Denna uppsats skall undersöka kopplingen mellan mental visualisering och ledarskap. Då tiderna förändras så ändras även rollen för en god ledare efter de nya förutsättningarna. Jag skall först undersöka vad som utmärker en ledarroll och vilka egenskaper som karktäriserar en god ledare. En sådan egenskap som jag tittar djupare på är mental visualisering; vart och hur är denna egenskap aktiv i en hjärna? Slutligen kommer jag försöka besavara hur eller om visualisering är en kritisk egenskap hos en god ledare. / This paper will examine the link between mental visualization and leadership. As times change so will also the role for a good leader change. I will first examine what distinguishes such a leadership and which qualities characterize a good leader. Futhermore, I will examine the possible problems  that might occur with using modern neuroscience techniques to identify the characteristics that are considered relevant for a good leadership. One such feature that I will examine closer is mental visualization. Where and how is this property active in the brain? Finally, I will try to answer how or if,  visualization is a critical characteristic of good leadership.

<p>The three evolutionarily related peptides neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) are ligands to at least five G-protein coupled receptors in mammals, which are denoted by numbers. NPY has many physiological effects including stimulation of appetite and regulation of circadian rhythm and blood pressure. This work describes the ancient origin of the NPY receptor genes as deduced from molecular cloning of six receptors in four distantly related vertebrate species. Three of the receptors have been functionally expressed <i>in vitro</i> to determine ligand binding properties. </p><p>The first Y2 receptor from any non-mammalian species was cloned from the chicken. The receptor was found to exhibit substantial structural and pharmacological differences to mammalian Y2, but showed similar anatomical distribution. </p><p>A receptor was cloned in a primitive vertebrate, an agnathan fish, the river lamprey <i>Lampetra fluviatilis</i>. Phylogenetic analyses indicated that it represents an orthologue to the ancestor of Y4 and the teleost subtypes Yb and Yc. </p><p>Three NPY receptors were cloned from a shark, the spiny dogfish <i>Squalus acanthias</i>. These were found to correspond to the three mammalian subtypes Y1, Y4 and y6, and was thereby the first complete Y1 subfamily in any species outside the mammalian lineage. This suggests that all three receptor subtypes arose in the common ancestor of sharks and mammals 420-450 million years ago. </p><p>The sixth described receptor was cloned from the zebrafish, <i>Danio rerio</i>, and was shown to have equal identity to all three mammalian Y1 subfamily receptors. Phylogenetic analyses including the shark and lamprey sequences suggested that Yb may represent a fourth Y1 subfamily gene.</p><p>It has previously been found that the genes for Y1, Y4 and y6 are located on separate chromosomes. Taken together, these results show that the NPY receptor family expanded by chromosomal duplications early in vertebrate evolution, prior to the origin of gnathostomes. This work will be important for the determination of the time points for the origin of the many functions of NPY as well as for the understanding of the processes that shaped the vertebrate genome.</p>

<p>Alzheimer’s disease (AD) is the most common cause of dementia. A characteristic feature of AD is the presence of amyloid plaques in the cortex and hippocampus of the brain. The principal component of these plaques is the amyloid-β (Aβ) peptide, a cleavage product from proteolytic processing of amyloid precursor protein (APP). A central event in AD pathogenesis is the ability of Aβ monomers to aggregate into amyloid fibrils. This process involves the formation of various Aβ intermediates, including protofibrils. Protofibrils have been implicated in familial AD, as the Arctic APP mutation is associated with enhanced rate of protofibril formation <i>in vitro.</i></p><p>This thesis focuses on Aβ aggregation and neurotoxicity <i>in vitro</i>, with special emphasis on protofibril formation. Using synthetic Aβ peptides with and without the Arctic mutation, we demonstrated that the Arctic mutation accelerated both Aβ1-42 protofibril- and fibril formation, and that these processes were affected by changes in the physiochemical environment. </p><p>Oxidation of Aβ methionine delayed trimer and protofibril formation <i>in vitro</i>. Interestingly, these oxidized peptides did not have the neurotoxic potential of their un-oxidized counterparts, suggesting that formation of trimers and further aggregation into protofibrils is necessary for the neurotoxic actions of Aβ. In agreement, stabilization of Aβ wild type protofibrils with the omega-3 (ω3) fatty acid docosahexaenoic acid (DHA) sustained Aβ induced neurotoxicity; whereas in absence of DHA, neurotoxicity was reduced as Aβ fibrils were formed. These results suggest that the neurotoxic potential of Aβ is mainly confined to soluble aggregated forms of Aβ, not Aβ monomer/dimers or fibrillar Aβ. </p><p>Stabilization of Aβ protofibrils with DHA might seem contradictory, as ω3 fatty acids generally are considered beneficial for cognition. However, we also demonstrated that DHA supplementation reduced Aβ levels in cell models of AD, providing a possible mechanism for the reported beneficial effects of DHA on cognitive measures <i>in vivo</i>.</p>

The three evolutionarily related peptides neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP) are ligands to at least five G-protein coupled receptors in mammals, which are denoted by numbers. NPY has many physiological effects including stimulation of appetite and regulation of circadian rhythm and blood pressure. This work describes the ancient origin of the NPY receptor genes as deduced from molecular cloning of six receptors in four distantly related vertebrate species. Three of the receptors have been functionally expressed in vitro to determine ligand binding properties. The first Y2 receptor from any non-mammalian species was cloned from the chicken. The receptor was found to exhibit substantial structural and pharmacological differences to mammalian Y2, but showed similar anatomical distribution. A receptor was cloned in a primitive vertebrate, an agnathan fish, the river lamprey Lampetra fluviatilis. Phylogenetic analyses indicated that it represents an orthologue to the ancestor of Y4 and the teleost subtypes Yb and Yc. Three NPY receptors were cloned from a shark, the spiny dogfish Squalus acanthias. These were found to correspond to the three mammalian subtypes Y1, Y4 and y6, and was thereby the first complete Y1 subfamily in any species outside the mammalian lineage. This suggests that all three receptor subtypes arose in the common ancestor of sharks and mammals 420-450 million years ago. The sixth described receptor was cloned from the zebrafish, Danio rerio, and was shown to have equal identity to all three mammalian Y1 subfamily receptors. Phylogenetic analyses including the shark and lamprey sequences suggested that Yb may represent a fourth Y1 subfamily gene. It has previously been found that the genes for Y1, Y4 and y6 are located on separate chromosomes. Taken together, these results show that the NPY receptor family expanded by chromosomal duplications early in vertebrate evolution, prior to the origin of gnathostomes. This work will be important for the determination of the time points for the origin of the many functions of NPY as well as for the understanding of the processes that shaped the vertebrate genome.

Alzheimer’s disease (AD) is the most common cause of dementia. A characteristic feature of AD is the presence of amyloid plaques in the cortex and hippocampus of the brain. The principal component of these plaques is the amyloid-β (Aβ) peptide, a cleavage product from proteolytic processing of amyloid precursor protein (APP). A central event in AD pathogenesis is the ability of Aβ monomers to aggregate into amyloid fibrils. This process involves the formation of various Aβ intermediates, including protofibrils. Protofibrils have been implicated in familial AD, as the Arctic APP mutation is associated with enhanced rate of protofibril formation in vitro. This thesis focuses on Aβ aggregation and neurotoxicity in vitro, with special emphasis on protofibril formation. Using synthetic Aβ peptides with and without the Arctic mutation, we demonstrated that the Arctic mutation accelerated both Aβ1-42 protofibril- and fibril formation, and that these processes were affected by changes in the physiochemical environment. Oxidation of Aβ methionine delayed trimer and protofibril formation in vitro. Interestingly, these oxidized peptides did not have the neurotoxic potential of their un-oxidized counterparts, suggesting that formation of trimers and further aggregation into protofibrils is necessary for the neurotoxic actions of Aβ. In agreement, stabilization of Aβ wild type protofibrils with the omega-3 (ω3) fatty acid docosahexaenoic acid (DHA) sustained Aβ induced neurotoxicity; whereas in absence of DHA, neurotoxicity was reduced as Aβ fibrils were formed. These results suggest that the neurotoxic potential of Aβ is mainly confined to soluble aggregated forms of Aβ, not Aβ monomer/dimers or fibrillar Aβ. Stabilization of Aβ protofibrils with DHA might seem contradictory, as ω3 fatty acids generally are considered beneficial for cognition. However, we also demonstrated that DHA supplementation reduced Aβ levels in cell models of AD, providing a possible mechanism for the reported beneficial effects of DHA on cognitive measures in vivo.

Transmembrane proteins are gatekeepers of the cells; controlling the transport of substrates as well as communicating signals among cells and between the organelles and cytosol. Solute carriers (SLC) and G protein-coupled receptors (GPCR) are the largest family of membrane transporters and membrane receptors respectively. The overall aim of this thesis was to provide a basic understanding of some of the novel SLCs and GPCRs with emphasis on expression, transport property, evolution and probable function. The first part of the thesis directs towards the study of some novel solute carriers. In an initial study, we provided an overall picture of the sequence relationship and tissue expression of 14 diverse atypical SLCs confirming some of their evolutionary conservation and highly specific expression pattern. The focus then was on the SLC17 family (mainly vesicular proteins) and a novel member named Slc17a9. This study revealed that SLC17 family could be divided into four main phylogenetic clades which were all present before the divergence of the insect lineage with Slc17a9 having the most restricted evolutionary history. Detailed expression study of Slc17a9 in the mouse brain suggests that it is also expressed in some regions important for purinergic neurotransmission. Further, we deorphanised an aminoacid transporter Slc38a7 which was expressed in a majority of neurons in the CNS and showed that it preferably mediate transport of L–glutamine and L–histidine. The second part of the thesis focuses on the study of two GPCRs belonging to the Rhodopsin superfamily, Gpr162 and Gpr153. A phylogenetic analysis revealed that both Gpr153 and Gpr162 originated from a common ancestor before the radiation of the mammalian lineage. Expression study revealed that Gpr162 had a predominant expression in the CNS and relatively lower expression in the other tissue tested whereas Gpr153 had a more widespread and similar expression pattern in both CNS and peripheral tissues. The functional studies of the two GPCRs were done using the antisense oligodeoxynucleotide knockdown rat model. These studies provided evidence linking the orphan Gpr162 gene with the regulation of food intake– related behaviour whereas Gpr153 gene caused only a slight reduction in food intake.

Hjärnans uppbyggnad och funktion besvarar många intressanta frågor när det kommer till undervisning och ett neurodidaktiskt perspektiv bidrar till att bättre förstå hur elever på gymnasienivå kan behärska de kunskaper som efterfrågas i Läroplan, examensmål och gymnasiegemensamma ämnen för gymnasieskola 2011. Studiens förutsättningar har legat inom ramen för tio veckors verksamhetsförlagd utbildning och har genomförts hösten 2017  tillsammans med två klasser som läser kursen Samhällskunskap 1a1 på Herrgårdsgymnasiet. Forskningsstrategin är en fåfallsstudie och teoriprövande som ämnat till att förklara varför ungdomar och neurodidaktik är en lyckad kombination. Studien har utgått ifrån följande frågeställningar:   1)      Vad upplever elever i årskurs två vara det bästa sättet att lära sig samhällsvetenskapliga begrepp på?   2)      Hur kan detta förklaras ur ett neurodidaktiskt läroperspektiv? Metoder för materialinsamling har varit enkäter och intervjuer och genom en mest-lika-design går resultatet att generalisera till en större population. Resultatet visar att eleverna tycks relatera mer till termer än begrepp och att de föredrar att arbeta två och två. Framför allt anser de flesta elever i studien att de lär sig bäst när läraren har en genomgång. Men läraren måste vara intressant, tydlig och använda sig av visuellt material för att inlärningen ska fungera bäst, enligt eleverna själva. Ett neurodidaktiskt lärarperspektiv handlar om att kunna anpassa – och självfallet utveckla – undervisningen till hjärnans biologiska konstruktion.

Syftet med detta arbete har varit att undersöka möjligheten att konkretisera hjärnforskningens rön i förhållande till historiedidaktiken för att finna sätt att öka elevers motivation inför historieämnet. En genomgång av relevant forskning om motivation, historiedidaktik samt neuro- och kognitionsvetenskap kopplad till pedagogik, det senare en del av hjärnforskningen, visar på betydande överlappning vad gäller metodiska rekommendationer. Den empiriska undersökningen hade som syfte att undersöka två elevgruppers uppfattningar om historieundervisning, speciellt med avseende på begrepp som är centrala inom motivationsforskningen: erfarenheter, förväntningar, meningsfullhet och nytta. Undersökningens resultat visar att elevgrupperna, som studerar vid ettnaturbruksgymnasium, hade ganska höga förväntningar på ämnet historia. Trots detta varmåluppfyllelsen i kursen bristfällig. Detta arbete argumenterar för att hjärnforskningens rön kan användas för att belägga vissa didaktiska metoders effektivitet. Slutsatsen är dock att flera pedagogiska perspektiv måste kombineras för att skapa inre motivation, vilket kan öka elevens måluppfyllelse i ämnen som eleven initialt inte är intresserad av.

Spanska är idag det mest lästa av de valbara språken i den svenska skolan, men liksom de andra moderna språken lider spanskaämnet av problem med avhopp och motivation. Eleverna uppfattar språken som svåra, och inte så användbara.  Syftet i uppsatsen är att analysera och tolka styrdokumenten som gäller spanska på gymnasiet och kommunala vuxenutbildningen, samt konkreta exempel från undervisningsämnet spanska, från en ny kontext. Neurovetenskap och neuropsykologi används idag inom många områden där man vill arbeta med motivation, beteendedesign och förändringsprocesser. En förståelse för hur hjärnan fungerar har på andra områden lett till metoder, som också skulle kunna användas i skolan.  Arbetet utgår från ett analytiskt perspektiv, för att genom en kvalitativ analys tolka ämnesplan, läroplan, exempel från läroböcker, samt konkreta svårigheter i spanska språket i en undervisningssituation. Genom att analysera dessa från en ny kontext av beteendevetenskap och neurovetenskap vill jag dels undersöka om moderna kunskaper om hjärnan finns avspeglade i styrdokumenten, och dels hur dessa kan användas inom spanska som undervisningsämne.  Resultaterna från undersökningen visar att det finns en potential att styrka styrdokumenten och tala mer om hur undervisningen skall ske, istället för bara om vad som skall undervisas. Tekniker från beteendevetenskap och neuropsykologi kan också användas inom lärandet av moderna språk och spanska. Det finns goda möjligheter att styrka undervisningsämnet spanska och moderna språk genom att tillföra dessa kunskaper och denna erfarenhet.

<p>Patients suffering from different forms of neurodegenerative diseases, such as: Creutzfeldt Jacob Disease (CJD), Alzheimer disease (AD), mild cognitive impairment (MCI), frontotemporal dementia and Parkinson’s disease (PD) were examined with Positron Emission Tomography (PET) and the combination of different radiotracers: ¹⁵O-water, N-[¹¹C-methyl]-L-deuterodeprenyl (DED), [¹⁸F] 2-fluorodeoxyglucose: (FDG), N-methyl-[¹¹C]2-(4-methylaminophenyl)-6-hydroxybenzothiazole (PIB) and L-[¹¹C]-3,4-dihydroxiphenyl-alanine (DOPA). The radiotracers and the combinations of different radiotracers were selected with the intention to detect, in the brain, patterns of neuronal dysfunction, astrocytosis, axon degeneration or protein aggregation (amyloid), in the brain which are pathognomonic for specific diseases and may contribute to improve clinical differential diagnoses. Examinations in healthy volunteers were performed to allow comparisons with patients. In addition, animal studies were conducted to complement the information. In some cases, the PET findings could be compared with the results of autopsies.</p><p>In contrast to the micropathology, in which only a limited part of a tissue (obtained post-mortem or by biopsy) is inspected, one PET acquisition provides an image of the whole system (e.g.: the brain and the cerebellum). This form of imaging pathology is “<i>in vivo</i>”, where the examination is innocuous for the patient. </p><p>This thesis is an attempt to stimulate the development of new tracers, new tracer combinations and methods that directly or indirectly describe the anatomo-physiopathological changes produced in the brain in neurodegenerative diseases. A better description of different diseases can be obtained, confirming or questioning the clinical diagnoses and widening our understanding of the mechanisms underlying neurodegeneration. Different pathologies can produce similar symptoms and thus causing confusion regarding clinical diagnosis. The used PET combinations improved the accuracy of the diagnoses. The incipient knowledge emerging from a new neuroimaging pathology in combination with other disciplines may open the way to new classifications of dementias and neurodegenerative diseases based on an “<i>in vivo</i>” pathology. </p>