering with their membr ane potential or their synaptic release machinery. Temporal specificity will be induced by expressing exogenous light-activated channels in target cells in rats implanted with a fiber optic probe connected to a laser source. Stimulation at specific wavele ngths can activate the channel protein at a time scale of milliseconds. This approach provides entirely new opportunities for determining the function of specific components of the hippocampo-entorhinal system.

Microcircuits for spatial representation in hippocampus and entorhinal cortex

The western Society epidemic of life-style-related disease is an impending threat to public health, as well as economy, and calls thus for effective, affordable treatment and prevention strategies. The project has the potential to identify the key cellula r and molecular mechanisms underlying the beneficial effects of physical exercise on heart, arteries, and skeletal muscle in the context of prevention and management of main public diseases through the combination of experimental, clinical and epidemiolog ical studies. Identifying the cellular and molecular mechanisms associated with aerobic fitness is important, because it may help us develop new and better methods to prevent and treat cardiovascular disease. The relationship between physical activity and  health has been studied using either a top-down or bottom-up strategy. The top-down approach starts by epidemiological studies, and then works its way towards identifying possible general physiological mechanisms. The bottom-up strategy begins by studyin g the basic molecular mechanisms induced by exercise training, and thence upwards to a coherent view of improved public health. Neither approach has alone been successful in establishing firm links between molecules and public health. There is a lack of a n integrative approach fighting the major public health issues of inactivity, overweight, metabolic syndrome and the subsequent cardiovascular disease/mortality and economical (and social) burden on the society in terms of treatment of life-style related disease. The main focus of the activity of the current project is to combine the two strategies into a more integrative approach bringing epidemiological, experimental and clinical expertise together in the battle against life-style related disease. The n ovelty of the suggested centre is the combination of studies of physical activity ranging from the largest health survey in an unselected population in the world (HUNT-1, 2, 3) all the way down to molecules.

EXERCISE IN MEDICINE: BIO-EPIDEMIOLOGY OF FITNESS AND CARDIOVASCULAR DISEASE

The mechanisms behind the development of PD are still obscure, but it is clear that PD is heterogeneous both in terms of cause, phenotype, progression, and response to treatment. Reproducible biomarkers for PD susceptibility and/or progression that are se nsitive and specific have long been sought, but have yet to be defined.
Several genetic causes for PD have now been determined and the G2019S LRRK2 (Park8) gene, which codes for leucine-rich repeat kinase 2 (Lrrk2), a large, multidomain protein with unkno wn function has also been found in Norwegian patients. This gene accounts for over 3% of all PD patients in Central Norway (Aasly et al. 2005) with an avarage start of disease of 58 years. In February 2007 there are between 60 and 100 known cases in this area carrying this mutation and about two third are so-called presymptomatic individuals. In addition there are also a large group of family members followed who do not carry the mutation. All known Park8 patients in Norway are followed clinically by one neurologist (Dr. Aasly). The patients are seen twice yearly (or more frequent if necessary), the asymptomatic family members are seen once a year. 
The annual screening includes:
- Longitudinal study of healthy carriers of Lrrk2 G2019S.
- Regular clinical  monitoring (Aasly)
- Updating of database, recording environmental criteria possibly relevant for PD onset and progression 
- Regular blood sampling (every year
In addition, done once:
- Cerebrospinal fluid (CSF) sample (by dr. Aasly)
- Regular brain MRI  

In case of adequate funding:
- volumetric MRI 
- cerebral SPECT or PET

Two control groups (50 sporadic PD cases and 25 healthy controls) are also included.

The blood and CSF samples will be analyzed with metabolomics and proteomics methods.
- CSF a-s ynuclein and filaments will be analyzed.
- The MAPK-pathway in leukocytes will be used. 

These parameters will probably in combination give important clues to the pathogenesis of PD.

The genetically-defined Parkinson's disease. A study of biomarkers in patients and healthy carriers of the Park8 G2019S mutation.

Regular physical activity promotes health. An inactive lifestyle may alter gene expression, influence negatively on several organ systems and thereby cause chronic disease and increase mortality. These conditions may be reversed by regular activity and in creased level of physical fitness. Physical activity and fitness also parallel QoL, reduced depression and improved social welfare. Patients with chronic pain report reduced physical function, lower muscular strength and aerobic fitness. There is an urgen t need to investigate these aspects in large scale epidemiological studies and in prospective cohort studies. Through the establishment of a long term interdisciplinary research collaborative with scientists from physical exercise, clinical research, epid emiology, outcome assessment, pharmacology and molecular biology at the Faculty of Medicine, NTNU including international collaborators, physical activity, pain and general health and genomics will be targeted. In the first phase of the collaborative, one  will scientifically investigate how physical activity may cause, modulate and prevent chronic pain, general health, major diseases as well as improvement of Quality of life (QoL). In the next phase the collaborative will embark on intervention studies. T he Nord-Trøndelag Health Survey (HUNT), the largest population based health study in Norway, is the basis for the collaboration in this phase of the research. The study material will consist of data from HUNT-2 and HUNT-3 (study I) supplied by two studies . One will test physical activity and capacity of a representative cohort of approximately 10000 participants (study II), a representative sample of HUNT-3. Furthermore, a prospective follow-up study (study III) of 3000 participants followed over a five y ear period, a representative draw from the 10000 cohort and HUNT-3. The overall goal is to establish a long lasting collaborative to investigate the effect of physical activity and capacity on health.

Physical activity and chronic pain in HUNT 3 - A prospective cohort study

The single most important factor for the correct functioning of genomes is that their coding information is maintained intact and transferred unperturbed to future generations. DNA repair is highly coordinated- and integrated with other fundamental cellul ar processes such as transcription, replication, cell-cycle control and apoptosis. Core elements of DNA repair has even been adapted as essential parts of the adaptive immune system in higher vertebrates. Thus, a fundamental understanding of the molecular  mechanisms underlying genomic maintenance is central to our understanding of regulation of genomic function. 
This project focuses on the repair of misincorporated bases, AP-sites (missing bases) and well as bases subject to simple chemical modifications . Collectively such damages amounts to about 10 000 events in the genome of each human cell/day. The major pathway for repair of such lesions is base-excision repair (BER), anthough alternative pathways, such as direct repair of alkylation lesions by the human AlkB homologues contribute significantly. Although the core factors and enzymatic steps of these pathways have been identified, we still lack information on regulatory steps, accessory proteins, potential bottle-necks, regulation and significance of  interactions, and function of posttranslational modifications. We also lack information on subnuclear localisation of the processes and recruitment of the various factors to the site of damage. Almost certainly several additional factors remain to be ide ntified. The strong background of our research group within mammalian DNA repair and genomic maintenance, extensive collaboration with leading groups both nationally and internationally, and in-house state-of the art technology within protein isolation, m ass spectrometry, molecular imaging, array technology and X-ray chrystallography indicate that we have the competence required to take on this important project within functional genomics.

The Interactomics of DNA Repair

This is (hopefully) an improved version of an earlier application to NFR that was reviewed as both "a high quality research program" and "poorly written and non-competitive". The comments from the reviewers have been used to revise the project.

Patient e ducation has become a task that is dictated by law in Norway and is one of the four main tasks of Norwegian hospitals. Despite this, there is a lack of research and researchers in this area. Based on a grant from the Central Norway Regional Health Authori ty, a researcher has been employed to build up the first research group on patient education in Norway and this application is for a project that will recruit two doctoral students that can be future researchers in this area.

The aim for the present proj ect is to develop a patient education intervention, study the effect and the cost benefit of this intervention and to explore the experience of the patients taking part in the intervention for two different patients groups, namely patients with chronic ob structive pulmonary disease (COPD) and rheumatic disease.

The projects will be done as two doctoral works from august 2007 to July 2010. The results will be published in international peer review journals and as PhD thesis.

FUNN-3-Tilskudd til ulønnet FoU-innsats

28977 Utvikle parykkbunn

Awarded: NOK 42,700

Funding scheme:

FUNN-3-Tilskudd til ulønnet FoU-innsats

Thematic Areas and Topics