In study 1, thirty-eight healthy controls were used for optimization of the method. Fifteen patients with progressive supranuclear palsy and an equal number of age-matched healthy controls underwent diffusion tensor MRI and were then investigated and compared groupwise. It was shown that tractography analyses may preferably be performed regionally, such as along the tracts or in different segments of the tracts. Normalization of white matter tracts can be performed using anatomical landmarks. In study 2, 104 males and 153 females in the age interval 13 to 84 years of age participated as healthy individuals in order to investigate age-related changes with diffusion tensor MRI. It was shown that spatially differences in age-related changes exist between subdivided segments within white matter tracts. The aging processes within the CB and the IFO vary regionally. In study 3, 38 human brains were used for investigation of the white matter tract inferior longitudinal fasciculus (ILF) and its subcomponents. Of these, white matter anatomical dissection was performed in 14 post-mortem normal human brains. The remaining 24 brains were investigated in vivo with diffusion tensor MRI in healthy individuals. It was validated that fibers of the ILF in the occipito-temporal region have a clear, constant and detailed organisation. The anatomical connectivity pattern, and quantitative differences between the ILF subcomponents, confirmed a pivotal role of the ILF. In study 4, 12 patients with iNPH were included in the study and examined with diffusion tensor at three time points. For comparison, 12 healthy controls, matched by gender and age were also included. Controls were examined with MRI only once. It was shown that DTI measures differ significantly between patients with iNPH and healthy controls. DTI measures of the CC, the CST and the SLF, correlated to changes in clinical symptoms after shunt surgery. Deeper knowledge about functions of the brain increases possibilities to take advantages from DTI analyses with tractography.

Language skills increase as the brain matures and language specialization is linked to the left hemisphere. Among distinct language domains, sentence comprehension is particularly vital in language acquisition and, by comparison, requires a much longer time-span before full mastery in children. Although accumulating studies have revealed the neural mechanism underlying sentence comprehension acquisition, the development of the brain’s gray matter and its relation to sentence comprehension had not been fully understood. This thesis employs structural magnetic resonance imaging and diffusion-weighted imaging data to investigate the neural correlates of sentence comprehension in preschoolers both cross-sectionally and longitudinally. The first study examines how cortical thick- ness covariance is relevant for syntax in preschoolers and changes across development. Results suggest that the cortical thickness covariance of brain regions relevant for syntax increases from preschoolers to adults, whilst preschoolers with superior language abilities show a more adult-like covariance pattern. Reconstructing the white matter fiber tract connecting the left inferior frontal and superior temporal cortices using diffusion-weighted imaging data, the second study suggests that the reduced cortical thickness covariance in the left frontotemporal regions is likely due to immature white matter connectivity during preschool. The third study then investigated the cortical thickness asymmetry and its relation to sentence comprehension abilities. Results show that longitudinal cortical thick- ness asymmetry in the inferior frontal cortex was associated with improvements in sentence comprehension, further suggesting the crucial role of the inferior frontal cortex for sentence comprehension acquisition. Taken together, evidence from gray and white matter data provides new insights into the neuroscientific model of language acquisition and the emergence of syntactic processing during language development.

No description available.

During adolescence, the brain undergoes significant reorganization due to myelination and synaptic pruning. These changes are associated with risk-taking behaviors and the development of social relationships. Recent advancements in adolescent brain development can potentially enhance strategies for preventing and treating mental health disorders. This systematic review focuses on structural changes in the adolescent brain, specifically emphasizing a decrease in gray matter and an increase in white matter changes. Four longitudinal MRI studies were included in this systematic review to identify changes in brain volume among healthy adolescents with an age range of 10 to 19 years. The results revealed observable changes in gray and white matter volume in various brain regions during this period. A decrease in gray matter was observed in the frontal, temporal, and parietal cortex, and several subcortical regions. Contrary to our expectations, the amygdala displayed an increase in gray matter in early adolescence. We expected this findings to occur in late childhood. The results also indicated that males undergo more significant changes in the brain during this period than females. Considering the Social Process Network (SIPN) and triadic model, changes occurring in the frontal cortex and the amygdala could be linked to social behavior. While the changes in the thalamus, hippocampus, and amygdala may be linked to heightened risk-taking and mental health disorders. Further research is necessary to clarify the relationship between mental health disorders, behaviors, and developmental processes during adolescence.

No description available.

While evidence suggests there is indeed a relationship between arterial stiffness and changes in brain structure and function cross-sectionally, the longitudinal relationship between arterial stiffness and changes in brain structure and function is unclear. Also unclear is whether a regional effect of arterial stiffness on brain structure exists, or if the effect is homogenous across brain regions. Using a healthy cohort of the UK Biobank study (N = 1858, meanSD: 61  7 years), we investigated the longitudinal association between changes in arterial stiffness index (ASI) and brain structure (grey matter cortical thickness, whole brain grey matter volume, white matter hyperintensity volume) and function (cognitive performance in 6 tests) over 2.5  1 years. We also examined the association between baseline ASI and all structural and functional brain outcomes 8-11 years post-baseline (N = 630). Prior to post-hoc correction, we observed a significant effect of changes in ASI over 2.5  1 years on grey matter cortical thickness in 11 brain regions contributing to reductions between 0.0004-0.0024mm annually, but none of the 11 regions remained significant post-correction. Following correction there was also no effect of changes in ASI on whole brain grey matter volume (p = 0.76), white matter hyperintensity volume (p = 0.84), or cognitive performance in the domains of interest. Baseline ASI was not associated with regional grey matter cortical thickness, white matter hyperintensity volume, or cognitive function, but did have a significant negative association with whole brain grey matter volume 8.5  1.05 (p = 0.015) years later and 11  1.02 (p = 0.03) years later. Our findings suggest that taken with the effect of age, elevations in ASI may have an additive effect to accelerate changes in brain structure beyond the range that is to be expected as a part of normal aging. Our findings also suggest the relationship between ASI and reductions in whole brain grey matter volume may require long-term exposure to elevations in arterial stiffness in otherwise healthy older adults. / Thesis / Master of Science in Kinesiology / Arterial stiffening both accompanies the normal aging process and can progress due to acquired health conditions. As arteries begin to stiffen the ability to buffer high pressure blood flow is impaired and can put microvasculature at risk of damage. Microvascular damage in the brain can disrupt blood and subsequent oxygen delivery to the brain. When delivery to the brain does not meet the metabolic demand, changes in brain structure brain can occur. Changes in brain structure are associated with impaired brain function, as well as potentially accelerating the progression of neurological diseases. What remains unclear is whether arterial stiffness impacts brain structure differently across regions or all regions homogenously. The purpose of this thesis was to examine the relationship between arterial stiffness and structural and functional changes in the brain over time (objective 1: 2-5 years; objective 2: 8-11 years). Our observations suggest that the progression of arterial stiffness had an effect that was equivalent to approximately 30% of the rate of grey matter tissue loss associated with normal healthy aging (~0.25% reduction in grey matter per year). We found no effect of changes in arterial stiffness on the progression of total grey matter volume, white matter lesions or brain function. We did observe a significant negative relationship between arterial stiffness at baseline and total grey matter volume 8-11 years later. We found no relationship between baseline arterial stiffness and brain structure or function 8–11-years post-baseline. Taken with the effects of normal aging, the loss of tissue in select brain regions associated with changes in arterial stiffness may result in grey matter reductions beyond the range associated with what is considered healthy or normal aging. The association of arterial stiffness and total grey matter volume 8-11 years later suggests that changes in whole brain structure are the product of long-term exposure to arterial stiffness.

Accurate delineation of anatomical structures in the white matter of the human brain is of paramount importance for multiple applications, such as neurosurgical planning, characterization of neurological disorders, and connectomic studies. Diffusion Magnetic Resonance Imaging (dMRI) techniques can provide, in-vivo, a mathematical representation of thousands of fibers composing such anatomical structures, in the form of 3D polylines called streamlines. Given this representation, a task of invaluable interest is known as white matter bundle segmentation, whose aim is to virtually group together streamlines sharing a similar pathway into anatomically meaningful structures, called white matter bundles. Obtaining a good and reliable bundle segmentation is however not trivial, mainly because of the intrinsic complexity of the data. Most of the current methods for bundle segmentation require extensive neuroanatomical knowledge, are time consuming, or are not able to adapt to different data settings. To overcome these limitations, the main goal of this thesis is to develop a new automatic method for accurate white matter bundle segmentation, by exploiting, combining and extending multiple up-to-date supervised learning techniques. The main contribution of the project is the development of a novel streamline-based bundle segmentation method based on binary linear classification, which simultaneously combines information from atlases, bundle geometries, and connectivity patterns. We prove that the proposed method reaches unprecedented quality of segmentation, and that is robust to a multitude of diverse settings, such as when there are differences in bundle size, tracking algorithm, and/or quality of dMRI data. In addition, we show that some of the state-of-the-art bundle segmentation methods are deeply affected by a geometrical property of the shape of the bundles to be segmented, their fractal dimension. Important factors involved in the task of streamline classification are: (i) the need for an effective streamline distance function and (ii) the definition of a proper feature space. To this end, we compare some of the most common streamline distance functions available in the literature and we provide some guidelines on their practical use for the task of supervised bundle segmentation. Moreover, we investigate the possibility to include, in a streamline-based segmentation method, additional information to the typically employed streamline distance measure. Specifically, we provide evidence that considering additional anatomical information regarding the cortical terminations of the streamlines and their proximity to specific Regions of Interest (ROIs) helps to improve the results of bundle segmentation. Lastly, significant attention is paid to reproducibility in neuroscience. Following the FAIR (Findable, Accessible, Interoperable and Reusable) Data Principles, we have integrated our pipelines of analysis into an online open platform devoted to promoting reproducibility of scientific results and to facilitating knowledge discovery.

Motivated by the rising prevalence of obesity worldwide and the global need for greater sustainability, I dedicated this dissertation to exploring new perspectives on food decision-making and to advancing neuroimaging and food-related research methods. Despite the awareness that unfavourable food choices can have serious long-term consequences on individual health and on the environment, people often struggle to break out of their dietary habits. Vicious cycles seem to inhibit individuals from shifting to healthier, more sustainable diets. Successful therapies and policies are required to prevent the pandemic development of obesity. Hence, there is an acute need to understand the complex mosaic of food choices, including cognitive, physiological and neuroanatomical factors. Using a randomized controlled trial (RCT) and diffusion-weighted magnetic resonance imaging (DWI), I was able to uncover a so far undetected potentially vicious cycle of reward-enhanced and calorie-biased food recognition memory. Consequently, the reward- and calorie-bias combined with the over-representation of high-caloric food in our environment might be inhibiting healthier food choices. On the neural level, I assessed the microstructural coherence of the uncinate fasciculus (UF) which connects reward with memory brain areas. The UF's coherence did not influence the enhancement of memory by 'desire-to-eat' in our healthy, overweight study participants. Weight-loss interventions could profit from reward-enhanced memorability by promoting the desire to eat healthier food options. In obese individuals, though, white matter coherence is often decreased and could counteract the success of such interventions. To facilitate and encourage further research on eating behaviour and interventions, I co-developed methodological advancements such as food-related tasks for MRI use, an open-access stimulus database, a tool to evaluate nutrient intake, and the extension of a food picture database by important characteristics. As DWI revealed to be noise- and artefact-sensitive, I also aimed to optimize DWI processing pipelines, namely artefact reduction and white matter skeleton reconstruction. Replicability and sustainability efforts in this dissertation are reflected in the choice of statistical tools and application of Open Science practices.:1 Introduction 1.1 The scope of food decisions 1.1.1 Individuals and their well-being and health 1.1.2 Societal well-being and functioning 1.1.3 Environment and climate change 1.2 The cognition of food decisions 1.2.1 Neural mechanisms of food choices 1.2.2 Food decision-making in obesity 1.3 The research on food decision-making—Methods and Tools 1.3.1 Assessing dietary habits and food intake 1.3.2 Functional neuroimaging 1.3.3 Experimental stimuli 1.3.4 Diffusion-weighted imaging of brain microstructure 1.3.5 Statistical Analysis 1.4 Interim Summary 2 Publications 2.1 art.pics Database: An Open Access Database for Art Stimuli for Experimental Research. 2.2 Same Brain, Different Look?—The Impact of Scanner, Sequence and Preprocessing on Diffusion Imaging Outcome Parameters. 2.3 Nutrient scoring for the DEGS1-FFQ—from food intake to nutrient intake. 2.4 Neurocognitive predictors of food memory in healthy adults—a preregistered analysis. 3 Conclusions Summary Neurocognitive determinants of food memory Implications for the obesity pandemic DWI in Neuroimaging Stimuli in Neuroimaging Food and nutrient intake assessment Open Science and Sustainability References Darstellung des eigenen Beitrags Erklärung über die eigenständige Abfassung der Arbeit Curriculum vitae Verzeichnis der wissenschaftlichen Veröffentlichungen und Vorträge Danksagung / Motiviert durch die steigende Prävalenz von Adipositas weltweit und den globalen Bedarf an mehr Nachhaltigkeit widmete ich diese Dissertation der Erforschung neuer Perspektiven auf Essentscheidungen und der Weiterentwicklung von Methoden zur Hirnbildgebung und Erforschung von Ernährung. Obwohl bekannt ist, dass ungünstige Nahrungswahl langfristig gravierende Folgen für die individuelle Gesundheit und die Umwelt haben kann, fällt es Menschen oft schwer, ihre Ernährungsgewohnheiten zu ändern. Teufelskreise scheinen Individuen daran zu hindern, zu gesünderen, nachhaltigeren Ernährungsweisen zu wechseln. Erfolgreiche Therapien und politische Maßnahmen sind erforderlich, um den globalen Anstieg von Adipositas zu verhindern. Daher besteht ein akuter Bedarf, das komplexe Mosaik der Essentscheidungen zu verstehen, einschließlich kognitiver, physiologischer und neuroanatomischer Faktoren. Durch eine randomisierte kontrollierte Studie und diffusionsgewichtete Magnetresonanztomographie (dwMRT) konnte ich einen bislang unentdeckten potenziellen Kreislauf des belohnungsverstärkten und kalorienverzerrten Lebensmittelgedächtnis aufdecken. Diese Kombination aus Belohnungs- und Kalorienbias, zusammen mit der Überrepräsentation hochkalorischer Lebensmittel in unserer Umgebung, könnte gesündere Essentscheidungen behindern. Auf neuronaler Ebene evaluierte ich die mikrostrukturelle Kohärenz des Fasciculus uncinatus (FU), der Belohnungs- mit Gedächtnisarealen des Gehirns verbindet. Die Kohärenz des FU hatte keinen Einfluss auf die Verstärkung des Gedächtnisses durch das „Verlangen zu essen“ bei unseren übergewichtigen Studienteilnehmenden, da deren Nervenfasern noch gesund waren. Gewichtsreduktionstherapien könnten daher von der belohnungsverbesserten Einprägsamkeit profitieren, indem sie das Verlangen nach gesünderen Nahrungsmitteln fördern. Bei Personen mit Adipositas ist die Kohärenz der weißen Substanz jedoch oftmals verringert, was den Erfolg solcher Interventionen schon beeinträchtigen könnte. Um weitere Forschung zu Essverhalten und Interventionen zu erleichtern und zu fördern, entwickelte ich Methoden wie Aufgaben zu Essentscheidungen und Essensgedächtnis für die Verwendung im MRT, eine öffentlich zugängliche Stimulusdatenbank, ein Tool zur Auswertung der Nährstoffaufnahme und die Erweiterung einer Lebensmitteldatenbank um wichtige Merkmale. Da sich dwMRT als anfällig für Rauschen und Artefakte erwies, hatte ich auch das Ziel, die dwMRT-Verarbeitungs-Pipelines zu optimieren, insbesondere die Artefaktreduzierung und die Rekonstruktion der Nervenbahnen der weißen Substanz. Die Reproduzierbarkeits- und Nachhaltigkeitsbemühungen dieser Dissertation spiegeln sich in der Wahl der statistischen Methoden und der Anwendung von Open-Science-Praktiken wider.:1 Introduction 1.1 The scope of food decisions 1.1.1 Individuals and their well-being and health 1.1.2 Societal well-being and functioning 1.1.3 Environment and climate change 1.2 The cognition of food decisions 1.2.1 Neural mechanisms of food choices 1.2.2 Food decision-making in obesity 1.3 The research on food decision-making—Methods and Tools 1.3.1 Assessing dietary habits and food intake 1.3.2 Functional neuroimaging 1.3.3 Experimental stimuli 1.3.4 Diffusion-weighted imaging of brain microstructure 1.3.5 Statistical Analysis 1.4 Interim Summary 2 Publications 2.1 art.pics Database: An Open Access Database for Art Stimuli for Experimental Research. 2.2 Same Brain, Different Look?—The Impact of Scanner, Sequence and Preprocessing on Diffusion Imaging Outcome Parameters. 2.3 Nutrient scoring for the DEGS1-FFQ—from food intake to nutrient intake. 2.4 Neurocognitive predictors of food memory in healthy adults—a preregistered analysis. 3 Conclusions Summary Neurocognitive determinants of food memory Implications for the obesity pandemic DWI in Neuroimaging Stimuli in Neuroimaging Food and nutrient intake assessment Open Science and Sustainability References Darstellung des eigenen Beitrags Erklärung über die eigenständige Abfassung der Arbeit Curriculum vitae Verzeichnis der wissenschaftlichen Veröffentlichungen und Vorträge Danksagung

Temporomandibular disorders (TMD) are a family of prevalent chronic pain disorders affecting masticatory muscles and/or the temporomandibular joint. There is no unequivocally recognized peripheral aetiology for idiopathic TMD. The central nervous system (CNS) may initiate and/or maintain the pain in idiopathic TMD due to sustained or long-term nociceptive input that induces maladaptive brain plasticity, and/or to inherent personality-related factors that may reduce the brain's capacity to modulate nociceptive activity. The main aim of this thesis is to determine whether there are structural neural abnormalities in patients with TMD, and whether these abnormalities are related to TMD pain characteristics, or to neuroticism. The specific aims are to delineate in TMD: (1) gray matter (GM) brain abnormalities and the contribution of pain and neuroticism to abnormalities; (2) the contribution of abnormal brain GM aging in focal cortical regions associated with nociceptive processes; and (3) abnormalities in brain white matter and trigeminal nerve and the contribution of pain. In groups of 17 female patients with TMD and 17 age- and sex- matched controls, magnetic resonance imaging revealed that patients with TMD had: (1) thicker cortex in the somatosensory, ventrolateral prefrontal and frontal polar cortices than controls, (2) cortical thickness in motor and cognitive areas that was negatively related to pain intensity, orbitofrontal cortical thickness that was negatively correlated to pain unpleasantness, and thalamic GM volume correlated to TMD duration, (3) an abnormal relationship between neuroticism and orbitofrontal cortical thickness, (4) abnormal GM aging in nociceptive, modulatory and motor areas, (5) widespread abnormalities in white matter tracts in the brain related to sensory, motor and cognitive functions, (6) reduced trigeminal nerve integrity related to pain duration, and (7) abnormal connectivity in cognitive and modulatory brain regions. In sum, this thesis demonstrates for the first time abnormalities in both peripheral nerve and CNS in patients with TMD.

Temporomandibular disorders (TMD) are a family of prevalent chronic pain disorders affecting masticatory muscles and/or the temporomandibular joint. There is no unequivocally recognized peripheral aetiology for idiopathic TMD. The central nervous system (CNS) may initiate and/or maintain the pain in idiopathic TMD due to sustained or long-term nociceptive input that induces maladaptive brain plasticity, and/or to inherent personality-related factors that may reduce the brain's capacity to modulate nociceptive activity. The main aim of this thesis is to determine whether there are structural neural abnormalities in patients with TMD, and whether these abnormalities are related to TMD pain characteristics, or to neuroticism. The specific aims are to delineate in TMD: (1) gray matter (GM) brain abnormalities and the contribution of pain and neuroticism to abnormalities; (2) the contribution of abnormal brain GM aging in focal cortical regions associated with nociceptive processes; and (3) abnormalities in brain white matter and trigeminal nerve and the contribution of pain. In groups of 17 female patients with TMD and 17 age- and sex- matched controls, magnetic resonance imaging revealed that patients with TMD had: (1) thicker cortex in the somatosensory, ventrolateral prefrontal and frontal polar cortices than controls, (2) cortical thickness in motor and cognitive areas that was negatively related to pain intensity, orbitofrontal cortical thickness that was negatively correlated to pain unpleasantness, and thalamic GM volume correlated to TMD duration, (3) an abnormal relationship between neuroticism and orbitofrontal cortical thickness, (4) abnormal GM aging in nociceptive, modulatory and motor areas, (5) widespread abnormalities in white matter tracts in the brain related to sensory, motor and cognitive functions, (6) reduced trigeminal nerve integrity related to pain duration, and (7) abnormal connectivity in cognitive and modulatory brain regions. In sum, this thesis demonstrates for the first time abnormalities in both peripheral nerve and CNS in patients with TMD.