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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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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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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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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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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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Schwarb, Hillary. "Optimized cognitive training: investigating the limits of brain training on generalized cognitive function." Diss., Georgia Institute of Technology, 2012. http://hdl.handle.net/1853/47599.
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Since antiquity, philosophers, theologians, and scientists have been interested in human memory; however, researchers today are still working to understand the capabilities, boundaries, and architecture. While the storage capabilities of long-term memory are seemingly unlimited (Bahrick, 1984), working memory, or the ability to maintain and manipulate information held in memory, seems to have stringent capacity limits (e.g., Cowan, 2001). Individual differences, however, do exist and these differences can often predict performance on a wide variety of tasks (cf. Engle, 2001). Recently, researchers have promoted the enticing possibility that simple behavioral training can expand the limits of working memory which indeed may also lead to improvements on other cognitive processes as well (cf. Morrison&Chein, 2011). The current study investigated this possibility. Recommendations from the skill training literature (cf. Schneider, 1985) were incorporated to create optimized verbal and spatial working memory training tasks. Significant performance improvements were evident across eight days of cognitive training using verbal and spatial adaptive n-back procedures. Training-related improvements were also evident for some untrained measures of visual short-term memory, attentional control, and working memory. These training effects, however, were not universal. Other measures of visual short-term memory and attentional control, as well as measures of fluid intelligence were unaffected by training.
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Parker, Tonya Moreland. "Recovery of motor and cognitive function following concussion /." view abstract or download file of text, 2006. http://proquest.umi.com/pqdweb?did=1188883691&sid=1&Fmt=2&clientId=11238&RQT=309&VName=PQD.
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Thesis (Ph. D.)--University of Oregon, 2006.<br>Typescript. Includes vita and abstract. Includes bibliographical references (leaves 113-119). Also available for download via the World Wide Web; free to University of Oregon users.
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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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Clavenstam, Isabell. "The Effect of Methamphetamine Abuse on Brain Structure and Function." Thesis, University of Skövde, School of Humanities and Informatics, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-3106.
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<p>The great amount of METH abuse all over the world causes enormous social and criminal justice problems. In the human brain the abuse of METH causes implications on both structures and functions given rise to acute as well as long term symptoms. In this essay the effects of METH abuse is described in the manner of the drug mechanism such as the impact on neurotransmitters, structural deficits with decreased and increased volumes and the implication on attention, memory, decision making and emotions. Results from studies showing brain structural and cognitive impairments in METH abusers and in prenatal METH exposed children.</p>
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Pham, Therese M. "Effects of neonatal handling and enriched environment on neurotrophins and cognitive function /." Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4362-1/.
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Osher, David Eugene. "Function follows form : how connectivity patterns govern neural responses." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/81731.
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Thesis (Ph. D. in Neuroscience)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2013.<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>Connectivity restricts and defines the information that a network can process. It is the substance of information processing that underlies the patterns of functional activity in the brain. By combining diffusion-weighted imaging or DWI, with fMRI, we are able to non-invasively measure connectivity and neural responses in the same individuals and directly relate these two measures to one another. In Chapter 2, I first establish the proof-of-principle that anatomical connectivity alone can predict neural responses in cortex, specifically of face-selectivity in the fusiform gyrus. I then extend this novel approach to the rest of the brain and test whether connectivity can accurately predict neural responses to various visual categories in Chapter 3. Finally, in Chapter 4, I compare and contrast the resulting models, which are essentially networks of connectivity that are functionally-relevant to each visual category, and demonstrate the type of knowledge that can be uncovered by directly integrating structure and function.<br>by David Eugene Osher.<br>Ph.D.in Neuroscience
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Martiros, Nuné. "Characterizing corticostriatal circuit function during performance of habitual action sequences." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/106437.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2016.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references (pages 101-111).<br>The striatum is the largest nucleus in the basal ganglia and the recipient of dense dopamine input. Multiple cortico-basal ganglia-thalamic loops are thought to function together during the learning and performance of reinforced behaviors, with the dorsolateral circuit being particularly critical for the learning of habitual chains of action sequences. However, how this circuit works to generate such behavior is poorly understood. To explore the nature of striatal neural representations during learned action sequences, I designed a task targeted at disambiguating movement-related responses from habit representations in striatum. In combination with this task, I employed electrophysiology and optogenetics techniques to characterize task-related neuronal activity in the corticostriatal circuit. I found that, unlike in motor cortex, neurons in striatum did not respond simply to particular individual actions, but responded preferentially at the initiation and termination of learned action sequences. These experiments provide a test for the existence of a generalized striatal signal marking the start and end of units of habitual behaviors which may be produced with the contribution of striatal interneurons, providing a mechanism by which striatum can control the encoding and performance of chunked action sequences. In a separate set of experiments, I explored the effect of dopamine depletion on local field potential oscillations in the same region of striatum. My goal was to investigate the interaction between abnormal oscillations caused by dopamine depletion in Parkinson's disease and the functional task-related oscillations that normally occur in healthy striatum. Against our expectations, I found that local unilateral dopamine depletion in dorsolateral striatum did not result in changes in pre-task baseline strength of oscillations, but rather in the overexpression of the normal task-related oscillations. These studies add support to theories of striatal function and dysfunction that emphasize selective network modulation by learned behaviors.<br>by Nuné Martiros.<br>Ph. D.
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Solé, Padullés Cristina. "Function and brain structure in aging with and without cognitive impairment." Doctoral thesis, Universitat de Barcelona, 2007. http://hdl.handle.net/10803/2705.
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L'interès general d'aquest projecte de tesi doctoral es centra en l'estudi dels patrons d'activació cerebral subjacents a l'envelliment cognitiu, tant en condicions clíniques normals com patològiques (Alteració cognitiva relacionada amb l'edat, alteració cognitiva lleu o Alzheimer inicial). Per aquest motiu hem empleat la tècnica de la RMf i hem estudiat com diferents variables intrínseques i extrínseques als individus estudiats influeixen la seva activació cerebral.<br/><br/>En un primer estudi ens vam plantejar l'estudi de les relacions entre el cervell i conducta en subjectes envellits amb queixes subjectives de memòria, segons criteris de Levy (1994). Així, el primer objectiu era estudiar com una tècnica capaç de modificar l'excitabilitat cortical de forma transitòria, l'estimulació magnètica transcranial (EMT) podia modular l'activació cerebral observada amb RMf i de retruc influir l'execució d'una tasca d'aprenentatge.<br/><br/>Posteriorment, després d'haver observat un efecte facilitador de l'EMT en el rendiment en memòria d'aquest subjectes vam voler tenir en compte com el fet de ser portador de la variant ε4 del gen de l'apolipoproteïna E (APOE), podria modular l'activació cerebral després d'una sessió d'EMT. Aquest al.lel s'ha relacionat amb disfuncions de tipus tant metabòlic com d'activació cerebral durant la realització de tasques cognitives, similars als observats en la MA, per tant l'objectiu d'aquest estudi era veure com dos factors, un intrínsec (ser portador de ε4) i una altre extrínsec (EMT), ambdós amb un efecte conegut en l'activació cerebral s'influïen mútuament per modular els patrons funcionals i com això afectava en últim terme l'execució en memòria. <br/><br/>Seguint amb l'estudi de les diferències funcionals entre portadors ε4 i no ε4, ens va interessar determinar els patrons de connectivitat cerebral de l'hipocamp en aquests dos grups de subjectes, amb queixes de memòria, durant l'execució d'una tasca de memòria associativa. <br/><br/>Finalment, després d'haver observat les diferents graus de manifestacions clíniques en subjectes amb una neuropatologia equiparable o les diferències en patrons d'activació causades per un emergent patologia cerebral vam considerar l'estudi d'aquestes diferències individuals (descrites com a factors de reserva cognitiva) per investigar els seus efectes en la funció i estructura cerebral de subjectes envellits pertanyents a diferents categories clíniques (envelliment normal, ACL i MA).<br/><br/>En resum, els objectius específics de la tesi es podrien concretar en els següents punts: <br/><br/>1) Estudiar els efectes de l'Estimulació Magnètica Transcranial (EMT) en l'activitat cerebral i el rendiment cognitiu durant una prova d'aprenentatge visual en una mostra de pacients envellits amb queixes de memòria. <br/><br/>2) Estudiar els efectes de la interacció entre l'EMT i el genotip de l'APOE en una mostra de pacients amb queixes de memòria. <br/><br/>3) Estudiar com el fet de tenir un determinat genotip del polimorfisme de l'APOE podria afectar els patrons d'activitat i connectivitat cerebrals mentre es realitza una tasca d'aprenentatge en pacients amb alteració cognitiva relacionada amb l'edat. <br/><br/>4) Estudiar la influència de les variables de reserva cognitiva en l'estructura cerebral per tal de provar la hipòtesi de la reserva cerebral, així com investigar com un determinat nivell de reserva cognitiva pot influenciar els patrons d'activitat cerebral per tal d'explorar els models actius (compensació) en l'envelliment normal, ACL i MA inicial.
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Su, Susan C. (Susan Chih-Chieh). "Regulation of synaptic function and plasticity by cyclin-dependent kinase 5." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/79141.
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Thesis (Ph. D. in Neuroscience)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, February 2013.<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. "February 2013." Page 192 blank.<br>Includes bibliographical references.<br>The neuronal serine/threonine kinase cyclin-dependent kinase 5 (Cdk5) is activated by its regulatory subunit, p35, to post-translationally modify substrates through phosphorylation. In this thesis, I provide several lines of evidence that Cdk5 plays a critical role in synaptic function and plasticity. First, we characterized the function of Cdk5 in learning and memory by region-specific Cdk5 ablation. From multiple Cdk5 conditional knockout mouse models, we determined that Cdk5 is essential for memory formation and synaptic plasticity. Loss of Cdk5 in the hippocampus disrupts the cAMP pathway due to increased phosphodiesterase proteins. This dysregulation of cAMP signaling can be attenuated by a phosphodiesterase inhibitor to restore levels of protein phosphorylation, synaptic plasticity, and memory. Moreover, forebrain-specific deletion of Cdk5 affected multiple aspects of behavior that can partially be rescued by lithium treatment. We next identified the N-type calcium channels as a presynaptic substrate of Cdk5. We described how Cdk5-mediated phosphorylation of the N-type calcium channel increased calcium influx and channel open probability. This in turn enhanced the association of the N-type calcium channel with the active zone protein RIM1, which impacted vesicle docking and neurotransmission. Finally, we identified the postsynaptic density protein Shank3 as a Cdk5 substrate and observed that Cdk5-mediated phosphorylation of Shank3 plays a critical role in maintaining dendritic spine morphology and synaptic plasticity. Our collective results demonstrate a central role for Cdk5 in regulating both presynaptic and postsynaptic functions and provide better insight into how specific targets of Cdk5 can impact a general mechanism underlying synaptic transmission, synaptic plasticity, and cognitive function.<br>by Susan C. Su.<br>Ph.D.in Neuroscience
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Blunk, Aline D. (Aline Dorret). "Regulation of synaptic structure and function at the Drosophila neuromuscular junction." Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/84874.
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Thesis (Ph. D. in Neuroscience)--Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2013.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>Neuronal communication requires a spatially organized synaptic apparatus to coordinate neurotransmitter release from synaptic vesicles and activation of postsynaptic receptors. Structural remodeling of synaptic connections can strengthen neuronal communication and synaptic efficacy during development and behavioral plasticity. Here, I describe experimental approaches that have revealed how the actin cytoskeleton participates in transynaptic signaling to control synapse assembly. I also describe my studies on how regulation of endocytic trafficking controls synaptic growth during neuronal development. To identify regulators of synapse assembly, I carried out a large-scale EMS mutagenesis screen of the second chromosome. From this screen I identified a mutation in actin 57B that disrupts synaptic morphology and presynaptic active zone organization. Actin 57B is one of six actin genes in Drosophila and is expressed in body wall muscle during larval development. The isolated allele harbors a point mutation disrupting a highly conserved amino acid present throughout the actin family. Homozygous mutant larvae show impaired alignment and spacing of presynaptic active zones. Additionally, disruption of the organization of the postsynaptic density is observed, with mislocalization of the Spectrin cytoskeleton and the PSD-homolog Disc-Large. Phallodin staining reveals a severe disruption of postsynaptic actin surrounding presynaptic boutons, with the formation of aberrant large actin swirls. Based on these results, we hypothesize that the loss of a synaptic interaction mediated by actin 57B leads to disruption of postsynaptic cytoskeletal organization and dysregulation of signals required to organize presynaptic active zones. Additionally, I present data that provide new insights into the mechanisms controlling synaptic growth signaling during transit through the endocytic pathway. Nervous Wreck (Nwk) is a presynaptic F-BAR/SH3 protein that regulates synaptic growth signaling in Drosophila. Here, I show that Nwk acts through a physical interaction with Sorting Nexin 16 (SNX16). SNX16 promotes synaptic growth signaling by activated BMP receptors, and live imaging in neurons reveals that SNX16-positive early endosomes undergo transient interactions with Nwkcontaining recycling endosomes. We identify an alternative signal termination pathway in the absence of Snx16 that is controlled by ESCRT-mediated internalization of receptors into the endosomal lumen. Our results define a presynaptic trafficking pathway mediated by SNX116, NWK and the ESCRT complex that functions to control synaptic growth signaling at the interface between endosomal compartments. Together, these experiments have expanded our understanding of the molecular mechanisms that control synaptic growth and assembly, highlighting the role of the postsynaptic actin cytoskeleton and the presynaptic endosomal trafficking pathway as key regulators.<br>by Aline D. Blunk.<br>Ph.D.in Neuroscience
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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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Cooke, Michael Alan. "Insight in schizophrenia : relationship to cognitive function, coping style and brain structures." Thesis, King's College London (University of London), 2006. https://kclpure.kcl.ac.uk/portal/en/theses/insight-in-schizophrenia--relationship-to-cognitive-function-coping-style-and-brain-structures(58fbfb60-3fdf-4e76-a927-1c85e814c96f).html.
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Inne, Hoff Erik. "Vascular cognitive impairment and cholinergic function an integrative analysis in rat brain /." [Maastricht] : Maastricht : [Maastricht University] ; University Library, Universiteit Maastricht [host], 2009. http://arno.unimaas.nl/show.cgi?fid=15082.
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Runyan, Caroline A. (Caroline Anne). "Distinct roles for inhibitory neuron subtypes in cortical circuits : an examination of their structure, function, and connectivity." Thesis, Massachusetts Institute of Technology, 2012. http://hdl.handle.net/1721.1/73772.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2012.<br>"June 2012." Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>Parvalbumin-containing (PV+) neurons and somatostatin-containing (SOM+) neurons are two key cortical inhibitory cell classes that are poised to play distinct computational roles in cortical circuits: PV+ neurons form synapses on the perisomatic region near the spike initiation zone of target cells, while SOM+ neurons form synapses on distal dendrites. The goals of this thesis are to better understand the functional roles of these two cell types with four major lines of questioning. 1) When and how do PV+ and SOM+ neurons respond to visual stimuli? 2) How do inhibitory neurons obtain their response selectivity? 3) How do PV+ and SOM+ neurons affect the responses of their targets? and 4) What are the targets of PV+ and SOM+ neurons? We used Cre-lox recombination to introduce either fluorescent protein or channelrhodopsin to PV+ or SOM+ neurons, targeting these cells for two-photon targeted physiological recording and morphological reconstruction, or selectively stimulating the population of PV+ or SOM+ neurons or stimulating single PV+ or SOM+ neurons. We find diverse response properties within both groups, suggesting that further functional subclasses of PV+ and SOM+ neurons may exist. Furthermore, orientation selectivity was strongly correlated to dendritic length in PV+ neurons, whose orientation preferences matched the preferences of neighboring cells, implying that inhibitory neurons may obtain selectivity by spatially limiting their sampling of the local network. When we stimulated PV+ and SOM+ neurons, we found that they perform distinct inhibitory operations on their targets: PV+ neurons divide responses while SOM+ neurons subtract. Even single PV+ and SOM+ neurons were capable of suppressing responses of other cells in the local network, but their functional targeting was sparse and followed different rules of wiring: PV+ neurons functionally suppressed a higher percentage of cells that shared their own tuning, while SOM+ neurons seemed to target other neurons independently of their preferred orientations. By studying the response properties and functional impacts of PV+ and SOM+ neurons in the intact primary visual cortex, we have gained insight into what information these cells are carrying and how they contribute to the response properties of other cells, which apply to cortical circuits in general.<br>by Caroline A. Runyan.<br>Ph.D.
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Buhl, Lauren Kaye. "Synaptic structure and function at the Drosophila larval neuromuscular junction : a molecular analysis of complexin and radish." Thesis, Massachusetts Institute of Technology, 2011. http://hdl.handle.net/1721.1/65285.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2011.<br>Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>From yeast to humans, the fusion of vesicles with target membranes is driven by the formation of a parallel four-helix bundle of SNARE proteins that are present on both the vesicular (v-SNAREs) and target plasma membranes (t-SNAREs). The full zippering of this bundle is thought to provide the driving force for membrane fusion. At synapses, vesicle fusion is exquisitely regulated by Ca2+ such that neurotransmitter release can occur within 1 ms of an action potential reaching the presynaptic terminal. This feat implies the presence of both a Ca2+ sensor and a fusion clamp that prevents vesicles from fusing in the absence of Ca2+. The presynaptic Ca2+ sensor for synchronous vesicle release is widely accepted to be Synaptotagmin-1 (Syt1), and there is growing evidence that Complexin (Cpx), which binds to the SNARE complex with high affinity and 1:1 stoichiometry, can act as a vesicle fusion clamp. As suggested by its name, however, Cpx appears to play a more complex role in vesicle release, carrying out different functions in spontaneous vs. evoked fusion events. Here we show the Drosophila express at least two Cpx isoforms that differ in the C-terminus (Cpx7A and Cpx7B) and can be further regulated by RNA editing and phosphorylation. These isoforms show different effects on spontaneous vs. evoked neurotransmitter release, with Cpx7A being a better fusion clamp and Cpx7B being a better fusion promoter. In addition, these isoforms have different effects on synaptic growth, which may be linked to their effects on synaptic physiology.<br>by Lauren Kaye Buhl.<br>Ph.D.
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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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Cader, Sarah. "Cognitive function in multiple sclerosis and its modulation by cholinergic drugs." Thesis, University of Oxford, 2005. http://ora.ox.ac.uk/objects/uuid:d07ad815-4fc6-43b7-96dc-97a2705d6c6a.
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In order to assess cognitive function in multiple sclerosis (MS) and the effect of cholinergic modulation, experiments were conducted using functional magnetic resonance imaging (fMRI) to assess the brain activation during cognitive tasks. A study comparing the processing of verbal working memory with an N-back task found that patients showed smaller increase in activation than healthy controls with greater task difficulty, suggesting a reduced functional reserve. Controls and patients showed differences of correlations between brain regions activated. Interactions between prefrontal regions may provide an adaptive mechanism that could limit clinical expression of the disease distinct from recruitment of novel processing regions. The effect of Rivastigmine on the cognitive processing in MS patients was tested in a longitudinal study, involving serial fMRI scans. Changes in the brain activation patterns were demonstrated with drug administration, without any changes in behavioural measures. Rivastigmine may act to increase the functioning of the normal neural network reducing the need for previously recruited compensatory mechanisms in MS patients. A study on healthy subjects examined the effect of cholinergic inhibition on cognitive processing and brain activation. Changes in functional activation due to Hyoscine during verbal working memory were found analogous to that in MS patients without any changes in behavioural measures. Processes that potentially impair brain cognitive function may recruit similar compensatory functional adaptive mechanisms. Studies on rats and MS patients explored the effect of Rivastigmine on the relationship of the BOLD fMRI signal with the underlying neural activity. Rivastigmine may be influencing the cortical excitability after direct cortical stimulation but showed only a small effect on the BOLD signal under more physiological neural activity. The neural activity in response to visual stimulation is slightly increased with Rivastigmine in MS patients, a change not detected with functional imaging. These studies suggest that changes in BOLD signal do represent sufficiently large changes of underlying neural activity in the presence of Rivastigmine. The relationship of damage in MS to measures of connectivity was studied using diffusion tensor imaging (DTI). Correlation was found between measures of connectivity and callosal size, a measure of fibre loss. The distribution of lesions was spatially correlated with changes in connectivity due to MS. Thus DTI could be utilized to explore the connectivity changes associated with MS, and the relationship with changes in functional activation.
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Loeb, Eric Peter. "Uses of statistical muscle models, including a test of an equilibrium point control theory of spinal cord function in Rana catesbiana." Thesis, Massachusetts Institute of Technology, 1996. http://hdl.handle.net/1721.1/10891.
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Ferguson, Stewart C. "Type 1 diabetes mellitus and the brain : influence of clinical complications and genetic factors on brain structure and cognitive function." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/29100.
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Microvascular disease, manifest as retinopathy, neuropathy or nephropathy, frequently complicates diabetes, the risk being related to long-term glucose control and increasing disease duration. Microvascular disease may also affect the cerebral circulation and could potentially compromise brain structure and intellectual performance. Type 1 diabetes commonly develops in childhood before maturation of the central nervous system and the developing brain may exhibit relative vulnerability to damage as a consequence of exposure to severe hypoglycaemia, or the development of Diabetic Keto-Acidosis, in early childhood. Genetic factors influence the vulnerability of an individual to develop cognitive impairment following pathological processes known to disadvantage the central nervous system. Polymorphism of the Apolipoprotein-E gene has been identified as one such factor and is known to influence the prognosis and cognitive outcomes following a wide variety of cerebral results. The studies contained within this Thesis explore the long-term consequences the clinical factors described above on brain structure and the cognitive performance of young adults with Type 1 diabetes mellitus of long duration. The effects of polymorphism of the Apolipoprotein-E gene on the cognitive performance of young adults who have Type 1 diabetes mellitus are also evaluated.
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Nilsson, Malin. "Effects of the Mediterranean Diet on Brain Function : Underlying mechanisms." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-17531.
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The Mediterranean diet (Medi) has been highlighted as the golden diet rich in protective properties associated with cognitive- and emotional health. The foundation of the Medi comprises vegetables, fruits, nuts and seeds, legumes, and extra virgin olive oil. Research has been conducted in both holistic dietary approach and single nutrient approach regarding the impact of nutrition and diet, in this case, the Medi‟s effect on brain health. This review aims to give an up to date overview of the Mediterranean diet, outline some of the diet's abundant nutrients, and discuss studies linking the nutrient's potential effect on depression, cognitive decline, dementia, and brain structure and function. In addition, this review will attempt to assess whether the Medi as a whole or if a single nutrient approach is accountable for the health-promoting findings. Furthermore, the gut-brain axis, and other potential underlying mechanisms involved in the modulation of food- and nutrient intake and their effects on the brain, will be outlined. A diet high in fruit-, vegetable-, polyunsaturated fatty acid-, and monounsaturated fatty acid content has great power for health-maintenance and decreases the risk of suffering cognitive decline, dementia, and potentially depression. More randomized controlled trials are however eagerly awaited to give more substance to previous findings.
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Papmeyer, Martina. "Structural brain imaging and cognitive function in individuals at high familial risk of mood disorders." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15915.
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Bipolar disorder (BD) and major depressive disorder (MDD) are characterised by a fundamental disturbance of mood, with strong support for overlapping causal pathways. Structural brain and neurocognitive abnormalities have been associated with mood disorders, but it is unknown whether these reflect early adverse effects predisposing to mood disorders or emerge as a consequence of illness onset. The Bipolar Family Study is well-suited to examine the origin of structural brain and neuropsychological abnormalities in mood disorders further. The volumes of subcortical brain regions, cortical thickness and surface area measures of frontal and temporal regions of interest and neuropsychological performance over a two-year time interval was compared at baseline and longitudinally between three groups: young individuals at high risk of mood disorders who subsequently developed MDD during the follow-up period (HR-MDD), individuals at high risk of mood disorders who remained well (HR-well), and healthy control subjects (HC). The longitudinal analysis of cortical thickness revealed significant group effects for the right parahippocampal and right fusiform gyrus. Cortical thickness in both of these brain regions across the two time points was reduced in both high-risk groups relative to controls, with the HR-MDD group displaying a thinner parahippocampus gyrus than the HR-well group. Moreover, a significant interaction effect was observed for the left inferior frontal and left precentral gyrus. The HR-well subjects had progressive thickness reductions in these brain regions relative to controls, while the HR-MDD group showed cortical thickening of these areas. Finally, longitudinal analyses of neuropsychological performance revealed a significant group effect for long delay verbal memory and extradimensional set-shifting performance. Reduced neurocognitive performance during both tasks across the two time points was found in the HR-well group relative to controls, with the HR-MDD group displaying decreased extradimensional set-shifting abilities as compared to the HC group only. These findings indicate, that reduced left parahippocampal and fusiform thickness constitute a familial trait marker for vulnerability to mood disorders and may thus form potential neuroanatomic endophenotypes. Particularly strong thickness reductions of the parahippocampal gyrus appear be linked to an onset of MDD. Moreover, progressive thickness reductions in the left inferior frontal and precentral gyrus in early adulthood form a familial trait marker for vulnerability to mood disorders, potentially reflecting early neurodegenerative processes. By contrast, an absence of cortical thinning of these brain regions in early adulthood appears to be linked to the onset of MDD, potentially reflecting a lack or delay of normal synaptic pruning processes. Reduced long delay verbal memory and extradimensional set-shifting performance across time constitute a familial trait marker for vulnerability to mood disorders, likely representing disturbances of normal brain development predisposing to illness. These findings advance our understanding of the origin of structural brain and neurocognitive abnormalities in mood disorders.
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Holt, Rosemary. "Investigating individuals with autism spectrum conditions and their siblings : cognitive measures, brain structure and function." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607896.
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Johnston, Harriet N. "Cognitive and brain function in adults with Type 1 diabetes mellitus : is there evidence of accelerated ageing?" Thesis, University of St Andrews, 2013. http://hdl.handle.net/10023/3446.
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The physical complications of Type 1 diabetes mellitus (T1DM) have been understood as an accelerated ageing process (Morley, 2008). Do people with T1DM also experience accelerated cognitive and brain ageing? Using findings from research of the normal cognitive and brain ageing process and conceptualized in theories of the functional brain changes in cognitive ageing, a combination of cognitive testing and functional magnetic resonance imaging (fMRI) techniques were used to evaluate evidence of accelerated cognitive and brain ageing in middle-aged adults with T1DM. The first part of this thesis comprises a cognitive study of 94 adults (≥ 45 years of age) with long duration (≥ 10 years) of T1DM. Participants completed cognitive assessment and questionnaires on general mood and feelings about living with diabetes. Findings highlighted the importance of microvascular disease (specifically retinopathy) as an independent predictor of cognitive function. The incidence and predictors of mild cognitive impairment (MCI) were then explored. Results indicate a higher percentage of the group met criteria for MCI than expected based on incidence rates in the general population, providing initial evidence of accelerated cognitive ageing. Psychological factors were explored next. The relationship between the measures of well-being, diabetes health, and cognitive function highlighted the need for attention to patient's psychological well-being in diabetes care. Finally, a subgroup of 30 participants between the ages of 45 and 65 who differed on severity of retinopathy were selected to take part in an fMRI study. Blood oxygen level dependent (BOLD) activity was evaluated while participants were engaged in cognitive tasks and during rest. The findings provided evidence that the pattern of BOLD activation and functional connectivity for those with high severity of retinopathy are similar to patterns found in adults over the age of 65. In line with the theories of cognitive ageing, functional brain changes appear to maintain a level of cognitive function. Evidence of accelerated brain ageing in this primarily middle-aged group, emphasizes the importance of treatments and regimens to prevent or minimize microvascular complications.
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Janoos, Firdaus H. "Spatio-Temporal Representations and Analysis of Brain Function from fMRI." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1295643292.
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Chua, Eldrich Norwin Siy, and 蔡季延. "The effects of noninvasive brain stimulation on cognitive function in patients with stroke : a systematic review." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206919.
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Introduction: Cognitive impairments occur frequently in stoke survivors, yet current conventional post-stroke care focuses mainly on motor function. Transcranial direct current stimulation (tDCS) and repetitive transcranial magnetic stimulation (rTMS) are noninvasive brain stimulation techniques (NIBS) that are used in neurological rehabilitation. Its efficacy is well-established in motor recovery post-stroke, but research on its effects on the associated cognitive decline after stroke is fairly new. The aim of this review is to evaluate recent studies and provide a summary on the effects of NIBS on post-stroke cognitive decline.
Methods: PubMed and CINAHL were searched using the keywords: “cerebrovascular accident”, “stroke”, “NIBS” or “noninvasive brain stimulation”, “tDCS” or “transcranial direct current stimulation”, and “TMS” or “transcranial magnetic stimulation”. PEDro system was used to assess the quality of the studies that passed the inclusion and exclusion criteria.
Results: The initial search returned 1081 citations, among which 12 were included in this review. The mean PEDro score of the studies was 7.5 out of 10. The trials had a total of 176 participants with stroke. Lesion site was heterogeneous. Six trials investigated tDCS, and the other 6 investigated rTMS. The main outcome measures were grouped into 3 domains: memory, visuospatial, and attention. Both tDCS and rTMS resulted in significant changes in the visuospatial domain in terms of improving spatial neglect. The results on memory and attention are mixed, but tDCS shows more consistent results.
Conclusion: NIBS is a safe and low-cost treatment that can improve cognitive decline post-stroke. However, the evidence is still lacking due to the small number of trials and sample sizes. More studies need to be conducted in order to establish a proper guideline for usage. Long term effects also need to be investigated.<br>published_or_final_version<br>Public Health<br>Master<br>Master of Public Health
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Yin, Yu Shen. "Spontaneous injury-induced hippocampal neurogenesis following kainic acid-mediated neurodegeneration and its effects on cognitive function." Thesis, The University of Sydney, 2018. http://hdl.handle.net/2123/20771.
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Adult mammalian neurogenesis occurs throughout life within two discrete brain regions; subventricular zone (SVZ) and subgranular zone (SGZ). Acute brain insults are associated with spontaneous increases in neurogenesis. This has been observed in both the SVZ and SGZ, as well as non-neurogenic regions. In some cases, this neurogenic response has been linked to cognitive recovery, although a direct functional relationship between injury-induced neurogenesis and cognitive recovery remains to be elucidated. The present work aimed to explore the functional relevance of spontaneous injury-induced neurogenesis in relation to recovery of hippocampal-dependent memory functions following acute brain injury. The kainic acid (KA) model of acute excitotoxic injury is a widely used model of acute neurodegeneration. Increases in SGZ neurogenesis have been well documented to occur following KA-induced injury, while evidence of neurogenesis occurring outside the SGZ is sparse. Prior work by our group had established the occurrence of neurogenesis in discrete non-neurogenic hippocampal regions; CA1 and CA3. However, several questions have remained, such as where the newborn cells are initially generated and whether or not they functionally integrate into existing circuits. In our efforts to establish a reproducible model of KA-induced hippocampal neurodegeneration that facilitated subsequent neuronal repopulation, we investigated the impact of several variables that may have been affecting the inconsistencies we observed in our initial attempts to reproduce the model. In parallel, we investigated the origin and functional significance of the KA-induced neurogenic response previously observed by our group. Lastly, we undertook histopathological analyses of the APPswe/PS1ΔE9 mouse model of Alzheimer’s disease (AD), a neurodegenerative disease where neurogenesis appears dysregulated, and established a baseline phenotype for future investigations into dysregulation of neurogenesis in AD.
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Quigley, Andrea. "EFFECTS OF HYPERTONIC SALINE ON RECOVERY OF FUNCTION FOLLOWING CONTROLLED CORTICAL IMPACT BRAIN INJURY." Available to subscribers only, 2009. http://proquest.umi.com/pqdweb?did=1967963291&sid=6&Fmt=2&clientId=1509&RQT=309&VName=PQD.
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Tinker, Jennifer Ruby Zillmer Eric. "Reported visual disturbance and post-concussion cognitive function in collegiate athletes : the relationship between symptom report and neurocognitive outcome /." Philadelphia, Pa. : Drexel University, 2010. http://hdl.handle.net/1860/3264.
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Niogi, Sumit Narayan. "Quantification of white matter integrity accounts for differences in specific cognitive function in adults with and without traumatic brain injury /." Access full-text from WCMC:, 2007. http://proquest.umi.com/pqdweb?did=1432771681&sid=3&Fmt=2&clientId=8424&RQT=309&VName=PQD.
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Zeigler, Michael. "THE EFFECTS OF bFGF TREATMENT IN THE AGED BRAIN FOLLOWING TRAUMATIC BRAIN INJURY." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/2227.
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The mature mammalian brain continually generates new neurons in the subventricular zone and hippocampus throughout life. Adult neurogenesis in the hippocampus is associated with hippocampal-dependent learning and memory function. During aging, this endogenous neurogenic potential is reduced which is accompanied by decreased cognitive function seen in the aging population. We have previously found that the injured adult brain shows heightened levels of endogenous neurogenesis and this response is associated with innate cognitive recovery. We have also found that basic fibroblast growth factor (bFGF), a potent neurotrophic polypeptide, can enhance injury-induced hippocampal neurogenesis and improve cognitive recovery following TBI. In this study, we administered bFGF into the lateral ventricle of aged rats following TBI and assessed the effect of bFGF treatment on hippocampal neurogenesis and cognitive recovery in aged animals. Specifically, male Fisher-344 rats at the age of 20 months received intraventricular infusion of bFGF for 7 days through osmotic mini-pump immediately following a moderate lateral fluid percussion injury. To label cell proliferation, animals received daily single i.p. BrdU injections for 6 days beginning 48 hr after injury. One group of animals was perfused at 1 wk after injury to assess cell proliferation. Another group of animals was first assessed for cognitive performance using the Morris water maze (MWM) at 21-25 days post-injury, then sacrificed at 4 weeks after injury to examine differentiation of newly generated cells. Brain sections were sliced and immunostained for BrdU, early neuronal marker doublecortin (DCX) and other cell type specific markers. Results showed that at 1 week post-injury, injured-aged animals infused with either vehicle or bFGF had a significantly higher number of cell proliferation in the dentate gyrus compared to sham animals. However, cell proliferation in the bFGF-infused animals was not significantly higher than vehicle-treated animals. Nevertheless, the number of DCX-labeled early stage neurons was significantly higher in the injured bFGF-treated animals than in vehicle-treated sham and injured animals. In MWM tests, unlike what we have observed in bFGF-treated younger animals, injured aged rats treated with bFGF did not show improved cognitive function. Furthermore, at 4 weeks post-injury, higher numbers of BrdU-labeled proliferative cells persisted in both injured groups, many of these cells labeled with glial and inflammatory cell markers. Collectively, the current data suggests that bFGF can enhance neurogenesis in the injured-aged hippocampus; however, this effect is not sufficient to improve functional recovery of aged rats following TBI due to the profound injury-induced inflammatory response.
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Phillips, Madison Leigh. "Impact of Gender on Acute Aerobic Exercise Induced Brain-Derived Neurotrophic Factor and Cognitive Function in Older Adults." Cleveland State University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=csu1575880466536442.
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Camm, Emily Jane 1976. "The effects of prenatal hypoxia on postnatal cognitive function : a behavioural, pharmacological and structural analysis." Monash University, Dept. of Physiology, 2002. http://arrow.monash.edu.au/hdl/1959.1/7907.
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Dedovic, Katarina. "Psychological stress and vulnerability for Major Depressive Disorder: cortisol, brain structure, function, and cognitive processing in young adults." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=96675.
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Psychological stress has an important impact on one's physical and mental health. Activation of the hypothalamic-pituitary-adrenal (HPA) stress axis and the subsequent increase in the stress hormone cortisol constitutes the organism's main response to stress. Individual differences in stress response contribute to one's vulnerability and resilience to a host of physical and psychological ills. Understanding the regulatory networks underlying stress processing in both healthy and vulnerable populations is essential. The work presented in this thesis aimed to investigate neural correlates of psychological stress processing and the HPA axis function in samples of healthy individuals as well as those with distinct vulnerability to a stress-related illness, Major Depressive Disorder. Our literature review revealed that only studies using serial subtraction or the Montreal Imaging Stress Task (MIST), a task that combines mental arithmetic and negative social evaluation components, were able to induce a significant cortisol stress response. Deactivation in orbitofrontal regions and the limbic system were most consistently observed in response to psychological stress. Exposing healthy subjects to a new, event-related version of MIST revealed that reduction of brain activity in the limbic system observed previously was specifically associated with the processing of social evaluative threat, a key component of psychological stress. We then examined HPA axis function (both basal and reactive) and the HPA regulatory brain areas for evidence of dysregulation in a sample of healthy young adults who showed varying levels of depressive tendencies, but at subclinical levels. This was the first time that these concepts were assessed in a subclinically depressed population. The subjects with increased subclinical levels of depression showed impairments in HPA function (in a form of blunted cortisol awakening response and blunted stress response), as well as impairment in certain key regions within the HPA axis regulatory network (for e.g. small hippocampal volumes and dysregulated medial orbitofrontal cortex). I conclude the thesis by proposing a basic model of a neural network underlying stress processing in a healthy population, and also outline nodes at which this network might be affected in subclinically depressed populations. Some research avenues for future studies are also highlighted.<br>L'expérience de stress psychologique peut compromettre la santé mentale et physiologique d'un individu. L'activation de l'axe hypothalamo-surrénalien, caractérisée par la libération subséquente de cortisol, constitue la principale réponse physiologique de stress. La susceptibilité ou la résilience pour un ensemble de maladies d'ordre physiques ou psychologiques est influencée par la variabilité interindividuelle dans la réponse de stress. Il est donc essentiel de comprendre le fonctionnement des systèmes régulateurs de la réponse de stress comparativement chez des sujets sains et vulnérables. Le travail présenté dans cette thèse investigue les processus neuronaux et endocrinologiques du stress psychologique chez des sujets sains exprimant divers degré de susceptibilité à la dépression majeure, une psychopathologie reliée au stress. Notre revue de la littérature suggère que l'exposition à une épreuve de soustraction en série de même que l'exposition au Montreal Imaging Stress Task (MIST), une épreuve de calcul mentale dans lequel le sujet est évalué négativement, peuvent induire une augmentation significative de cortisol. Au niveau neuronal, la réponse de stress psychologique se manifeste par une réduction de l'activité du cortex orbitofrontal et des régions du système limbique. L'exposition de sujets sains à une nouvelle version du MIST, employant un paradigme événementiel, a démontré que la réduction de l'activité du système limbique était spécifiquement associée aux éléments de menace psychosocial, une composante clé dans l'induction de la réponse de stress. Nous avons ensuite étudié l'activité de l'axe hypothalamo-surrénalien, (basale et réactive) en relation avec les régions cérébrales régulatrices afin d'observer certaines irrégularités chez de jeunes adultes sains qui présente divers degré de susceptibilité au développement de trouble dépressifs tout en demeurant sous le seuil clinique. Les sujets présentant un profil dépressif sous clinique élevée on démontrer un dysfonctionnement de l'axe hypothalamo-surrénalien, (une suppression des niveaux de cortisol à l'éveil et en réponse de stress) ainsi que l'altération de régions cérébrales régulatrices de la réponse de stress (volume hippocampique réduit, dysfonctionnement de l'activité du cortex orbitofrontale médial). Je conclue cette thèse en proposant un modèle d'interaction cérébrale impliqué dans la réponse de stress chez des sujets sains en soulignant les possibles sites de dysfonctionnement chez les sujets présentant un seuil dépressif sous clinique élevée. Finalement, quelques projets futurs seront présentés.
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Bois, Catherine. "Investigation in the relationship between childhood adversity and cognitive function in psychosis and individuals at clinical high risk of psychosis." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/33089.
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Background An increasing body of research is suggesting that childhood trauma and adversity may be associated with various adverse mental health outcomes, including psychosis. Cognitive functioning is often compromised in psychosis, and research has shown that there may be a link between early trauma and cognitive impairment in people with psychosis. No systematic review of the literature of this link has been undertaken, and very few studies have examined samples of individuals at high clinical risk for psychosis, to assess whether the potential link between adversity and cognitive functioning exists, without the confounding factors of length of illness, antipsychotic medication and chronicity of symptoms. Method The systematic review of all relevant electronic databases investigates the research to date on the association between childhood adverse experiences and cognitive ability in psychosis, and the conclusions that can be drawn from the existing literature, taking into account relevant considerations regarding sample, methodology and statistical analysis. The subsequent empirical study utilizes a sample at clinical high risk of developing psychosis, and a healthy control group to investigate whether any putative association in specific domains of cognitive functioning, or global cognitive ability and childhood adversity exist in those at clinical high risk, compared to controls. Results The systematic review indicated that at present, the literature looking into childhood adversity and cognitive ability in relation to psychosis is heterogeneous, with some studies finding that this association only occurs in patients, whilst others suggest it only occurs in the control groups. Some studies found it to be specific to certain cognitive domains, whilst others suggest it was a more global impairment. Methodology, samples and analysis differed considerably across studies, and likely contribute to the heterogeneity of the literature. The empirical paper showed a significant interaction effect between group (high risk versus controls) in the high childhood adversity group, in relation to global cognitive ability. Interestingly, this was not related to psychotic symptom severity or distress. Conclusion Several limitations of the existing studies limit the conclusions that can be drawn from the existing evidence regarding the link between childhood adversity and cognitive ability, and future research in prodromal samples is essential. The empirical study showed that there is a link between childhood adversity and cognitive ability in those at clinical high risk of developing psychosis, before disorder onset, that is not present in controls. This suggests that this may form a vulnerability in those at high risk for psychosis, rather than a more general mechanism present in the typical population.
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Blair, Hannah. "Subjective evaluation of quality of life after brain injury : measuring quality of life and the impact of response shift." Thesis, University of Stirling, 2014. http://hdl.handle.net/1893/21458.
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Introduction: After a brain injury there are often long term consequences impacting on QoL. However, this is a complex issue influenced by many factors. As someone recovers and adjusts it is likely that the way in which they evaluate QoL will also change. The theory of response shift suggests people will change the way they evaluate QoL in the face of changes in their life. The aim of this thesis is to investigate what influences a QoL judgement; examining the possibility of response shift. Methods: Quantitative and qualitative methods were used in 4 studies. These were a cross-sectional design utilising an individualised QoL measure (SEIQoL-DW); a longitudinal study utilising a ‘then-test’ approach; a cross-sectional questionnaire study; and a qualitative study using Interpretative Phenomenological Analysis. Study 1 (Ch.3) Results: Correlations between the QoL measures confirm the validity of the SEIQoL-DW; however, correlations were generally stronger for the simpler Hadorn Scale. There was little overall change in mean QoL when current and retrospective judgements were compared. There was evidence for a change in what areas of life were considered most important to QoL following injury. Study 2 (Ch.4) Results: Improvements in reported QoL between baseline and follow-up were small. A then-test indicates that any effect of response shift is small, and non-significant in the current research. There was also little evidence for reprioritisation or re-conceptualisation. Examination of other factors associated with QoL suggest that brain-injury specific factors (BIGI, RBANS) play a role in predicting QoL. Study 3 (Ch.5) Results: QoL was reported as worse post-injury on both Hadorn’s scale and the QOLIBRI-OS; a difference that was more pronounced on the QOLIBRI-OS. Differences were also reported in the importance of different areas of functioning. Change in QoL as measured by the QOLIBRI-OS was significantly influenced by disability as measured by the GOSE, emotional and informational support, and upwards social comparison. Optimism as measured by the LOT, but not upwards social comparison was a significant predictor of change on Hadorn’s scale; GOSE and emotional and informational support remain significant predictors. The GOSE, emotional and informational support, emotional coping styles and optimism were significant predictors of current QoL on the QOLIBRI-OS; and emotional and informational support and optimism were significant predictors of QoL on Hadorn’s scale. Little evidence was found to suggest that the factors proposed in Sprangers and Schwartz’s (1999) model of response shift have predicted relationships with QoL. Two candidate variables were studied: optimism and social support. However neither showed the predicted pattern of relationships. Nonetheless the study supports previous work indicating an influence of optimism and social support on QoL, and indicates that these warrant further study. There were systematic difference between current and retrospective ratings of importance of domains. The level of importance given to the areas of life defined by the QOLIBRI-OS is higher after injury than before, with the exception of “personal and social life” for which there is no significant difference. The areas of life chosen to reflect that which is measured by the GOSE (“work”, “close relationships”, and “social and leisure activities”) are rated as less important with the exception of “close relationships”. These findings provide further support for the idea that QoL domains are re-evaluated after brain injury. Study 4: This was an in depth qualitative investigation of the experience of recovery and adjustment following TBI. Semi-structured interviews and Interpretative Phenomenological Analysis (IPA) were used. Interviews were conducted with 4 men who were 3, 7, 12, and 18 years post injury. Main Outcome and Results: Themes emerging from the analysis were ‘Change: In Self and World’; ‘Reaching a point of realisation’; ‘Support’; ‘Adjusting to change/Coping with day to day life’; and ‘Participation, Goals and Focus’. These themes cover how participants felt both they and their lives had changed as a consequence of their injury; ways they went about coping and adjusting to changes; the importance of support; and the significance of social integration and participation in feeling satisfied with life. Summary and Conclusions: These studies provide evidence for response shift in different ways. There is little evidence for recalibration but there is some indication that reprioritization or reconceptualization may take place. Changes in how important different areas of life are before and after injury suggest that participants are changing the way they view and make evaluations of QoL. Factors identified as being important to QoL judgements were disability, social support (emotional and informational support identified in the questionnaire study and support in the IPA), upwards social comparison, and optimism. The IPA study suggests that functional outcome and participation are important after TBI; while also identifying ways of coping and providing an insight into the experience of recovery from brain injury. The different QoL measures used provides both evidence for their validity, but also evidence for the different conceptualisations of QoL that are measured by different instruments. The findings have implications both for understanding the QoL of the individual and for research on QoL after TBI.
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Leimbach, F. M. M. "Effects of deep brain stimulation of the subthalamic nucleus and the pedunculopontine nucleus on cognitive function in Parkinson's disease." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10052871/.
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The general aim of this thesis was to investigate the cognitive effects of deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the pedunclopontine nucleus (PPN) in Parkinson’s disease (PD). In Study 1, acute STN stimulation did not induce impulsivity on a probabilistic decisionmaking task, suggesting STN-DBS induced impulsivity may occur in tasks involving conflict, reward or time pressure. This study has clarified that the inhibitory deficits associated with STN-DBS are situation and task specific, which makes it clear why new cases of post-operative impulse control disorders are only reported in some patients. In Study 2, the STN-DBS induced decline in verbal fluency (VF), greater for semantic than phonemic fluency, was found to be a surgical rather than an acute stimulation effect, mainly due to reduced switching but no change in cluster size. Therefore, future work in identifying the mechanisms of the STN-DBS induced VF decline should focus on surgical rather than stimulation effects. In Study 3, patients failed to benefit from corrective feedback to enhance their learning relative to a trial-and-error version when performing visual conditional associative learning tasks (VCLT) with STN-DBS on versus off. STN-DBS seemed to influence proactive interference resolution on the VCLTs. These results have implications for the use of adjunct interventions such as speech therapy or physiotherapy following STN-DBS surgery. In Study 4, PPN-DBS surgery did not have an impact on most aspects of cognition assessed and the only consistent decline was in switching category VF. For the two patients who developed dementia after PPN-DBS surgery, resuming low frequency stimulation improved working memory and attention. The findings from these studies provide further evidence and clarity regarding the cognitive sequel of STN-DBS and PPN-DBS for PD and confirm that the former can be a good treatment of choice for mid to late-stage Parkinson’s disease without the risk of major cognitive adverse effects.
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Rylands, Angela J. "An investigation of cognitive function and the brain serotonin (5HT) system in impulsive aggression (IA), using positron emission tomography." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511920.
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Maumet, Camille. "From group to patient-specific analysis of brain function in arterial spin labelling and BOLD functional MRI." Phd thesis, Université Rennes 1, 2013. http://tel.archives-ouvertes.fr/tel-00863908.
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This thesis deals with the analysis of brain function in Magnetic Resonance Imaging (MRI) using two sequences: BOLD functional MRI (fMRI) and Arterial Spin Labelling (ASL). In this context, group statistical analyses are of great importance in order to understand the general mechanisms underlying a pathology, but there is also an increasing interest towards patient-specific analyses that draw conclusions at the patient level. Both group and patient-specific analyses are studied in this thesis. We first introduce a group analysis in BOLD fMRI for the study of specific language impairment, a pathology that was very little investigated in neuroimaging. We outline atypical patterns of functional activity and lateralisation in language regions. Then, we move forward to patient-specific analysis. We propose the use of robust estimators to compute cerebral blood flow maps in ASL. Then, we analyse the validity of the assumptions underlying standard statistical analyses in the context of ASL. Finally, we propose a new locally multivariate statistical method based on an a contrario approach and apply it to the detection of atypical patterns of perfusion in ASL and to activation detection in BOLD functional MRI.
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Lodha, Jyoti. "The Effects of Notch Signaling on Functional Recovery Following Traumatic Brain Injury." VCU Scholars Compass, 2019. https://scholarscompass.vcu.edu/etd/5999.
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2.5 million people sustain a traumatic brain injury (TBI) annually in the United States. Although there is potential for functional recovery following TBI, there is no definitive treatment to improve recovery after TBI. Our lab has shown that TBI enhances an endogenous neurogenic response in the subventricular zone and hippocampus. TBI-induced neural stem cells (NSCs) can integrate into regions such as the hippocampus and olfactory bulb. Although the mechanism behind TBI-enhanced neurogenesis remains unknown, the Notch signaling pathway has been implicated as a regulator in the maintenance and survival of NSCs.
This thesis explores the effects of Notch pathway manipulation on functional recovery following TBI. We hypothesize that Notch signaling plays a critical role in recovery after TBI. Activation of this pathway via a Notch agonist (Notch1) will facilitate post-injury recovery while inhibition of this pathway via a Notch antagonist (recombinant Jagged-1 Fc) will deter post-injury recovery. Functional recovery was assessed within 30 days or 60 days post-injury in two different cohorts of animals. The behavior assays conducted in this study included motor, cognitive, and olfactory assessment.
In the 30-day phase, Notch pathway manipulation following TBI did not affect functional performance. In the 60-day study, significant group differences were found. While the FPI+Vehicle animals exhibited a functional recovery in Morris water maze, injured animals with Notch inhibition failed to show this cognitive recovery, indicating the involvement of the Notch pathway in cognitive recovery at the chronic stage following TBI. Motor and olfaction were not significantly affected by Notch pathway manipulation.
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Rogers, Heather L. "Cognitive function and emotional status of middle-aged chinese hypertensive patients without detectable white matter brain lesions or lacunar infarctions /." Download the thesis in PDF, 2006. http://www.lrc.usuhs.mil/dissertations/pdf/Rogers2006.pdf.
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Eakin, Katharine Coryell. "The Effect and Chronic Acute Pre-Treatment with Methylphenidate on Recovery of Cognitive Function Following Experimental Traumatic Brain Injury In Rats." VCU Scholars Compass, 2006. http://scholarscompass.vcu.edu/etd/755.
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Adolescent and young adult males are at a higher risk for traumatic brain injury (TBI) compared to the general population. Diagnosis of Attention Deficit Hyperactivity Disorder (ADHD) is also more prevalent for males in these age groups. The most commonly prescribed medication for ADHD is methylphenidate (MPH). Based on the increase in the number of new diagnoses of ADHD and the number of children who continue taking MPH into adulthood, it is important to evaluate how chronic or acute MPH administered prior to injury may influence recovery following TBI. In both studies, cognitive abilities of male Sprague-Dawley rats were assessed on post-injury using the Morris Water Maze. There was no effect of chronic MPH treatment on cognitive outcome following TBI. In contrast, acute MPH pre-treatment improved cognitive outcome as measured by the MWM. The MPH + injury group reached sham-injury levels on days 4 and 5 in the MWM.
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Christie, Zara. "Cognitive function and traumatic brain injury in refugees and asylum-seekers attending mental health services : a preliminary study, and Clinical Research Portfolio." Thesis, University of Glasgow, 2014. http://theses.gla.ac.uk/5702/.
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Objective: Every year, an estimated 10 million people suffer a traumatic brain injury (TBI; Hyder, Wunderlich, Puvanachandra, Gururaj, & Kobusingye, 2007). Refugees and asylum-seekers fleeing persecution have often experienced war and torture and are at a greater risk of TBI (Priebe & Esmaili, 1997). Following a TBI, cognitive, behavioural and psychosocial difficulties can significantly impact on independence (Cohen, 2001). This preliminary study investigated whether cognitive function is poorer in refugees and asylum-seekers who report a severe TBI, compared to those who do not. The study also compared cognitive performance in refugees and asylum-seekers attending mental health services with Western controls from normative data. Assessing the cognitive performance of this group against Western expectations is important, to inform the clinical work as well as UK asylum law and policy. Methods: The study employed a between-subjects design, comparing 14 refugees and asylum-seekers with a self-report of one or more severe TBIs and 11 without a history of TBI. Participants attended for one assessment session and completed the Colour Trails Test (CTT; D’Elia, Satz, Uchiyama, & White, 1996) as well as other cognitive tests. Where necessary, an interpreter was present. Results: Refugees and asylum-seekers who self-reported a history of severe TBI were not more cognitively impaired on the CTT than those without TBI. The combined groups performed significantly worse on the CTT compared to normative data. Conclusions: This preliminary study suggests that refugees and asylum-seekers attending mental health services are performing much poorer cognitively than healthy Western counterparts. This highlights the value of assessing cognition in this complex group, as on a case-by-case basis, results informed the practice of mental health clinicians and GPs. Furthermore, these results raise issues about the expectations placed on cognitively impaired individuals throughout the asylum process if these expectations are based on experience of cognitive function typical of that represented by Western norms. Additional research may instigate policy-makers to make adjustments to the asylum process to better acknowledge mental health and cognitive impairment.
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Milham, Donald John. "AN ASSOCIATION BETWEEN A STRUCTURED WALKING PROGRAM AND COGNITIVE FUNCTION, BALANCE, MOBILITY, AND ACTIVITIES OF DAILY LIVING IN PERSONS WITH ALZHEIMER'S DISEASE." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/42640.
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Kinesiology<br>Ph.D.<br>Alzheimer’s disease (AD), an age-related neurodegenerative disorder, progresses across a continuum of severity that leads to serious neurological dysfunction and eventually death. Initially manifesting as mild impairment in cognition and executive function, AD eventually leads to serious disturbances in memory, decision-making, language, mobility and sensing the environment. AD affects approximately 27 million people worldwide, over 5 million in the United States alone, and is one of the most debilitating diseases that costs society billions of dollars annually and is a primary cause of death in the elderly. Pharmacological treatments produce only moderate symptomatic benefits and do not attenuate or prevent the progression of AD with some medications associated with increased symptomatic behavior such as decreased motor function and increased likelihood of falls. Conversely, research utilizing animal models indicates exercise may play an important role to attenuate AD symptoms and delaying AD onset as regular aerobic activity increases the expression of brain-derived neurotrophic factor, a peptide that plays a major role in neural function, neural plasticity, and attenuation of neuritic plaque; a ß-amyloid derived plaque that is recognized as the primary cause of neural degradation associated with AD. To examine this exercise hypothesis, participants (N = 19; mean age 85.5 ±5.2 years) completed a single treatment, regular walking activity over time (30-min per day, 3 days per week for 12 weeks), with pre-test post-test evaluations undertaken utilizing valid research instruments designed to measure cognition, executive function, and motor capabilities in persons with AD. T-test with repeated measures ANOVA with various categorical variables as between-group factors were used to test the hypothesis. Analysis of change indicated significant change occurred in Cognitive function [t(18) = 5.74, p < .001], Balance [t(18) = 7.43, p < .001], and Mobility [t(18) = 3.82, p < .001], with no significant change in Activities of Daily Living (t[18] = 1.48, p < .156). A significant decrease in the number of falls was also found (z = 2.392, p < .017). No main effect was associated with AD stage, gender, or education level. The results of this study indicate regular aerobic activity enhances neural function in persons with AD, thus supporting the exercise hypothesis which posits regular aerobic exercise attenuates AD symptoms and delays AD onset. While the results provide important evidence regarding the impact of aerobic exercise on neural function in the AD populations, further research is necessary to identify the mechanisms by which brain-derived neurotrophic factor is induced with exercise and to examine the effectiveness of different exercise modalities (e.g., specificity, duration, and intensity) on neural function in the AD population.<br>Temple University--Theses
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Xu, Dong. "The relationship between executive function, postural instability and gait disturbance in Parkinson's disease." Thesis, Queensland University of Technology, 2015. https://eprints.qut.edu.au/91606/1/Dong%20Xu%20Thesis.pdf.
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The thesis investigated the relationships between executive function, balance and gait using assessments of cognitive and executive function, a wide range of clinical and biomedical measures of balance and gait, and different dual task paradigms in people with Parkinson's disease (PD) and healthy controls. Furthermore, functional association between executive function and brain activation in the prefrontal cortex was explored using functional near-infrared spectroscopy. The study has revealed greater postural instability and profound changes of gait parameters under dual-tasking for people with PD. Improving executive function may be an effective intervention to improve balance and gait in people with PD.