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1

Cada, Amy Marie. "Brain energy metabolism and spatial memory dysfunction /." Digital version accessible at:, 1998. http://wwwlib.umi.com/cr/utexas/main.

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2

Edrissi, Hamidreza. "Blood Brain Barrier Dysfunction in Chronic Cerebral Ischemia." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32531.

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Cerebral small vessel pathology is now known to be associated with the development of cognitive impairment and mild motor impairments such as gait disturbance in a variety of neurodegenerative diseases. This dissertation explores the hypothesis that blood brain barrier dysfunction is an early event in cerebral ischemia and contributes to the development of cerebral small vessel disease (CSVD). A common rodent model of CSVD is permanent bilateral common carotid artery occlusion in the rat. This model was used to study several aspects of the progression of CSVD including the timecourse of blood
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3

Conrad, Joseph Samuel. "Vision Therapy for Binocular Dysfunction Post Brain Injury." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306554563.

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4

Lu, Ran [Verfasser]. "Metabolic syndrome, olfactory dysfunction, and brain morphology / Ran Lu." Bonn : Universitäts- und Landesbibliothek Bonn, 2019. http://d-nb.info/1240761252/34.

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5

Marrerios, Rita [Verfasser]. "Protein homeostasis dysfunction in chronic brain disorders / Rita Marrerios." Düsseldorf : Universitäts- und Landesbibliothek der Heinrich-Heine-Universität Düsseldorf, 2020. http://d-nb.info/1219299618/34.

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6

Yonutas, Heather M. "NOVEL TARGETS FOR MITOCHONDRIAL DYSFUNCTION FOLLOWING TRAUMATIC BRAIN INJURY." UKnowledge, 2016. https://uknowledge.uky.edu/neurobio_etds/15.

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Mitochondrial dysfunction is a phenomenon observed in models of Traumatic Brain Injury (TBI). Loss of mitochondrial bioenergetics can result in diminished cellular homeostasis leading to cellular dysfunction and possible cellular death. Consequently, the resultant tissue damage can manifest as functional deficits and/or disease states. Therapeutic strategies to target this mitochondrial dysfunction have been investigated for models TBI and have shown promising effects. For this project, we tested the hypothesis that mitoNEET, a novel mitochondrial membrane protein, is a target for pioglitazone
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7

Salvadore, Christopher P. "Brain cell injury: metabolic dysfunction in ischemia and hypoxia." Thesis, Boston University, 1988. https://hdl.handle.net/2144/38099.

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Thesis (M.A.)--Boston University<br>PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.<br>A sequence of biochemical events responsible for the destruction of brain cells during oxygen deprivation has been proposed based on available experimental evidence reviewed in the text. Oxygen deficiency resu
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8

Salar, Seda [Verfasser]. "Blood-brain barrier dysfunction and pharmacoresistance of seizures / Seda Salar." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237906/34.

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9

Heinly, Matthew T. "Language Dysfunction in Traumatic Brain Injury While Controlling for Effort." ScholarWorks@UNO, 2007. http://scholarworks.uno.edu/td/610.

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The present study included three traumatic brain injury (TBI) groups (good effort mild TBI, poor effort mild TBI, and good effort moderate/severe TBI) and two neurologic control groups (dementia and unilateral left hemisphere stroke). Language impairment was examined using the following measures: Wechsler Adult Intelligence Scale-III Verbal Comprehension Index and the Vocabulary, Similarities, Information, and Comprehension subtests; the Boston Naming Test; the Phonemic and Semantic cue conditions of the Controlled Oral Word Association Test; the Auditory Comprehension subtest of the Co
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10

Bonnelle, Valerie. "Disconnection, network dysfunction and cognitive impairment after traumatic brain injury." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9782.

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It is now widely accepted that cognitive functions depend on the integrated operation of large-scale distributed brain networks. Recent methodological advances allow both structural and functional connectivity within these networks to be studied non-invasively in vivo. These approaches hold the promise of dramatically extending our understanding of the impact of traumatic brain injury (TBI) on cognition, which should help determine strategic targets for the rehabilitation of individuals with TBI. In this thesis, I present three studies that combine structural and functional magnetic resonance
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11

Payette, Daniel. "Neuronal dysfunction and degeneration in Alzheimer's disease and brain trauma." Oklahoma City : [s.n.], 2008.

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12

Sukhina, Alona. "Developments on Post-Traumatic Brain Injury-Induced Hypothalamic Pituitary Dysfunction: A Pediatric Case." Thesis, The University of Arizona, 2018. http://hdl.handle.net/10150/626895.

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13

Sánchez, Guerrero Ángela. "High-resolution microdialysis to detect metabolic dysfunction after traumatic brain injury." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/402271.

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El traumatismo craneoencefálico (TCE) es la primera cause de muerte y discapacidad en la población mundial menor de 40 años. La mayoría de los pacientes que sobreviven a un TCE grave tienen secuelas con importantes repercusiones médicas, familiares y socioeconómicas. Hasta la fecha, ningún tratamiento neuroprotector ha resultado efectivo en ensayos clínicos controlados. Los avances en este campo se han visto limitados por la falta de conocimiento sobre los cambios bioquímicos, celulares y moleculares implicados en la fisiopatología de la lesión cerebral. Los mecanismos fisiopatológicos del TCE
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14

Shao, Changxing. "OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION IN TRAUMATIC BRAIN INJURY IN AGING." UKnowledge, 2007. http://uknowledge.uky.edu/gradschool_diss/533.

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Traumatic brain injury (TBI) is a prominent disease in developed countries, and age is an important factor in functional outcome. Although aged patients typically show diminished recovery compared to young patients, and have higher mortality and morbidity following TBI, the mechanism is not well understood. To date, there is no effective therapeutic for TBI. Previous studies indicate a secondary injury in TBI begins immediately after impact, and is likely the major contribution to delayed neuron dysfunction and loss. Studies also suggest mitochondrial dysfunction and increased free radical spe
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15

Bailey, Emma Louise. "Pathophysiology of lacunar stroke : ischaemic stroke or blood brain barrier dysfunction?" Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6529.

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Lacunar strokes account for approximately a quarter of all ischaemic strokes and traditionally are thought to result from occlusion of a small deep perforating arteriole in the brain. Lacunar infarcts can be up to 2cm in diameter and are found in deep brain structures such as the thalamus and internal capsule. Despite their prevalence and specific accompanying clinical syndromes, the cause of lacunar stroke and its associated vascular pathology remain unclear. Many hypotheses as to the cause exist, which fall broadly into two categories; firstly, a direct occlusion via emboli or thrombus usual
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16

Ord, Jonathan. "Executive Dysfunction following Traumatic Brain Injury and Factors Related to Impairment." ScholarWorks@UNO, 2007. http://scholarworks.uno.edu/td/626.

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Deficits in executive function are commonly reported following Traumatic Brain Injury (TBI) and are important for establishing functional impairments. Understanding the nature of executive dysfunction following TBI is often complicated by secondary factors that can impact measured ability. This study sought to clarify the persistent effects of TBI on executive function, as measured by the Wisconsin Card Sorting Test (WCST), while accounting for effort given during testing, as measured by the Portland Digit Recognition Test. Results suggested a dose-response relationship between TBI seve
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17

Jilka, Sagar Ramesh. "Salience network and default mode network dysfunction after traumatic brain injury." Thesis, Goldsmiths College (University of London), 2015. http://research.gold.ac.uk/11157/.

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It is now widely accepted that cognitive control depends on the integrated operation of large-scale distributed brain networks. Recent methodological advances allow both structural and functional connectivity (FC) within these networks to be studied non- invasively in vivo. These approaches hold the promise of dramatically extending our understanding of the impact of traumatic brain injury (TBI) on cognitive control, which has the potential to help determine strategic targets for the rehabilitation of individuals with TBI. In the current thesis, structural and functional magnetic resonance ima
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18

ORNAGHI, SARA. "Antiepileptic Drugs to Treat Cytomegalovirus Infection during Early Brain Development." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2018. http://hdl.handle.net/10281/199053.

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Il citomegalovirus (CMV) é la causa infettiva più frequente di malformazioni cerebrali e disturbi neurologici in feti e neonati. Le possibilità terapeutiche durante momenti critici di sviluppo intrauterino e post-natale sono significativamente limitate dalla tossicità e teratogenicità dei farmaci anti-CMV ad oggi disponibili sul mercato. Questo lavoro di ricerca riporta per la prima volta che il valpromide (VPD) e il valnoctamide (VCD), due farmaci strutturalmente simili con attività anti-epilettica e stabilizzatrice dell’umore e privi di potenziale tossico o teratogenico, esercitano una speci
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19

Nukala, Vidya Nag. "ROLE OF CALCIUM AND NITRIC OXIDE SYNTHASE (NOS) IN BRAIN MITOCHONDRIAL DYSFUNCTION." UKnowledge, 2007. http://uknowledge.uky.edu/neurobio_etds/8.

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Mitochondria are essential for promoting cell survival and growth through aerobic metabolism and energy production. Mitochondrial function is typically analyzed using mitochondria freshly isolated from tissues and cells because they yield tightly coupled mitochondria, whereas those from frozen tissue can consist of broken mitochondria and membrane fragments. A method, utilizing a well-characterized cryoprotectant such as dimethyl sulfoxide (DMSO), is described. Such mitochondria show preserved structure and function that presents us with a possible strategy to considerably expand the time-fram
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20

CASTELNOVO, VERONICA. "BRAIN FUNCTIONAL CONNECTIVITY AND COGNITIVE DYSFUNCTION IN PATIENTS WITH MOTOR NEURON DISORDERS." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/128276.

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Motor neuron diseases (MND) are heterogeneous neurodegenerative disorders in which the possible presence of cognitive and/or behavioural symptoms is a universally known neuropsychological feature. Detecting even subtle cognitive changes in MND, monitoring them over time and identifying new markers both in terms of cognition and of neuroimaging is critical due to their considerable clinical impact. This thesis examines the presence of early markers of cognitive and behavioural alterations, of disease progression and brain correlates in MND patients, using specific neuropsychological evaluations
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21

Sherman, Elisabeth Mary Suzanne. "Neuropsychological correlates of social skills." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. https://dspace.library.uvic.ca//handle/1828/9778.

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Case studies and a small number of group studies in the neuropsychological literature on adults and children with brain dysfunction suggest that certain cognitive skills are important determinants of social skills. However, standardised measures of social skills designed expressly to measure this construct have not been used previously in the neuropsychological field. The goal of this study was to determine neuropsychological correlates of social skills in children referred for neuropsychological assessment, and compare the findings to the cognitive skills identified in social informati
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22

Geng, Li. "The role of NADPH oxidase 2 in ageing-related brain oxidative stress, cerebral endothelial damage and brain dysfunction." Thesis, University of Reading, 2018. http://centaur.reading.ac.uk/80438/.

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The average age of our population continues to grow as a result of increasing longevity. Indeed, according to WHO, by the year 2100, nearly one third of the global population will be 60+ years old. However, the key factors and signalling pathways involved in cellular ageing remain largely unknown. Our hypothesis is that oxidative stress generated by the activation of a Nox2-containing NADPH oxidase plays a key role in ageing-related vascular and neuro-degenerative disorder. Therefore, the overall aim of this PhD research project is to investigate the role of Nox2 activation in ageing-related b
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23

Kurowski, Brad G. "Executive Dysfunction after Moderate and Severe Pediatric Traumatic Brain Injury Predicts Clinical Dysfunction on the Child and Adolescent Functional Assessment Scale." University of Cincinnati / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1342543308.

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24

Gulati, Gaurav. "Blood Brain Barrier and Anti-NR2 Antibody in SLE Patients with Cognitive Dysfunction." University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1427882673.

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25

Nunez, Ivette Ariela. "Traumatic Brain Injury Causes Endothelial Dysfunction In Mesenteric Arteries 24 Hrs After Injury." ScholarWorks @ UVM, 2015. http://scholarworks.uvm.edu/graddis/362.

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Traumatic brain injury (TBI) is the most frequent cause of death in children and young adults in the United States. Besides emergency neurosurgical procedures, there are few medical treatment options to improve recovery in people who have experienced a TBI. Management of patients who survive TBI is complicated by both central nervous system and peripheral systemic effects. The pathophysiology of systemic inflammation and coagulopathy following TBI has been attributed to trauma-induced endothelial cell dysfunction; however, there is little knowledge of the mechanisms by which trauma might impac
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26

Paul, Carolyn. "Analysis and treatment of pathological blood-brain barrier dysfunction during experimental allergic encephalomyelitis." Thesis, University of Bath, 1996. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320434.

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27

Bailey, Mark Arnott William. "The relationship between lateralized motor impairment and verbal/visuospatial deficits in children with suspected brain dysfunction." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32703.pdf.

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28

Leaver, Amber Michelle. "Magnetic resonance imaging (MRI) studies of the human auditory brain objects, sequences, and dysfunction /." Connect to Electronic Thesis (CONTENTdm), 2010. http://worldcat.org/oclc/642698715/viewonline.

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29

Rasmussen, Lars Simon. "Postoperative cognitive dysfunction : incidence, risk factors, and correlation with biochemical markers for brain damage /." Københavns : Lægeforeningens Forlag, 2007. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=016143662&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.

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30

Sauerbeck, Andrew David. "TRICHLOROETHYLENE EXPOSURE AND TRAUMATIC BRAIN INJURY INTERACT AND PRODUCE DUAL INJURY BASED PATHOLOGY AND PIOGLITAZONE CAN ATTENUATE DEFICITS FOLLOWING TRAUMATIC BRAIN INJURY." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/133.

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The development of Parkinson's disease (PD) in humans has been linked to genetic and environmental factors for many years. However, finding common single insults which can produce pathology in humans has proved difficult. Exposure to trichloroethylene (TCE) or traumatic brain injury (TBI) has been shown to be linked to PD and it has also been proposed that multiple insults may be needed for disease development. The present studies show that exposure to TCE prior to a TBI can result in pathology similar to early PD and that the interaction of both insults is required for impairment in behaviora
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31

Kelly, Kimberly A. "The role of NADPH oxidase in blood-brain barrier dysfunction following stroke in aged rats." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10635.

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Thesis (Ph. D.)--West Virginia University, 2009.<br>Title from document title page. Document formatted into pages; contains x, 121 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 84-118).
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Meier, Shelby. "PATHOLOGICAL TAU AS A CAUSE, AND CONSEQUENCE, OF CELLULAR DYSFUNCTION." UKnowledge, 2019. https://uknowledge.uky.edu/physiology_etds/44.

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Tauopathies are a group of neurodegenerative diseases characterized by the abnormal deposition of the protein tau, a microtubule stabilizing protein. Under normal physiological conditions tau is a highly soluble protein that is not prone to aggregation. In disease states alterations to tau lead to enhanced fibril formation and aggregation, eventually forming neurofibrillary tangles (NFTs). The exact cause for NFT deposition is unknown, but increased post-translational modifications and mutations to the tau gene can increase tangle formation. Tauopathic brains are stuck in a detrimental cycle,
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33

Haya, Hidalgo Jenny Rosario 1978. "Neurogenic bowel dysfunction in subjects with brain injury : prevalence, risk factors, clinical characterization and physiopathology." Doctoral thesis, Universitat Pompeu Fabra, 2018. http://hdl.handle.net/10803/665842.

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To date, there are scarce data on bowel dysfunction (BD) in patients after brain injury (BI). Until now, only fecal incontinence (FI) has received attention and it has been mainly associated to patients’ age or performance status after the brain damage. In this thesis we report on the elevated incidence of BD in patients after an acute BI event, including FI but also diarrhea, severe constipation, abdominal pain and distention. We have characterized the clinical manifestations of these gut dysfunctions and measured their impact on QOL. We have also explored risks factors and underlying pathoph
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34

Swan, Alicia, Jeremy T. Nelson, Terri K. Pogoda, et al. "Association of Traumatic Brain Injury with Vestibular Dysfunction and Dizziness in Post-9/11 Veterans." Digital Commons @ East Tennessee State University, 2020. https://dc.etsu.edu/etsu-works/7777.

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Objective:To describe the prevalence and impact of vestibular dysfunction and nonspecific dizziness diagnoses and explore their associations with traumatic brain injury (TBI) severity, mechanism, and postconcussive comorbidities among post-9/11 veterans. Setting:Administrative medical record data from the US Departments of Defense and Veterans Affairs (VA). Participants:Post-9/11 veterans with at least 3 years of VA care. Design:Cross-sectional, retrospective, observational study. Main measures:International Classification of Diseases, Ninth Revision, Clinical Modification diagnosis codes for
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35

Gardner, Ann. "Mitochondrial dysfunction and alterations of brain HMPAO SPECT in depressive disorder : perspectives on origins of "somatization" /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-903-X/.

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36

Sundman, Mark H., Nan-kuei Chen, Vignesh Subbian, and Ying-hui Chou. "The bidirectional gut-brain-microbiota axis as a potential nexus between traumatic brain injury, inflammation, and disease." ACADEMIC PRESS INC ELSEVIER SCIENCE, 2017. http://hdl.handle.net/10150/626124.

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As head injuries and their sequelae have become an increasingly salient matter of public health, experts in the field have made great progress elucidating the biological processes occurring within the brain at the moment of injury and throughout the recovery thereafter. Given the extraordinary rate at which our collective knowledge of neurotrauma has grown, new insights may be revealed by examining the existing literature across disciplines with a new perspective. This article will aim to expand the scope of this rapidly evolving field of research beyond the confines of the central nervous sys
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Ashbrook, Richard McBride. "Memory organization in attention deficit disorder children." The Ohio State University, 1985. http://rave.ohiolink.edu/etdc/view?acc_num=osu1371733849.

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38

Mohamed, Hala Alhadi Ali. "Alterations in cytoskeletal proteins and microtubule stability following 26S proteasome dysfunction in mouse brain cortical neurons." Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/47188/.

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The mechanisms involved in the cause and progression of chronic neurodegenerative diseases are still unclear. The ubiquitin proteasome system (UPS) plays an essential role in the maintenance of intracellular protein homeostasis by degrading unwanted proteins. The accumulation of ubiquitinated proteins is a hallmark of major neurodegenerative diseases, including Alzheimer’s and Parkinson’s diseases. In most cases, these diseases are also associated with changes in cytoskeletal proteins and microtubule stability. We previously reported decreased levels of microtubule destabilizing protein stathm
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Avlonitis, Vassilios S. "The role of brain death in donor lung injury and primary graft dysfunction after pulmonary transplantation." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.416646.

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40

Anzalone, Steven J. "Cholinergic cortical dysfunction in an animal model of diencephalic amnesia." Diss., Online access via UMI:, 2009.

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41

Colaluca, Beth. "Validation of the Expanded McCarron-Dial System for Diagnosis of Neuropsychological Dysfunction in Adults." Thesis, University of North Texas, 1998. https://digital.library.unt.edu/ark:/67531/metadc279403/.

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The McCarron-Dial System (MDS) has successfully predicted vocational and independent living outcomes with neuropsychologically disabled individuals receiving rehabilitation services. In addition, preliminary validation studies suggest that the abbreviated MDS is useful for clinical neuropsychological diagnosis. The present study represents part of an ongoing research project aimed at validating the expanded version of the MDS for diagnosis of neuropsychological dysfunction. Specifically, it was hypothesized that the expanded MDS would be able to accurately discriminate between brain-damaged an
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42

Nord, Camilla Laxmi. "The role of dorsolateral prefrontal cortex dysfunction in depression and its treatment with non-invasive brain stimulation." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038161/.

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Major depression is a common and debilitating condition. However, initial treatment is ineffective for almost half of all patients. This thesis aims to clarify the mechanisms of a novel putative treatment for depression, transcranial direct current stimulation (tDCS), which targets the dorsolateral prefrontal cortex (DLPFC). The first experimental chapter tests whether DLPFC tDCS alters emotional face perception, akin to the acute effects of antidepressant drugs. Our analyses revealed that tDCS does not exert an antidepressant-like effect on emotion perception, but may affect non-emotional cog
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43

Olivecrona, Zandra, Per Dahlqvist, and Lars-Owe Koskinen. "Acute neuro-endocrine profile and prediction of outcome after severe brain injury." Umeå universitet, Institutionen för farmakologi och klinisk neurovetenskap, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-73085.

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Object: The aim of the study was to evaluate the early changes in pituitary hormone levels after severe traumatic brain injury (sTBI) and compare hormone levels to basic neuro-intensive care data, a systematic scoring of the CT-findings and to evaluate whether hormone changes are related to outcome. Methods: Prospective study, including consecutive patients, 15-70 years, with sTBI, Glasgow Coma Scale (GCS) score &lt;= 8, initial cerebral perfusion pressure &gt; 10 mm Hg, and arrival to our level one trauma university hospital within 24 hours after head trauma (n = 48). Serum samples were colle
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44

VanGilder, Reyna. "Examining the protective effects of sesamol on oxidative stress associated blood-brain barrier dysfunction in streptozotocin-induced diabetic rats." Morgantown, W. Va. : [West Virginia University Libraries], 2009. http://hdl.handle.net/10450/10541.

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Thesis (Ph. D.)--West Virginia University, 2009.<br>Title from document title page. Document formatted into pages; contains xi, 165 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 131-163).
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Ganci, Maria. "A Comprehensive Neuropsychological Screening Device for Adults: Reliability of Parallel Forms." Thesis, University of North Texas, 1991. https://digital.library.unt.edu/ark:/67531/metadc500815/.

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The purpose of the present study was to evaluate the reliability of parallel-forms of the Comprehensive Neuropsychological Screening Device (CNS). Forty-five subjects ranging in age from 16 to 69 were administered Form A and Form B of the CNS at two week intervals. Results indicated that the CNS has adequate test-retest reliability. The results suggest the applicability of using the CNS as a screening device for brain dysfunction.
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Rajani, Rikesh Mukesh. "Is small vessel disease a disease of the blood brain barrier?" Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25866.

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Cerebral small vessel disease (SVD) is a vascular neurodegenerative disease which is the leading cause of vascular dementia and causes 20% of strokes. 20-30% of those over 80 show signs of the disease as white matter hyperintensities on MRI scans, doubling their risk of stroke and trebling their risk of dementia. Sporadic SVD is thought to be caused by hypertension but 30% of sufferers are normotensive and an alternative hypothesis implicates loss of integrity of the blood brain barrier (BBB). To investigate this, I studied brains from normotensive people with early stage SVD and found reduced
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47

Luna, Brenda. "Prenatal Environmental Exposure and Neurodevelopmentally Important Gene Expression in Malformed Brain Tissue from Pediatric Intractable Epilepsy Patients." FIU Digital Commons, 2011. http://digitalcommons.fiu.edu/etd/445.

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The primary objective of this proposal was to determine whether mitochondrial oxidative stress and variation in a particular mtDNA lineage contribute to the risk of developing cortical dysplasia and are potential contributing factors in epileptogenesis in children. The occurrence of epilepsy in children is highly associated with malformations of cortical development (MCD). It appears that MCD might arise from developmental errors due to environmental exposures in combination with inherited variation in response to environmental exposures and mitochondrial function. Therefore, it is postulated
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48

Irving, Stephanie [Verfasser], and Andreas [Akademischer Betreuer] Zwergal. "Gaze behaviour and brain activation patterns during real-space navigation in hippocampal dysfunction / Stephanie Irving ; Betreuer: Andreas Zwergal." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2019. http://d-nb.info/1198111895/34.

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Alamu, Olufemi Akinyinka. "Differential toxicity of two murine endothelial cells to ROS duress: Understanding oxidative stress-induced blood-brain barrier dysfunction." University of the Western Cape, 2020. http://hdl.handle.net/11394/7876.

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Philosophiae Doctor - PhD<br>The blood-brain barrier (BBB) is a critical interface between the blood circulation and brain tissue which performs critical selection of circulating molecules that gain access to the brain tissue. Its unique ability to adjust to changes in the constituents of the blood circulation confer in the BBB a dynamic nature enabling changes in its properties to suit the homeostatic needs of the brain. Dysfunction of the BBB has been established to be pivotal to the initiation and/or maintenance of an array of neurological disorders, most of which involve the production of
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Saracino, Emanuela <1988&gt. "“Nanoglial interfaces: nanostructured materials, interfaces and devices to unveil the role of astrocytes in brain function and dysfunction”." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2022. http://amsdottorato.unibo.it/10173/1/E.Saracino%20XXXIV%20Cycle%20Nanoscience%20in%20the%20Medicine%20and%20the%20Environment%20submitted.pdf.

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The role of non-neuronal brain cells, called astrocytes, is emerging as crucial in brain function and dysfunction, encompassing the neurocentric concept that was envisioning glia as passive components. Ion and water channels and calcium signalling, expressed in functional micro and nano domains, underpin astrocytes’ homeostatic function, synaptic transmission, neurovascular coupling acting either locally and globally. In this respect, a major issue arises on the mechanism through which astrocytes can control processes across scales. Finally, astrocytes can sense and react to extracellular stim
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