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Tidswell, Alexander Thomas. "Functional Electrical Impedance Tomography of adult and neonatal brain function." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445123/.
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Electrical Impedance Tomography (EIT) is a fast, portable imaging technique that produces tomographic images of the internal impedance of an object from surface electrode measurements. This thesis reports the first use of EIT to image evoked brain activity in adults and neonates and determines whether accurate EIT images could be obtained from the adult and neonatal brain. In addition, a realistic head-tank phantom was developed to test the performance of EIT with known impedance changes placed within a real human skull. Two EIT systems were used. Images were obtained using 31 or 21 Ag/AgCl EEG scalp electrodes in adults and neonates, respectively, with either 256 or 187 individual impedance measurements from different electrode combinations: 2 applied a safe, alternating current and 2 measured the resultant scalp voltage. Imaging was performed using a block design with 6-15 stimulation periods of between 10-75s during either: 1) Visual, 2) Somatosensory or 3) Motor stimuli. Impedance changes were detected in 38/39 adults and 9/9 neonates within 0.6-5.8s after stimulus onset, and returned to baseline 7.6-36s after stimulus cessation. Reconstructed images were noisy: -20-70% images showed correct localisation to the expected area of cortex stimulated by the visual, motor or somatosensory paradigms. As EIT images from the head-tank localised changes within 10% of the impedance perturbation, this indicated that poor localisation in humans was not due to the head-shape or the skull, but may be related to unknown physiological factors. An improved EIT reconstruction algorithm, using a computerised finite-element model of the head, showed improved localisation for the adult images. This is the first demonstration that EIT can detect and image impedance changes in the head, probably due to increased regional cerebral blood volume in the activated cortex. Improvements may enable more accurate neuroimaging of the adult and neonatal brain for use in clinical practice.
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Deshpande, Gopikrishna. "Nonlinear and network characterization of brain function using functional MRI." Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/24760.
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Thesis (Ph.D.)--Biomedical Engineering, Georgia Institute of Technology, 2007.<br>Committee Chair: Hu, Xiaoping; Committee Member: Brummer, Marijn; Committee Member: Butera, Robert; Committee Member: Oshinski, John; Committee Member: Sathian, Krish.
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McCorry, N. K. "Prenatal prediction of postnatal brain function." Thesis, Queen's University Belfast, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411140.
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MacLullich, Alasdair Maurice Joseph. "Cognitive function, the brain and glucocorticoids." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/24879.
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Several domains of cognitive function show lower mean scores and increasing variability with increasing age. Little is known about the biological mechanisms underlying these changes. There is evidence, largely from animal studies, that prolonged exposure to high levels of glucocorticoids is associated with (a) atrophy of brain regions known to be essential for cognitive functioning, such as the hippocampus, and (b) decrements in cognitive function with ageing. There are few human studies examining these links. The studies in this thesis were aimed at testing the hypotheses that elevated levels in Cortisol are associated with relative cognitive impairment, with relative atrophy of the hippocampus and other brain regions, and also with variations in the levels of brain metabolites, and also that cognitive function is associated with brain size and metabolites. Additionally, measures of glucose homeostasis (fasting glucose and glycosylated haemoglobin (HbAlc)) were hypothesised to be negatively correlated with cognitive function. Ill healthy, unmedicated men aged 65-70 were recruited. Subjects had blood taken for 9am, 2.30pm, and post-dexamethasone (0.25mg) Cortisol levels, fasting glucose, and HbAlc, and did a battery of cognitive tests, including tests of 'premorbid' intelligence, fluid intelligence, verbal and visuospatial memory and processing speed. 100 of the subjects underwent two modalities of neuroimaging: (a) structural magnetic resonance imaging, with intracranial area, hippocampus, temporal lobe and frontal lobe volumes measured, and (b) magnetic resonance spectroscopy (MRS), with N-acetylaspartate (NAA), choline (Cho) and creatine (Cr) levels measured. Principal components analyses showed that a single component (designated the 'general cognitive factor') accounted for 51% of the variance in cognitive performance; rotation yielded two correlated components representing fluid intelligence/visuospatial memory tasks, and verbal memory tasks. Intracranial area and several regional brain volumes correlated positively and significantly with 'premorbid' and fluid intelligence and visuospatial memory. Verbal memory and verbal fluency did not correlate significantly with any brain volumes. Structural equation modelling showed that the relationships between cognitive tests and brain volumes could best be summarised by a significant positive relationship between overall brain size and the general cognitive factor (r=0.42, p < 0.05), and not by associations between individual tests and particular brain regions. Both NAA/Cr and Cho/Cr ratios correlated positively with tests of verbal memory and a verbal memory factor (e.g. NAA/Cr and Logical Memory: r=0.24, p < 0.05). Cho/Cr ratios also correlated positively with visuospatial memory (eg. Visual Reproduction: r=0.21, p < 0.05). There were several small but statistically significant correlations in the predicted (negative) direction between brain volumes and Cortisol levels. Left temporal lobe volumes correlated with 9am Cortisol (r=-0.22) and 2.30pm Cortisol (r=-0.26), right temporal lobe volumes correlated with 9am Cortisol (r=-0.21), right hippocampal volumes correlated with 9am Cortisol (r=-0.22) and postdexamethasone Cortisol (r=-0.24). These correlations were significant at p < 0.05, 2- tailed. There were no significant correlations between Cortisol measures and metabolite ratios (from MRS). Correlations between Cortisol measures and cognitive tests were largely in the predicted direction, though few of these correlations reached conventional levels of statistical significance. The general cognitive factor and the fluid/intelligence factor, adjusted for 'premorbid' intelligence, correlated significantly and negatively with 9am Cortisol levels, at r=-0.23 (p=0.028, 2-tailed). HbAlc was significantly negatively correlated with two measures of verbal memory, but not with other cognitive tests (list-learning: r=-0.24, p=0.01; delayed paragraph recall r=-0.31, p=0.018, 2-tailed). These results demonstrate that in healthy, elderly men, overall brain size and metabolite ratios are significantly related to cognitive ability. A possible mechanistic link between these two domains is variations in Cortisol with ageing. The results of the present studies are supportive of the hypothesis that elevated glucocorticoids are associated with ageing-related changes in brain volumes, and, less clearly, cognitive function. Follow-up studies will help determine whether Cortisol levels are predictive of worsening brain atrophy and cognitive decline.
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Nakao, Akito. "Elucidation of Ca[2+] channel function in higher brain function." 京都大学 (Kyoto University), 2014. http://hdl.handle.net/2433/192194.
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Schott, Geoffrey. "Picturing the functions of the brain : 20th century graphic illustration of brain function ; observations and critical analysis." Thesis, Royal College of Art, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262785.
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Kinnunen, K. M. "Traumatic brain injury : relationships between brain structural abnormalities and cognitive function." Thesis, Goldsmiths College (University of London), 2011. http://research.gold.ac.uk/6498/.
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Traumatic brain injury (TBI) is the leading cause of disability in young adults and a major public health problem. Persistent cognitive impairments are common, and constitute a significant source of long-term disability. The specific pathophysiological mechanisms underlying these impairments remain poorly understood. As it disconnects brain networks, white matter damage can be a key determinant of cognitive impairment after TBI. Neuroimaging and neuropsychological methods were employed to explore the relationships between indices of brain structure and cognitive function. The participants were 40 TBI patients and 40 healthy controls. First, relationships between focal lesions and cognitive performance were investigated using structural magnetic resonance imaging (MRI) and a battery of neuropsychological tests. The results demonstrated that lesion location and load are not good indices of the cognitive deficits - probably because diffuse axonal injury is poorly assessed by standard MRI. By contrast, diffusion tensor imaging (DTI) can be used to quantify the microstructure of white matter. A ‘whole-brain’ technique, tract-based spatial statistics (TBSS), was used to flexibly analyse the structure of white matter tracts. Despite only small amounts of focal damage observed using standard MRI, TBSS revealed widespread white matter abnormalities after TBI. White matter damage was found in patients with no evidence of focal damage, and in patients classified as ‘mild’ clinically. Relationships between white matter tract structure and specific cognitive functions were then explored. The structure of the fornix, an important white matter pathway of the hippocampus, correlated with verbal associative memory across the patient and control groups. By contrast, structure of frontal lobe connections showed distinct relationships with executive function in these two groups. The results emphasise the importance of white matter pathology after TBI and suggest that disruption to specific white matter tracts is associated with particular patterns of cognitive impairment, but also highlight the complexity of these relationships.
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LaRoux, Charlene I. 1979. "Executive function deficits in traumatic brain injury." Thesis, University of Oregon, 2010. http://hdl.handle.net/1794/11063.
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xii, 98 p. : ill. (some col.)<br>The short and long term pathophysiology of traumatic brain injury (TBI) has not been fully elucidated. Individuals recently suffering a mild TBI (mTBI) or having a history of TBI frequently suffer deficits in their ability to maintain and allocate attention within and between tasks. This dissertation examines the influence of mild and chronic TBI on performance of task switching. We employed spatial and numerical task switching paradigms to assess the behavioral deficits in mTBI, and we used an internally generated switching and an externally cued switching task along with functional Magnetic Resonance Imaging (fMRI) to assess the long term deficits in executive function resulting from chronic TBI.
In the first experiment, individuals with mTBI were identified and tested within the first 48 hours of injury and then at a set interval 5, 14, and 28 days post injury. In the second investigation, individuals with chronic TBI were tested at least 12 months after their most recent injury. Healthy gender, age, and education matched controls were also tested in both studies.
This research demonstrated that mTBI subjects display deficits in switching behavior within 48 hours of injury that failed to resolve a month post-injury; however, these costs did not generalize across the switching task types. Chronic TBI subjects performed internally generated and externally cued switching paradigms with a degree of success equivalent to that of healthy controls but displayed larger amounts of activation and recruited more areas of the brain at lower levels of difficulty and did not increase recruitment in a stepwise fashion at higher levels of difficulty.
Mild TBI causes significant deficits in task switching, but there is specificity in these deficits. Chronic TBI patients performed at a level equivalent to that of controls but displayed different patterns and degree of activation. Taken together, these findings indicate that there may be a specific time frame during which task switching shows behavioral deficits, after which the subject may compensate for these deficits to produce normalized performance.<br>Committee in Charge: Dr. Paul van Donkelaar, Chair;
Dr. Li-Shan Chou;
Dr. Ulrich Mayr;
Dr. Marjorie Woollacott
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Yu, Yingwei. "Computational role of disinhibition in brain function." [College Station, Tex. : Texas A&M University, 2006. http://hdl.handle.net/1969.1/ETD-TAMU-1762.
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Furmark, Tomas. "Social Phobia. From Epidemiology to Brain Function." Doctoral thesis, Uppsala University, Department of Psychology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-546.
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<p>Social phobia is a disabling anxiety disorder characterized by an excessive fear of negative evaluation in social situations. The present thesis explored the epidemiology and neurobiology of the disorder. By means of a mailed questionnaire, the point prevalence of social phobia in the Swedish general population was estimated at 15.6%. However, prevalence rates varied between 1.9 and 20.4% across the different levels of distress and impairment used to define cases. Thus, although social anxiety is widespread within the community, the precise diagnostic boundaries for social phobia are difficult to determine. Social phobia was associated with female gender, low educational attainment, psychoactive medication use, and lack of social support. A cluster analysis revealed that subtypes of social phobia mainly differed dimensionally on a mild-moderate-severe continuum, with number of cases declining with increasing severity. Public speaking was the most common social fear in all groups of social phobics and in the population at large.</p><p>In the neurobiological studies, positron emission tomography was used to examine brain serotonin metabolism and changes in the regional cerebral blood flow (rCBF) response to public speaking stress following treatment with a selective serotonin reuptake inhibitor (SSRI) or cognitive-behavioral group therapy. Social phobics exhibited lowered serotonin turnover, relative to non-phobics, mainly in the medial temporal cortex including the bilateral rhinal and periamygdaloid regions. Symptom improvement with cognitive-behavioral- as well as SSRI-treatment was accompanied by a reduced rCBF-response to public speaking in the amygdala, hippocampus and adjacent temporal cortex, i.e. regions that serve important functions in anxiety. Thorough suppression of rCBF in limbic brain regions was associated with favorable long-term treatment outcome. These results provide neuroimaging evidence for a presynaptic serotonergic dysfunction in social phobia and for a common neural mechanism whereby psychological and pharmacological anti-anxiety treatments act.</p>
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Young, A. H. "Hormonal effects on brain 5-HT function." Thesis, University of Edinburgh, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.664142.
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The purpose of the work carried out in this thesis was to examine hormonal effects on central nervous system serotonergic (5-hydroxtryptamine; 5-HT) receptor function. Experiments were carried out using established rodent (mouse and rat) models of central 5-HT receptor function. Corticosteroids were administered, both acutely and chronically, and the effects on these models assessed. Corticosteroids were found to have relatively selective effects: in the mouse and rat certain models of 5-HT<SUB>1A</SUB> receptor function were attenuated and in the mouse corticosteroids enhanced behavioural models of 5-HT release. No effects were found on models of other central 5-HT receptor functions. These effects were found to be both time and dose dependent and to reverse after the administration of corticosteroids ceased. Removal of endogenous corticosteroids, by adrenalectomy, was found to cause an enhancement of 5-HT<SUB>1A</SUB> receptor function. A sex difference, in rodents, in 5-HT<SUB>1A</SUB> receptor function was found which was abolished by ovariectomy. The action of corticosterone in producing these effects could not be replicated by selective corticosteroid receptor antagonists. Further experiments were carried out in healthy human male volunteers. Buspirone was shown to induce a hypothermic response significantly greater than placebo. The effects of hydrocortisone administration (20mg, orally, twice daily) on the sensitivity of brain 5-HT<SUB>1A</SUB> receptors in healthy volunteers were then studied using a buspirone challenge paradigm. These experiments show that the effects of corticosteroids are relatively selective to 5-HT<SUB>1A</SUB> receptors. The effect of corticosteroids on 5-HT<SUB>1A</SUB> receptors may be the mechanism whereby exogenous corticosteroids affect mood. Furthermore, the effects of endogenous corticosteroids on 5-HT receptor function may be important in the pathophysiology of mood disorders.
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Nayak, Sahana. "Synthetic and function of DHEA in brain." Thesis, University of Nottingham, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298961.
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Saygin, Zeynep Mevhibe. "Structure-function relationships in human brain development." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/77843.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2012.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis. Page 125 blank.<br>Includes bibliographical references.<br>The integration of anatomical, functional, and developmental approaches in cognitive neuroscience is essential for generating mechanistic explanations of brain function. In this thesis, I first establish a proof-of-principle that neuroanatomical connectivity, as measured with diffusion weighted imaging (DWI), can be used to calculate connectional fingerprints that are sufficient to delineate fine anatomical distinctions in the human brain (Chapter 2). Next, I describe the maturation of structural connectivity patterns by applying these connectional fingerprints to over a hundred participants ranging from five to thirty years of age, and show that these connectional patterns have different developmental trajectories (Chapter 3). I then illustrate how anatomical connections may shape (or in turn be shaped by) function and behavior, within the framework of reading ability and describe how white matter tract integrity may predict future acquisition of reading ability in children (Chapter 4). I conclude by summarizing how these experiments offer testable hypotheses of the maturation of structure and function. Studying the complex interplay between structure, function, and development will get us closer to understanding both the constraints present at birth, and the effect of experience, on the biological mechanisms underlying brain function.<br>by Zeynep Mevhibe Saygin.<br>Ph.D.
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Bentley, P. I. "Effects of cholinesterase inhibition on brain function." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1301395/.
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Pharmacological-functional imaging provides a non-invasive method by which the actions of neurotropic drugs on the human brain can be explored. Simply put, it assesses how neural activity patterns associated with cognitive functions of interest are modified by a drug challenge. Since one of the most widely-used cognitive-enhancing drugs in clinical practice are cholinesterase inhibitors, this thesis applies pharmacological functional imaging to the question of understanding how such drugs work - both in healthy people and dementia. The experiments in this thesis describe how brain activations – as revealed by functional magnetic resonance imaging (fMRI) – are modulated by the cholinesterase inhibitor physostigmine, during tasks designed to isolate sensory, attentional, and memory processes. While non-human and human psychophysical studies suggest that all three of these cognitive functions are under the control of the endogenous cortical cholinergic system, understanding how neurobiological models of cholinergic function translate into human brain activation modulations is unclear. One main question that is particularly relevant in this regard, that recurs through all the experiments, is how physostigmine-induced neuromodulations differ between sensory-driven ‘bottom-up’, and task-driven ‘top-down’, brain activations. The results are discussed with reference both to non-human physiological data and to existing human cholinergic-functional imaging studies (fifty studies published to date), which are themselves reviewed at the outset. Furthermore, assumptions based upon the physical and physiological principles of pharmacological functional imaging, being critical to interpretation, are discussed in detail within a general methods section.
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Enfield, Louise C. "Electrical impedance tomography of human brain function." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1446415/.
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Electroencephalography (EEG) has been used for over 70 years to record the electrical signals of the brain. Electrical impedance tomography (EIT) is a more recent imaging technique which when applied to brain function and structure has the potential to provide a rapid portable bedside neuroimaging device. The purpose of this work has been to investigate several applications of EIT and EEG in the imaging of brain function. EEG does not always give the required spatial information, especially if the current generator is in the deep brain structures such as the hypothalamus. Dipole source localisation has become a common research tool that can be used estimate the current sources that are responsible for the EEG signals recorded on the scalp. Using this method, the accuracy and ease of use for four commercially available headnets was assessed. No headnet performed better at localisation, with all localising one dipole well, and two or three dipoles poorly. EIT has the potential to image the impedance changes that occur during neuronal depolarisation. Modelling work has been carried out to predict the size of these impedance changes and this thesis presents some work carried out in an attempt to record these changes in human subjects. The levels of noise at present are too great to record the impedance changes, but suggestion for improving the signal to noise ratio are given. Previous work on EIT and fMRI studies has shown that there are changes in blood volume (and as a result changes in impedance) after interictal spike activity. The impedance changes relating to the blood flow response to interictal epileptiform activity were recorded using EEG-correlated continuous EIT acquisition from scalp electrodes from patients on telemetry. Despite averaging up to 900 spikes, there was no recordable change in impedance after the interictal activity. Bioimpedance changes also occur due to pathological conditions. Multifrequcncy HIT makes use of the differences in impedance properties between healthy and ischaemic or tumour tissue, in an attempt to image these conditions. Data were collected from patients with tumours and other conditions and healthy volunteers, and the raw data and images compared. No differences were seen in the raw data between the different patients groups thought changes were seen in individual patients. . These results will inform the design of an EIT system which operates at a lower frequency band where the largest changes in impedance are seen.
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Soni, Garcia Adriana Lorena. "Latin American teachers' perceptions about the mind-brain relationship, brain function and neuroeducation." Thesis, University of Bristol, 2016. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.723455.
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Trachtenberg, Aaron J. "The effects of APOE genotype on brain function." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.542982.
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Vogiatzoglou, Anna. "Vitamin B12 status : determinants, biomarkers and brain function." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526422.
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Cahill, Louise Margaret. "Motor speech function following childhood traumatic brain injury /." [St. Lucia, Qld.], 2002. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16948.pdf.
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Elgh, Eva. "Neuropsychological Function in Relation to Structural and Functional Brain Changes in Alzheimer’s Disease." Doctoral thesis, Umeå universitet, Geriatrik, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-323.
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The aim of this doctoral thesis was to study neuropsychological function in relation to structural and functional brain changes in Alzheimer´s disease (AD). In the first study relations between hippocampal volume, neuropsychological function and limbic-hypothalamic-pituitary-adrenal (LHPA) axis disturbances in AD were investigated with magnetic resonance imaging (MRI). Reduced hippocampal CA1 volume and suppressed cortisol levels in combination, best predicted the variation in neuropsychological performance. The conclusion was that reduced hippocampal volume and LHPA axis disturbances are associated to level of cognitive function in AD. The second study focused on whether patients with early AD showed an altered regional cerebral blood flow (rCBF) pattern compared to control persons, correlation between performance on memory tests and rCBF in sub-lobar volumes of the brain were investigated. The rCBF was measured with single photon emission computed tomography (SPECT). AD-patients showed a significantly lower rCBF in temporoparietal regions including left hippocampus compared to controls. The diagnostic sensitivity and specificity for AD was high in temporoparietal regions. AD-patients had significantly lower performance on semantic and, in particular, episodic memory-tests compared to the controls, and their performance on several episodic tests correlated with rCBF in parietal and temporal regions including left hippocampus, which suggest that abnormalities in the rCBF pattern underlie impaired episodic memory functioning in AD. The conclusion was that an observer-independent analyzing method for SPECT with sub-lobar volumes VOI´s is promising in the diagnosis of AD. In a third study possible differences in memory-related functional brain activation between persons with high versus low risk for AD were examined with functional magnetic resonance imaging (fMRI). The high-risk individuals performed worse than low-risk individuals on tests of episodic memory. Patterns of brain activity during episodic encoding and retrieval showed significant group differences. During both encoding and retrieval, the low-risk persons showed increased activity relative to a baseline condition in prefrontal and hippocampal brain regions that previously have been implicated in episodic memory. By contrast, the high-risk persons did not significantly activate any prefrontal regions, but instead showed increased activity in visual occipito-temporal regions. The conclusion was that patterns of prefrontal brain activity related to episodic memory differed between persons with high versus low risk for AD, and lowered prefrontal activity may predict subsequent disease. In a final study SPECT was used to map patterns of rCBF in an activated state (an episodic encoding task) and in a rest condition in persons with mild AD and in healthy elderly control persons. A reduction of rCBF in temporoparietal regions that was more pronounced in mild AD in the activated encoding task was observed. The conclusion was that there are rCBF differences between mild AD patients and healthy controls in temporoparietal regions, and the temporoparietal reduction is more pronounced during activation than during rest which might be important in the early diagnosis of AD. Taken together, these findings show that level of neuropsychological function, notably episodic memory, can be systematically related to functional disturbances in the LHPA axis and to the function of temporoparietal and prefrontal brain regions in AD patients. These changes are detectable in patients with risk for AD and in an early phase of AD which suggests that the obtained results might be important for early diagnosis of AD.
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Elgh, Eva. "Neuropsychological function in relation to structural and functional brain changes in Alzheimer's disease /." Umeå : Geriatric medicine, Department of community medicine and rehabilitation, Umeå University, 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-323.
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Olesen, Pernille J. "Brain function and behaviour related to development and training of working memory /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-506-2/.
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Lind, Johanna. "Memory, genes, and brain imaging : relating the APOE gene to brain function and structure /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-110-4/.
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Lima, Brasil Fabricio [Verfasser], and Niels [Akademischer Betreuer] Birbaumer. "Brain-Machine Interfaces and Plasticity of Brain Function / Fabricio Lima Brasil ; Betreuer: Niels Birbaumer." Tübingen : Universitätsbibliothek Tübingen, 2019. http://d-nb.info/1194370411/34.
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Driessen, Anique Johanna Eduarda. "Exploring the combined use of electrical and hemodynamic brain activity to investigate brain function." Thesis, Oxford Brookes University, 2014. https://radar.brookes.ac.uk/radar/items/d5e7c357-e312-4fba-8cc5-774eff36180e/1/.
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This thesis explored the relationship between electrical and metabolic aspects of brain functioning in health and disease, measured with QEEG and NIRS, in order to evaluate its clinical potential. First the limitations of NIRS were investigated, depicting its susceptibility to different types of motion artefacts and the inability of the CBSI-method to remove them from resting state data. Furthermore, the quality of the NIRS signals was poor in a significant portion of the investigated sample, reducing clinical potential. Different analysis methods were used to explore both EEG and NIRS, and their coupling in an eyes open eyes closed paradigm in healthy participants. It could be reproduced that during eyes closed blocks less HbO2 (p = 0.000), more Hbb (p = 0.008), and more alpha activity (p = 0.000) was present compared to eyes open blocks. Furthermore, dynamic cross correlation analysis reproduced a positive correlation between alpha and Hbb (r: 0.457 and 0.337) and a negative correlation between alpha and HbO2 (r: -0.380 and -0.366) with a delayed hemodynamic response (7 to 8s). This was only possible when removing all questionable and physiological illogical data, suggesting that an 8s hemodynamic delay might not be the golden standard. Also the inability of the cross correlation to take non-linear relationships into account may distort outcomes. Therefore, In chapter 5 non-linear aspects of the relationship were evaluated by introducing the measure of relative cross mutual information. A newly suggested approach and the most valuable contribution of the thesis since it broadens knowledge in the fields of EEG, NIRS and general time series analysis. Data of two stroke patients then showed differences from the healthy group between the coupling of EEG and NIRS. The differences in long range temporal correlations (p= 0.000 for both cases), entropy (p< 0.040 and p =0.000), and relative cross mutual information (p < 0.003 and p < 0.013) provide the proof of principle that these measures may have clinical utility. Even though more research is necessary before widespread clinical use becomes possible.
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Martindale, Anthony John. "Investigating the relationship between neural activity and the haemodynamic response : modelling, theory and experiment." Thesis, University of Sheffield, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.269397.
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Tranberg, Mattias. "N-acetylaspartate in brain : studies on efflux and function /." Göteborg : Institute of Neuroscience and Physiology, Department of Physiology, The Sahlgrenska Academy, Göteborg University, 2006. http://hdl.handle.net/2077/718.
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Podjaski, Cornelia. "Netrins enhance blood-brain barrier function and regulate immune responses at the blood-brain barrier." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=116977.
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During development, netrin guidance cues control cell motility and cell adhesion. Cell-adhesion between endothelial cells at the blood-brain barrier makes the endothelium impermeable to blood-derivatives and immune cells. To establish and maintain this barrier during development, and adulthood, and as well as during disease, brain endothelial cells must develop and sustain these strong adhesive contacts, through expression of tight junction molecules. However, we do not know whether netrins support inter-endothelial cell adhesion at the blood-brain barrier. Given this, we hypothesize that netrin tightens the blood-brain barrier during development, adulthood, and protects it during disease. Methods: To test this, we used both human adult primary brain-derived endothelial cells and newborn netrin-1 knockout mice and evaluated netrin's effect on inter-endothelial cell adhesion and barrier permeability. We also assessed netrins' therapeutic potential to maintain the barrier and limit immune cell infiltration into the central nervous system (CNS) during experimental autoimmune encephalomyelitis (EAE). Results: Our results demonstrate that brain endothelial cells express netrins where they function in three ways. They help to form a tighter blood-brain barrier during development. They also maintain and protect the adult barrier by increasing the expression of endothelial junction molecules, thus promoting inter-endothelial adhesion and reducing protein leakage across the barrier. Netrins also reduce blood-brain barrier breakdown and diminish initial myeloid cell infiltration into the brain and spinal cord during EAE, which delays disease onset and ameliorates disease severity. However, during the chronic phase of EAE, netrin-1 treated mice have higher numbers and more activated T cells in their CNS and exhibit an ataxic gait and limb spasticity. Discussion: We conclude that netrins enhance BBB stability, but have dual functions on immune responses during neuroinflammatory disease. These findings favour the hypothesis that if netrin function was to be manipulated as a therapeutic, early short-term approaches would likely be the most effective.<br>Au cours du développement, les molécules de la famille des nétrines contribuent à la morphologénèse des organes en contrôlant la motilité et l'adhérence cellulaire. L'adhérence cellulaire entre les cellules endothéliales est une caractéristique importante de la barrière hémato-encéphalique (BHE), ce qui rend l'endothélium imperméable aux molécules sanguines et aux cellules immunitaires. Pour établir et maintenir cette barrière au cours du développement, à l'âge adulte et au cours de la maladie, les cellules endothéliales du cerveau doivent développer et maintenir ces contacts adhésifs en exprimant des molécules de jonction serrées. Cependant, nous ne savons pas si les molécules de la famille des nétrines influencent l'adhérence cellulaire inter-endothéliale de la BHE. Nous avons donc émis l'hypothèse que les nétrines resserrent la BHE au cours du développement, à l'âge adulte, et la protège au cours de la maladie.Méthodes: Pour valider notre hypothèse, nous avons utilisé des cellules endothéliales primaires dérivées des cerveaux humains adultes ou des cerveaux de souris nouveau-nés déficientes en nétrine-1 et évalué l'effet de la nétrine sur l'adhésion cellulaire endothéliale et inter-perméabilité de la barrière. Nous avons également évalué le potentiel thérapeutique des nétrines a restaurer la barrière et l'infiltration de cellules immunitaires limite dans le système nerveux central (SNC) pendant encéphalomyélite allergique expérimentale, un modèle animal de sclérose en plaques. Résultats: Nos résultats démontrent que les nétrines sont exprimées par les cellules endothéliales du cerveau, exprimes nétrines. Au cours du développement les nétrines aident à assurer l'étanchéité de la BHE. Chez les adultes, ils maintiennent et protègent la barrière adulte en augmentant l'expression des molécules de jonctions serrées, favorisant ainsi l'adhérence inter-endothéliale et diminuant les fuites de protéines à travers la BHE. Dans la pathologie de l'EAE, le rôle des nétrins diffère en fonction de la phase de la maladie. Au cours de la phase aigue, les nétrines atténuent la perte de l'intégrité de la BHE et diminuent l'infiltration des cellules myéloïdes dans le SNC. Ceci retarde l'apparition de la maladie et réduit sa sévérité. Au cours de la phase chronique de l'EAE, les souris traitées avec netrin-1 ont un plus grand nombre des cellules T activées dans leurs SNC et présentent une démarche ataxique ainsi qu'une spasticité des membres. Discussion: Nous concluons que les nétrins améliorent la stabilité de la BHE. Ces résultats suggèrent que les nétrines peuvent être envisagée comme agent thérapeutique dans les maladies neuroinflammatoire. Dans ce cas une approche précoce et à court terme serait probablement plus efficace.
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Sellers, Kathleen Walworth. "Role of brain soluble epoxide hydrolase in cardiovascular function." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0008356.
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Thesis (Ph.D.)--University of Florida, 2004.<br>Typescript. Title from title page of source document. Document formatted into pages; contains 156 pages. Includes Vita. Includes bibliographical references.
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Zemanová, Lucia. "Structure-function relationship in hierarchical model of brain networks." Phd thesis, Universität Potsdam, 2007. http://opus.kobv.de/ubp/volltexte/2008/1840/.
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The mammalian brain is, with its numerous neural elements and structured complex connectivity, one of the most complex systems in nature. Recently, large-scale corticocortical connectivities, both structural and functional, have received a great deal of research attention, especially using the approach of complex networks. Here, we try to shed some light on the relationship between structural and functional connectivities by studying synchronization dynamics in a realistic anatomical network of cat cortical connectivity. We model the cortical areas by a subnetwork of interacting excitable neurons (multilevel model) and by a neural mass model (population model). With weak couplings, the multilevel model displays biologically plausible dynamics and the synchronization patterns reveal a hierarchical cluster organization in the network structure. We can identify a group of brain areas involved in multifunctional tasks by comparing the dynamical clusters to the topological communities of the network. With strong couplings of multilevel model and by using neural mass model, the dynamics are characterized by well-defined oscillations. The synchronization patterns are mainly determined by the node intensity (total input strengths of a node); the detailed network topology is of secondary importance. The biologically improved multilevel model exhibits similar dynamical patterns in the two regimes. Thus, the study of synchronization in a multilevel complex network model of cortex can provide insights into the relationship between network topology and functional organization of complex brain networks.<br>Das Gehirn von Säugetieren stellt mit seinen zahlreichen, hochgradig vernetzten Neuronen ein natürliches Netzwerk von immenser Komplexität dar. In der jüngsten Vergangenheit sind die großflächige kortikale Konnektivitäten, sowohl unter strukturellen wie auch funktionalen Gesichtspunkten, in den Fokus der Forschung getreten. Die Verwendung von komplexe Netzwerke spielt hierbei eine entscheidende Rolle. In der vorliegenden Dissertation versuchen wir, das Verhältnis von struktureller und funktionaler Konnektivität durch Untersuchung der Synchronisationsdynamik anhand eines realistischen Modells der Konnektivität im Kortex einer Katze näher zu beleuchten. Wir modellieren die Kortexareale durch ein Subnetzwerk interagierender, erregbarer Neuronen (multilevel model) und durch ein Modell von Neuronenensembles (population model). Bei schwacher Kopplung zeigt das multilevel model eine biologisch plausible Dynamik und die Synchronisationsmuster lassen eine hierarchische Organisation der Netzwerkstruktur erkennen. Indem wir die dynamischen Cluster mit den topologischen Einheiten des Netzwerks vergleichen, sind wir in der Lage die Hirnareale, die an der Bewältigung komplexer Aufgaben beteiligt sind, zu identifizieren. Bei starker Kopplung im multilevel model und unter Verwendung des Ensemblemodells weist die Dynamik klare Oszillationen auf. Die Synchronisationsmuster werden hauptsächlich durch die Eingangsstärke an den einzelnen Knoten bestimmt, während die genaue Netzwerktopologie zweitrangig ist. Eine Erweiterung des Modells auf andere biologisch relevante Faktoren bestätigt die vorherigen Ergebnisse. Die Untersuchung der Synchronisation in einem multilevel model des Kortex ermöglicht daher tiefere Einblicke in die Zusammenhänge zwischen Netzwerktopologie und funktionaler Organisation in komplexen Hirn-Netzwerken.
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Kokotilo, Kristen J. "Reorganization of brain function during force production after stroke." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2723.
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Damage to motor areas of the brain, caused by stroke, can produce devastating motor deficits, including aberrant control of force. After stroke, reorganization of the brain’s motor system has been identified as one of the fundamental mechanisms involved in recovery of motor control after stroke. Yet, few studies have investigated how force production and modulation are encoded in the brain after stroke and how this relates to motor outcome. Thus, the purpose of this study was to (1) understand how past neuroimaging literature has contributed to establishing common patterns of brain reorganization during both relative and absolute force production after stroke, (2) examine how brain function is reorganized during force production and modulation in individuals with stroke, and (3) relate this task-related reorganization of brain function to the amount of paretic arm use after stroke. In the second chapter, we systematically reviewed all relevant literature examining brain activation during force production after stroke. The following chapters (chapters 3 and 4) applied functional magnetic resonance imaging (fMRI) to examine the neural correlates of force production and modulation after stroke. Chapter 2 supports differences in task-related brain activation dependent on features of stroke, such as severity and chronicity, as well as influence of rehabilitation. In addition, results suggest that activation of common motor areas of the brain during force production can be identified in relation to functional outcome after stroke. Results from the subsequent two chapters (3 and 4), demonstrate that brain function reorganizes in terms of absolute, and not relative force production after stroke. Specifically, stroke participants exhibit greater activation of motor areas than healthy controls when matched for absolute force production. Moreover, there is a relationship between paretic arm usage and brain activation, where stroke participants having less paretic arm use, as measured using wrist accelerometers, exhibit higher brain activation. Results of this thesis suggest that during absolute force production, brain activation may approach near maximal levels in stroke participants at lower forces than healthy controls. Furthermore, this effect may be amplified even further in subjects with less paretic arm usage, as increased activation in motor areas occurs in participants with less arm use after stroke. Ultimately, the results from this thesis will contribute to research relevant to brain reorganization in individuals with stroke and may lead to the development of new, beneficial therapeutic interventions that optimize brain reorganization and improve functional recovery after stroke.
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Odontiadis, John. "Effects of nutritional manipulation on brain 5-HT function." Thesis, Oxford Brookes University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397093.
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Cheyne, Christopher Paul. "Multivariate modelling of cognitive function and brain structural data." Thesis, University of Liverpool, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.569125.
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Previous studies have investigated links between cognitive ability and a number of factors including age, gender, handedness, musical ability as well as the volume and surface area of certain brain structures, However, in these studies either the explanatory variables are analysed independently of each other, or the investigation is based on a separate analysis for individual cognitive outcomes (e.g. language, visuospatial, etc.) The main objectives of this thesis are(1) to develop general multivariate models, which include mixed-effects terms, to account for the correlation in the data, (2) to explore the possible associations in children and adults between multiple cognitive ability test scores and the range of factors mentioned above by simultaneously applying the multivariate models designed in (1), and (3) to investigate the possible effects of missing data on the results. To meet these objectives, a range of statistical and stereological methods was employed: Multivariate linear and linear mixed models were developed and fitted to multiple datasets. The approach used took into account the correlation of clustered data, the correlation between outcomes as well as the association between explanatory variables and a linear combination of the outcomes. Stereological methods were used to estimate the volume and surface area of a region of the brain called Broca's area, using magnetic resonance images. Also, the latest formulae in error prediction for these stereological estimates were described and applied to the data. Results from the fitted multivariate linear mixed model to a dataset of l l-year old children (n= 1184 3) showed that children whose writing hand has less hand skill than the opposite hand performed worse, on average, in both reading and maths scores, than those children whose writing hand had more hand skill than the opposite hand. A multivariate linear model fitted to a dataset of adults (n=142) revealed that the gender difference found in the non-musician groups for the vocabulary and arithmetic scores was not present in the musician group. Multivariate linear models were subsequently fitted to a subset of this cohort containing volume and surface area estimates of Broca's area (n=39). Musicians were associated with Broca's area being less convoluted in the right hemisphere than non-musicians. Other associations investigated were not found to be statistically significant. Inverse probability weighting was then used to take the missing data into account for each of the analyses (aim (3)). The results and interpretations determined from the fitted multivariate models were consistent with the analyses when the missing data were accounted for. Only those results for the children dataset changed slightly, but not enough to alter the interpretations of the results. This adds weight to the belief that the results of the multivariate analyses gave a reasonably accurate description of the variability that exists within the children and adult datasets.
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黃德興 and Tak-hing Michael Wong. "Brain function and structure in violent metally abnormal offenders." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31981719.
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Holloway, Victoria. "Investigations of sensorimotor function in children with brain disease." Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.326156.
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Krishnaswamy, Pavitra. "Algorithms for enhanced spatiotemporal imaging of human brain function." Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95844.
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Thesis: Ph. D., Harvard-MIT Program in Health Sciences and Technology, 2014.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student-submitted PDF version of thesis.<br>Includes bibliographical references (pages 123-142).<br>Studies of human brain function require technologies to non-invasively image neuronal dynamics with high spatiotemporal resolution. The electroencephalogram (EEG) and magnetoencephalogram (MEG) measure neuronal activity with high temporal resolution, and provide clinically accessible signatures of brain states. However, they have limited spatial resolution for regional dynamics. Combinations of M/EEG with functional and anatomical magnetic resonance imaging (MRI) can enable jointly high temporal and spatial resolution. In this thesis, we address two critical challenges limiting multimodal imaging studies of spatiotemporal brain dynamics. First, simultaneous EEG-fMRI offers a promising means to relate rapidly evolving EEG signatures with slower regional dynamics measured on fMRI. However, the potential of this technique is undermined by MRI-related ballistocardiogram artifacts that corrupt the EEG. We identify a harmonic basis for these artifacts, develop a local likelihood estimation algorithm to remove them, and demonstrate enhanced recovery of oscillatory and evoked EEG dynamics in the MRI scanner. Second, M/EEG source imaging offers a means to characterize rapidly evolving regional dynamics within an estimation framework informed by anatomical MRI. However, existing approaches are limited to cortical structures. Crucial dynamics in subcortical structures, which generate weaker M/EEG signals, are largely unexplored. We identify robust distinctions in M/EEG field patterns arising from subcortical and cortical structures, and develop a hierarchical subspace pursuit algorithm to estimate neural currents in subcortical structures. We validate efficacy for recovering thalamic and brainstem contributions in simulated and experimental studies. These results establish the feasibility of using non-invasive M/EEG measurements to estimate millisecond-scale dynamics involving subcortical structures. Finally, we illustrate the potential of these techniques for novel studies in cognitive and clinical neuroscience. Within an EEG-fMRI study of auditory stimulus processing under propofol anesthesia, we observed EEG signatures accompanying distinct changes in thalamocortical dynamics at loss of consciousness and subsequently, at deeper levels of anesthesia. These results suggest neurophysiologic correlates to better interpret clinical EEG signatures demarcating brain dynamics under anesthesia. Overall, the algorithms developed in this thesis provide novel opportunities to non-invasively relate fast timescale measures of neuronal activity with their underlying regional brain dynamics, thus paving a way for enhanced spatiotemporal imaging of human brain function.<br>by Pavitra Krishnaswamy.<br>Ph. D.
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Chang, Jessica T. (Jessica Tzung-Min). "The formation and function of the brain ventricular system." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/72618.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2012.<br>This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.<br>Cataloged from student submitted PDF version of thesis.<br>Includes bibliographical references.<br>The brain ventricular system is composed of a highly conserved set of cavities that contain cerebrospinal fluid (CSF), a protein-rich fluid essential for brain function. However, little is known about the function of embryonic CSF (eCSF), or the mechanisms of CSF production, retention, and circulation that regulate brain ventricle shape and size. Here we present data that begins to dissect the mechanisms governing CSF dynamics during zebrafish embryonic development. Our data indicate that the Na,K-ATPase regulates three aspects of brain ventricle development essential for normal function - neuroepithelial formation, permeability, and CSF production. Formation of a cohesive neuroepithelium requires both the alpha subunit (Atp1a1) and the regulatory subunit, Fyxd1, while only Atp1a1 modulates neuroepithelial permeability. Further, RhoA regulates both neuroepithelium formation and permeability, downstream of the Na,KATPase. Finally, we identified a RhoA-independent process, likely CSF production, which requires Atp1a1, but not Fxyd1. Therefore, formation of the vertebrate brain ventricles requires both production and retention of CSF. Although the embryonic brain ventricles contain large quantities of eCSF little is known about the function of the fluid or the mechanisms that drive fluid production. We developed a method to manually drain eCSF from zebrafish brain ventricles and show that eCSF is necessary for cell survival within the neuroepithelium. Further, increased retinol binding protein 4 (Rbp4), retinoic acid synthesis, and retinoic acid signaling via the PPAR? (peroxisome proliferatoractivated receptor gamma) receptors, prevents neuroepithelial cell death. Thus, we present a novel role for Rbp4 and retinoic acid synthesis and signaling during embryonic brain development. Finally, we also developed an assay to visualize CSF flow in the embryonic zebrafish. We found that the midbrain-hindbrain boundary acts as a barrier preventing CSF movement between the midbrain and hindbrain, while CSF moves freely between the midbrain and forebrain. Additionally, the heartbeat contributes to CSF movement increasing mixing between the hindbrain and forebrain/midbrain compartments. Furthermore, we determined that hydrocephalic phenotypes observed in zebrafish are due to abnormalities in CSF production, retention and flow. These data demonstrate the importance of CSF dynamics during development and further suggest that disruption of these processes can all result in hydrocephalus.<br>by Jessica T. Chang.<br>Ph.D.
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Bahuguna, Jyotika. "Structure-Dynamics relationship in basalganglia: Implications for brain function." Doctoral thesis, KTH, Beräkningsvetenskap och beräkningsteknik (CST), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-186262.
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In this thesis, I have used a combination of computational models such as mean field and spikingnetwork simulations to study various sub-circuits of basal ganglia. I first studied the striatum(chapter 2), which is the input nucleus of basal ganglia. The two types of Medium SpinyNeurons (MSNs), D1 and D2-MSNs, together constitute 98% of the neurons in striatum. Thecomputational models so far have treated striatum as a homogenous unit and D1 and D2 MSNs asinterchangeable subpopulations. This implied that a bias in a Go/No-Go decision is enforced viaexternal agents to the striatum (eg. cortico-striatal weights), thereby assigning it a passive role.New data shows that there is an inherent asymmetry in striatal circuits. In this work, I showedthat striatum due to its asymmetric connectivity acts as a decision transition threshold devicefor the incoming cortical input. This has significant implications on the function of striatum asan active participant in influencing the bias towards a Go/No-Go decision. The striatal decisiontransition threshold also gives mechanistic explanations for phenomena such as L-Dopa InducedDyskinesia (LID), DBS-induced impulsivity, etc. In chapter 3, I extend the mean field model toinclude all the nuclei of basal ganglia to specifically study the role of two new subpopulationsfound in GPe (Globus Pallidus Externa). Recent work shows that GPe, also earlier consideredto be a homogenous nucleus, has at least two subpopulations which are dichotomous in theiractivity with respect to the cortical Slow Wave (SWA) and beta activity. Since the data for thesesubpopulations are missing, a parameter search was performed for effective connectivities usingGenetic Algorithms (GA) to fit the available experimental data. One major result of this studyis that there are various parameter combinations that meet the criteria and hence the presenceof functional homologs of the basal ganglia network for both pathological (PD) and healthynetworks is a possibility. Classifying all these homologous networks into clusters using somehigh level features of PD shows a large variance, hinting at the variance observed among the PDpatients as well as their response to the therapeutic measures. In chapter 4, I collaborated on aproject to model the role of STN and GPe burstiness for pathological beta oscillations as seenduring PD. During PD, the burstiness in the firing patterns of GPe and STN neurons are shownto increase. We found that in the baseline state, without any bursty neurons in GPe and STN,the GPe-STN network can transition to an oscillatory state through modulating the firing ratesof STN and GPe neurons. Whereas when GPe neurons are systematically replaced by burstyneurons, we found that increase in GPe burstiness enforces oscillations. An optimal % of burstyneurons in STN destroys oscillations in the GPe-STN network. Hence burstiness in STN mayserve as a compensatory mechanism to destroy oscillations. We also propose that bursting inGPe-STN could serve as a mechanism to initiate and kill oscillations on short time scales, asseen in the healthy state. The GPe-STN network however loses the ability to kill oscillations inthe pathological state.<br><p>QC 20160509</p>
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Brolin, Erika. "Growth hormone in the brain : Focus on cognitive function." Doctoral thesis, Uppsala universitet, Institutionen för farmaceutisk biovetenskap, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-317305.
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Cognitive impairments are an increasing health problem worldwide. In the developed countries, the average life expectancy has dramatically increased over the last decades, and with an elderly population more cases of cognitive impairments appear. Age, genetics, and different medical conditions such as diabetes mellitus, and substance use disorders may all contribute to declined cognitive ability. Physiological functions also decrease with increasing age, as does the activity of the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis. Interestingly, both GH and IGF-1 are recognized for their neuroprotective effects and cognitive enhancement. The overall aim of this thesis was to investigate the impact of the somatotrophic axis (i.e. GH/IGF-1 axis) in rodents with cognitive deficiencies induced by diabetes or long-term drug exposure. For the first time cognitive impairments were characterized in diabetic mice using a spatial learning and memory task called the Barnes maze (BM). In diabetic mice, impaired learning in the BM was associated with decreased expression of the GH receptor (GHR) in the frontal cortex, a region important for e.g. working memory. Treatment with GH reversed certain cognitive impairments seen in diabetic animals. In rats treated with gamma-hydroxybutyrate (GHB), a significant decrease of Igf1 mRNA expression in the frontal cortex was observed. This observation may explain the impaired cognitive function previously seen following GHB administration. Furthermore, rats exposed to chronic morphine delivered in mini-osmotic pumps displayed memory impairments in the Morris water maze (MWM), an effect that seems to be associated with the composition of the N-methyl-d-aspartate (NMDA) receptor complex in the frontal cortex. In conclusion, the result strengthens the evidence for GH being a cognitive enhancer. Moreover, the result within this thesis identifies the frontal cortex as an important brain region, where gene expression related to the somatotrophic system is affected in rodents with cognitive impairments. The thesis especially emphasizes the importance of the local somatotrophic system in the brain with regard to cognitive function.
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Smallman, Richard. "Schizotypy and the association with brain function and structure." Thesis, University of Manchester, 2012. https://www.research.manchester.ac.uk/portal/en/theses/schizotypy-and-the-association-with-brain-function-and-structure(c8f5a318-5a89-412d-b422-1eedb80e43f6).html.
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Introduction: Schizotypy is a personality trait that shares some of the characteristics of clinical disorders such as schizophrenia. Similarities are found in expression of psychotic-like experiences and presence of attenuated negative signs. Furthermore, schizotypal samples are associated with impairments in cognitive tasks, albeit in a less comprised form. For these reasons and others, schizotypy is considered a part of the extended-phenotype of schizophrenia and as such can be utilised as an analogue sample without some of theconfounds associated with illness. Objective: The aim of the PhD is to examine the relationship of schizotypal features and brain function and structure in a sample of adolescents and young adults (age 16-25 years). This will attempt to provide further evidence for the placement of schizotypy on the continuum, along with insights into pathophysiological mechanisms involved in schizophrenia and related disorders. Methods: The study involved three main phases: recruitment via an online survey, further neuropsychological testing and brain imaging on selected high schizotypes and controls. The thesis comprises 5 papers/experiments. Paper 1 utilises confirmatory factor analysis (CFA) to examine the factorial structure of the schizotypal personality questionnaire (SPQ) in a community sample aged 16-25 years. It also examined the effects of demographics on schizotypal levels. Paper 2 examined the association between schizotypy and measures of sustained attention and spatial working memory both in a total sample, and in samples split by age and by sex. Paper 3 further examined the association between schizotypy and cognition laboratory tests of attention, executive function and verbal learning/memory. Paper 4 tested the same participants on measures of functional brain asymmetry. Paper 5 used diffusion tensor imaging (DTI) to examine white matter structures in a sample of high schizotypes and controls. Results: Paper 1 confirmed that the SPQ is most appropriately modelled by a four-factor structure in an adolescent and young adult sample. Demographic effects on SPQ subscales scores mirrored those seen in clinical samples. Paper 2 found that where small associations between schizotypy and sustained attention/spatial working memory function occurred, these were in relation to either age of sex. Paper 3 demonstrated an association between increased schizotypal features and a slight reduction in performance on verbal learning/memory, but no association with tasks of executive function or attention. In Paper 4, schizotypy was associated with a left-hemifield bias on a computerised line bisection task. Paper 5 found that a group of high schizotypes had an increase in tract coherence in the uncinate fasciculus compared to controls. Furthermore, increasing subclinical hallucinatory experiences were associated with increased tract coherence in the right hemisphere arcuate fasciculus. Conclusions: Schizotypy was associated with changes in brain function and structure similar to that demonstrated in more serious mental illness, although to a lesser degree. The current studies suggested that schizotypy is associated with relatively intact prefrontal function, but slight performance bias on measures of medial temporal lobe function. There was also evidence for structural brain changes in schizotypes, with these being indicative of either a protective factor, or a marker of a pathological process. Correlations between hallucinatory experiences and white matter tracts between language regions support theories implicating hyperconnectivity and presentation of symptoms in clinical groups. The functional and structural data collected from this study suggests that the ‘schizotypal’ brain may represent an ‘early’ stage of pathology, but which is likely to be compensated enough such that transition to serious mental illness is unlikely. Further studies could examine similarities and differences between the schizotypal profile and clinical conditions, which would provide further insights into aetiological mechanisms in schizophrenia/psychosis.
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Wong, Tak-hing Michael. "Brain function and structure in violent metally abnormal offenders." Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21254163.
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Powell, Howell William Robert. "Investigating brain structure and function in temporal lobe epilepsy." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1446099/.
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Background Anterior temporal lobe resection (ATLR) is increasingly used in the treatment of patients with refractory temporal lobe epilepsy (TLE). Complications of surgery include a decline in language and memory abilities, and visual field defects. The principal aim of this thesis was to use magnetic resonance imaging (MRI) techniques to improve the planning of effective surgical treatment for patients with TLE by using functional MRI to localise areas in the brain involved in language and memory function, and MR-tractography to investigate the structural connections of these areas and those involved in visual function. Methods Ten control subjects underwent tractography to study the connections of the medial temporal lobe (MTL). Two patients underwent tractography pre- and post-operatively to look at the trajectory of the optic radiation. For the memory studies we scanned 10 control subjects and 15 presurgical patients with refractory TLE. For the combined language fMRI and tractography study, 10 control subjects and 14 patients with hippocampal sclerosis underwent both fMRI and tractography. All scans were performed on a 1.5T GE Signa Horizon scanner. Findings The connections of the MTL were identified in a group of control subjects. The optic radiation was mapped preoperatively and shown to be disrupted following ATLR in a patient with a visual field defect. A material-specific lateralisation of memory encoding activation was demonstrated in control subjects with reduced ipsilateral activation in patients with TLE. Increased ipsilateral hippocampal activation correlated with better preoperative memory function and with greater postoperative memory decline. fMRI and tractography were combined to study the structural connections of functional language areas in controls and TLE patients, demonstrating reduced left sided and increased right hemisphere connections in left TLE patients, findings that reflected the pattern of functional activation.
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Yanochko, Gina Marie. "Structure and function of the Drosophila protein Big Brain." Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/279810.
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big brain is a neurogenic gene which, when mutated causes defects in cell fate determination during Drosophila neurogenesis through an unknown mechanism. The protein Big Brain (BIB) has sequence identity with the Major Intrinsic Protein family including the water- and ion-conducting Aquaporin channels. We show here that BIB expressed heterologously in Xenopus oocytes is a non-selective monovalent cation channel with permeability to K⁺ > Na⁺ >> TEA⁺. BIB macroscopic conductance, activated in response to endogenous oocyte signaling pathways, was decreased after treatment with 20μM insulin and was enhanced with 10μM lavendustin A, a tyrosine kinase inhibitor. Current activation is not observed in control oocytes or in oocytes expressing a non-functional mutant BIB channel (E71N) that is expressed on the plasma membrane, as confirmed with confocal microscopy and western blotting. Cell-attached patch clamp experiments revealed a novel large conductance (300 ± 30pS) channel in BIB-expressing but not control oocytes. Divalent cations, such as calcium, are important developmental signaling molecules. We found that calcium and barium partially block currents in BIB-expressing oocytes. We further demonstrated that a conserved glutamate (E71) located in transmembrane domain 1 is crucial for channel properties of BIB. Mg²⁺ block was introduced in currents from oocytes expressing the BIB mutant E71D. The carboxy tail of BIB comprises 61% of the channel (431 of 700 residues) and contains sites of potential serine/threonine and tyrosine phosphorylation, SH3 binding domains, PDZ binding domains and three polyglutamine stretches. The importance of the carboxy tail for BIB channel activity was demonstrated by truncation of the channel at two sites. Truncated channels had reduced whole-cell conductance and at least one (Δ317) was not tyrosine phosphorylated. In summary, the results presented in this dissertation provide a novel function of the Drosophila protein Big Brain as a regulated cationic channel, indicate that BIB can participate in tyrosine kinase-regulated transmembrane signaling, and suggest a role for membrane depolarization in the neurogenic function of BIB in early development.
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Carr, Sheryl Teresa. "Insulin and Ketones: Their Roles in Brain Mitochondrial Function." BYU ScholarsArchive, 2017. https://scholarsarchive.byu.edu/etd/6810.
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The prevalence of both Type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD) is increasing worldwide, and the trends are unfortunately expected to continue. AD has recently been tied with mitochondrial dysfunction and insulin resistance, creating a mechanistic tie between AD and T2DM. Unfortunately, insulin resistance is often increased with aging and therefore, all individuals are at risk of brain mitochondrial dysfunction. Without proper mitochondrial function, the brain will degenerate, causing impaired cognitive function and reduced quality of life. The purpose of this study is two-fold: first, to understand the role of ceramides in insulin-induced brain mitochondrial dysfunction, and; second, to understand how ketones can restore brain mitochondrial function in aged brains. To evaluate the role of insulin resistance and ceramides in brain mitochondrial function, we induced hyperinsulinemia in ApoE4 mice. In addition to insulin, one group received myriocin injections to inhibit ceramide biosynthesis. We observed significant increases in brain ceramides in the insulin-treated group, which correlated with disrupted brain mitochondrial function. However, the group receiving myriocin alone, and, importantly, myriocin with insulin, had normal lipid profiles and normal mitochondrial bioenergetics. Altogether, these findings support the hypothesis of the key role of ceramides in insulin resistance-induced mitochondrial dysfunction within the brain. Next, young adult (5 months old) and old (28 months old) rats were assigned to either standard chow diets or very-low-carbohydrate, high-fat, ketogenic diets for 4 weeks. Following the treatment period, we analyzed brain mitochondrial function and oxidative stress. We found that the old rats fed the ketogenic diet had improved mitochondrial function in comparison to the old rats consuming standard rodent chow. In addition, the old rats fed a standard diet had significantly higher levels of oxidative stress than the aged rats on the very-low-carbohydrate, high-fat diet. These findings revealed that ketones can protect brain mitochondrial function in aging. Collectively, these results suggest that insulin resistance has a role in the development of brain mitochondrial dysfunction due to ceramide accumulation, while ketones can help mitigate some of the negative consequences of aging, perhaps some due to insulin resistance, on brain mitochondrial function.
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Ruiz, Susan Michelle Mosher. "Gender differences in brain function and structure in alcoholism." Thesis, Boston University, 2012. https://hdl.handle.net/2144/32050.
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Thesis (Ph.D.)--Boston University<br>PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>Traditionally, alcoholism research focusing on the brain included only men. Recently, inclusion of women in brain-based alcoholism research has shown that gender differences in physiology and drinking habits contribute to unique profiles of cognitive, emotional, and neuropsychological dysfunction, as well as dimorphic patterns of structural brain damage and recovery. The present study employed functional and structural magnetic resonance imaging (MRI) of alcoholic men and women and demographically-similar control participants to explore how gender and alcoholism interact to influence: (1) interference by reward-salient distractor stimuli on working memory, (2) emotional processing and memory, and (3) drinking pattern associations with structural brain abnormalities. [TRUNCATED]<br>2031-01-02
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Arichi, Tomoki. "Characterisation of the Haemodynamic Response Function (HRF) in the neonatal brain using functional MRI." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/14422.
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Background: Preterm birth is associated with a marked increase in the risk of later neurodevelopmental impairment. With the incidence rising, novel tools are needed to provide an improved understanding of the underlying pathology and better prognostic information. Functional Magnetic Resonance Imaging (fMRI) with Blood Oxygen Level Dependent (BOLD) contrast has the potential to add greatly to the knowledge gained through traditional MRI techniques. However, it has been rarely used with neonatal subjects due to difficulties in application and inconsistent results. Central to this is uncertainity regarding the effects of early brain development on the Haemodynamic Response Function (HRF), knowledge of which is fundamental to fMRI methodology and analysis. Hypotheses: (1) Well localised and positive BOLD functional responses can be identified in the neonatal brain. (2) The morphology of the neonatal HRF differs significantly during early human development. (3) The application of an age-appropriate HRF will improve the identification of functional responses in neonatal fMRI studies. Methods: To test these hypotheses, a systematic fMRI study of neonatal subjects was carried out using a custom made somatosensory stimulus, and an adapted study design and analysis pipeline. The neonatal HRF was then characterised using an event related study design. The potential future application of the findings was then tested in a series of small experiments. Results: Well localised and positive BOLD functional responses were identified in neonatal subjects, with a maturational tendency towards an increasingly complex pattern of activation. A positive amplitude HRF was identified in neonatal subjects, with a maturational trend of a decreasing time-to-peak and increasing positive peak amplitude. Application of the empirical HRF significantly improved the precision of analysis in further fMRI studies. Conclusions: fMRI can be used to study functional activity in the neonatal brain, and may provide vital new information about both development and pathology.
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Soehnlen, Steve G. "A Rat Model of Sleep Deprivation Prior to Traumatic Brain Injury." Cleveland State University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=csu1304627398.
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Breen, Mara E. "The identification and function of English prosodic features." Thesis, Massachusetts Institute of Technology, 2007. http://hdl.handle.net/1721.1/40974.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2007.<br>Includes bibliographical references (leaves 98-102).<br>This thesis contains three sets of studies designed to explore the identification and function of prosodic features in English. The first set of studies explores the identification of prosodic features using prosodic annotation. We compared inter-rater agreement for two current prosodic annotation schemes, ToBI (Silverman, et al., 1992) and RaP (Dilley & Brown, 2005) which provide guidelines for the identification of English prosodic features. The studies described here survey inter-rater agreement for both novice and expert raters in both systems, and for both spontaneous and read speech. The results indicate high agreement for both systems on binary classification, but only moderate agreement for categories with more than two levels. The second section explores an aspect of the function of prosody in determining the propositional content of a sentence by investigating the relationship between syntactic structure and intonational phrasing. The first study tests and refines a model designed to predict the intonational phrasing of a sentence given the syntactic structure. In further analysis, we demonstrate that specific acoustic cues-word duration and the presence of silence after a word, can give rise to the perception of intonational boundaries. The final set of experiments explores the relationship between prosody and information structure, and how this relationship is realized acoustically. In a series of four experiments, we manipulated the information status of elements of declarative sentences by varying the questions that preceded those sentences. We found that all of the acoustic features we tested-duration, f0, and intensity-were utilized by speakers to indicate the location of an accented element. However, speakers did not consistently indicate differences in information status type (wide focus, new information, contrastive information) with the acoustic features we investigated.<br>by Mara E. Breen.<br>Ph.D.
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Vernon, Amanda Ph D. Massachusetts Institute of Technology. "Enhanced striatal glutamatergic function upon chronic antipsychotic action." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/132750.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, June, 2019<br>Cataloged from the PDF version of thesis.<br>Includes bibliographical references (pages 186-208).<br>Schizophrenia is a psychiatric disorder characterized by multiple clusters of symptoms including positive symptoms, such as hallucinations and delusions, negative symptoms, such as decreased motivation and flattened affect, and cognitive symptoms, such as memory impairment and impaired executive function. Currently available antipsychotics mitigate some symptoms of schizophrenia, particularly the positive symptoms, but there is no preventive treatment nor cure after schizophrenia develops. Efforts to generate more effective antipsychotics are made particularly challenging by the fact that the therapeutic effect of currently prescribed antipsychotics is not well understood and the cell type(s) and brain circuits crucial for beneficial effects have not been conclusively identified. Here we show that chronic antipsychotic administration enhances glutamatergic function in the ventral striatum through translational alterations and increased synaptic function. Cell type-specific mRNA profiling on spiny projection neurons (SPNs) of the direct (dSPNs) and indirect (iSPNs) pathways following chronic antipsychotic administration revealed cell type-specific molecular alterations indicating increases in components of the glutamatergic postsynaptic density. Subsequent functional experiments demonstrated the presence of calcium-permeable AMPARs and increased mEPSC frequency following chronic administration of one especially effective antipsychotic, clozapine. Furthermore, we find that striatal astrocytes also respond to chronic antipsychotic treatment with translational alterations promoting synaptogenesis. Together, these data have identified a core molecular signature of increased glutamatergic transmission in the striatum induced by chronic antipsychotic treatment. This work provides evidence that effective antipsychotics address a lack of glutamatergic drive into the striatum in cases of schizophrenia. Additionally, it suggests that drug development efforts seeking improved antipsychotics may benefit by finding compounds that feature an increased glutamatergic drive into the striatum as a core function.<br>by Amanda Vernon.<br>Ph. D.<br>Ph.D. Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences
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Lai, Kam-ming. "Structure and function of 5'-nucleotidase of the rat brain /." [Hong Kong : University of Hong Kong], 1991. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12986343.
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