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1

Russell, Teresa. "Alzheimer's disease : expressed concern for problem behaviors /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p1390668.

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2

Navaratnam, Dasakumar Selveraj. "Cholinesterases in Alzheimer's disease." Thesis, University of Oxford, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306734.

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Newman, Tracey Anne. "Ageing and Alzheimer's disease." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246220.

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Montacute, Rebecca. "Infection in Alzheimer's disease." Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/infection-in-alzheimers-disease(a69fbf77-1455-4a78-a700-54815cad926d).html.

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Infections are a common co-morbidity in Alzheimer's disease (AD), and evidence suggests that infections can exacerbate neuroinflammation and increase cognitive decline in AD patients. In AD, immune changes are observed both in the central nervous system (CNS) and in the rest of the body. However, only a few studies have investigated immune responses to infection in AD. Here, two extensively studied infections, Toxoplasma gondii (T. gondii) and Trichuris muris (T. muris) were used to investigate infection in AD. T. gondii is a protozoan parasite which is common globally, including in the develo
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5

Zubair, Mohammed. "Metabolomics in Alzheimer's disease." Thesis, University of Manchester, 2013. https://www.research.manchester.ac.uk/portal/en/theses/metabolomics-in-alzheimers-disease(0872757b-d25a-4c43-bd52-915d4cad21c6).html.

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Metabolites are a potentially useful source of detecting and identifying disease specific biomarkers. This thesis investigates the possibility of using metabolomics applications to detect Alzheimer’s disease associated metabolite peaks in patients and to detect longitudinal changes of the disease. Serum samples and clinical data were collected from 60 healthy controls and 60 Alzheimer’s disease patients (60 at baseline and 60 at 12 month follow-up). The metabolic fingerprinting of serum samples using the FT-IR lacked discriminatory power to discriminate Alzheimer’s disease and non-disease samp
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Shie, Feng-Shiun. "Cholesterol and Alzheimer's disease /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6604.

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梁欣珮 and Yan-pui Irene Leung. "Potential impact of alzheimer's disease on retina." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42905059.

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8

Hynd, Matthew. "Excitotoxic neurodegeneration in Alzheimer's disease /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18145.pdf.

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9

Blom, Elin. "Genetic Studies of Alzheimer's Disease." Doctoral thesis, Uppsala universitet, Institutionen för folkhälso- och vårdvetenskap, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9397.

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Patients with Alzheimer's disease (AD) often have a family history of the disease, implicating genetics as a major risk factor. Three genes are currently known to cause familial early-onset AD (<65 years): the amyloid precursor protein (APP) and the presenilins (PSEN1 and PSEN2). For the much more common late-onset disease (>65 years), only the APOE gene has repeatedly been associated to AD, where the ε4 allele increases disease risk and decreases age at onset. As APOE ε4 only explains part of the total estimated disease risk, more genes are expected to contribute to AD. This thesis has
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10

Bakerink, Ronda Ann. "Semantic memory in Alzheimer's Disease." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27795.

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Alzheimer's Disease is characterized by a general decline in cognitive functioning. Although phonology are relatively unaffected, patients with Alzheimer's Disease have been reported to have deficits of semantic memory. Thirteen patients with dementia, five of whom had a confirmed diagnosis of dementia, participated in the study. The purpose of this investigation was to replicate a study performed by Mark Byrd (1984), using Alzheimer's Disease patients. Subjects were presented with category-word decision pairs, for which the task was to decide if the word was an exemplar of the category, and c
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11

Williams, Abigail J. "Cystatin C and Alzheimer's disease." Thesis, University of Sheffield, 2014. http://etheses.whiterose.ac.uk/8547/.

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Aggregation of amyloid-β in Alzheimer's disease (AD) is modulated in the presence of other amyloidogenic proteins including human cystatin C (hCC), which directly protects neuronal cells from Aβ-induced toxicity and inhibits fibril formation. Determination of the relevant conformations of the interacting Aβ and hCC is a key step to uncovering the molecular mechanism of hCC's activity in AD. A system for the production of recombinant Aβ1-40 has been established and is described here. It is also shown that hCC readily produces stable oligomeric species upon incubation in aggregating conditions,
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12

Beffert, Uwe. "Apolipoprotein E in Alzheimer's disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0021/NQ55300.pdf.

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13

Bothmer, John. "Phosphoinositides, aging and Alzheimer's disease." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=6504.

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14

Howell, Walter Mathias. "SNP technology and Alzheimer's disease /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-473-9/.

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15

Naidj, Sonia. "Visuospatial dysfunction in Alzheimer's disease." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=23924.

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The objective of this study was to identify subgroups in patients with Alzheimer's Disease (AD), based on a dissociation in their performance on visuospatial tasks: one subgroup with predominant impairment on object recognition or the "What" system, and another subgroup with predominant impairment in spatial recognition or the "Where" system. Also, an attempt was made to clarify the relationship between attention on these two visuospatial processes. Amongst twenty-four patients with AD, we identified two pairs of patients with dissociated performances. However, except for one case, the dissoci
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16

Xu, Chun. "Morphological subtypes of Alzheimer's disease." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61223.

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Initiating a computerized population-based registry of Alzheimer's disease (AD), the IMAGE Project has developed a multimatrix model to investigate the disease. Part of the IMAGE Project 1, the neuropathological study, is designed to correlate clinical, neuropsychological and neuropathological features of AD for characterization of subtypes. This thesis reports mainly the morphometrical studies associated with project 1.<br>The study, based on (a) brain autopsy, (b) standardized histopathology, and (c) quantitative morphometry, shows heterogeneity in pathophenotypes of AD. Four morphological s
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17

Spillantini, Maria Grazia. "Molecular neuropathology of Alzheimer's disease." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282037.

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18

Bourne, Nathan T. "Molecular mechanisms of Alzheimer's disease." Thesis, University of Sheffield, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521906.

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19

Smith, M. A. "Protein structures and Alzheimer's disease." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.291081.

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20

Treanor, James J. S. "Neurotrophic factors and Alzheimer's disease." Thesis, University of Bristol, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385730.

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21

Bucks, Romola Starr. "Intrusion errors in Alzheimer's disease." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285578.

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22

Fox, Sarah. "Oscillations memory and Alzheimer's disease." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/oscillations-memory-and-alzheimers-disease(bbacb2f0-74f3-4071-b02f-19c0c5570227).html.

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Damage precipitating cognitive decline in Alzheimer's disease (AD) begins long before behavioural alterations become clinically apparent. At this prodromal stage, communication between networks of neurons connecting different brain regions starts to break down; setting in motion a chain of events leading to clinical AD. A significant challenge facing Alzheimer's researchers today is finding a cheap, easy-to-perform test capable of detecting prodromal AD. Such a test would afford significant benefits to patients, including a chance of early intervention. Perhaps, more importantly, it would also
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23

Benjamin, Maxwell J. "Autobiographical memory in Alzheimer's Disease." Thesis, Canterbury Christ Church University, 2013. http://create.canterbury.ac.uk/12348/.

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Retrieval of autobiographical memories (AMs) is important for “sense of self”. Current theoretical understanding of AM retrieval predicts that working memory (WM) and executive functions (ExF) enable the hierarchical search for, and reliving of past, personal events in the mind’s eye. However, there remains a lack of consensus as to the nature of the relationships between these cognitive functions and semantic and episodic aspects of AM. The present study therefore aimed to explore the associations between these variables in a sample with a wide range of ability on measures of WM, ExF, and AM.
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24

Davidson, Madeiene E. "Alzheimer's Disease: The Triple Threat." Scholarship @ Claremont, 2016. http://scholarship.claremont.edu/cmc_theses/1287.

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Many Americans know Alzheimer’s disease for its devastating physical, emotional, and financial impact on patients as well as their family members and friends. According to the Alzheimer’s Association’s recent national survey, 73 million voters have had a family member or friend with the disease, indicating that the nation is aware of the disease’s affect on patients, their relatives, friends, and caretakers. Many are unaware, however, that Alzheimer’s could impose an enormous economic burden on the nation. Harry Johns, the president and CEO of the Alzheimer’s Association, calls Alzheimer’s “a
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25

Kim, Sohee. "Computational modeling in Alzheimer's disease." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1267541374.

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26

Huseby, Carol. "Molecular Neuropathology in Alzheimer's Disease." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1543314678552794.

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27

Morshed, Nader Francis. "Phosphoproteomics analysis of Alzheimer's disease." Thesis, Massachusetts Institute of Technology, 2021. https://hdl.handle.net/1721.1/130816.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, February, 2021<br>Cataloged from the official PDF version of thesis.<br>Includes bibliographical references (pages [137]-[153]).<br>Alzheimer's disease (AD) is a form of dementia characterized by the appearance of amyloid-[beta] plaques, neurofibrillary tangles, and inflammation in brain regions involved in memory. Despite numerous clinical trials, a limited understanding of disease pathogenesis has prevented the development of effective therapies. Several lines of genetic and biomolecular evidence ind
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28

Townsend, Kirk Phillip. "Microglia activation in Alzheimer's disease." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000489.

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29

Morris, Eva Marie. "Semantic Memory in Alzheimer's Disease." W&M ScholarWorks, 1999. https://scholarworks.wm.edu/etd/1539626235.

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30

Wang, Juelu. "Selective neurodegeneration in Alzheimer's disease and Parkinson's disease." Thesis, University of British Columbia, 2017. http://hdl.handle.net/2429/63267.

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Alzheimer’s disease (AD) and Parkinson’s disease (PD) are featured by cholinergic and dopaminergic neuron loss, respectively. As a unique pathological hallmark of AD, neuritic plaques contain aggregated amyloid β protein (Aβ), generated from amyloid β precursor protein (APP). APP mutations cause familial AD; mutations in the alpha-synuclein (SNCA) and leucine-rich repeat kinase 2 (LRRK2) genes are associated with PD. Recent studies suggest that the level of LRRK2 affects its toxicity in neurons. Therefore, understanding the mechanisms underlying LRRK2 expression would help to examine its p
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31

Rickle, Annika. "PTEN and Akt signalling in Alzheimer's disease /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-514-3/.

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32

Holt, Jim. "Alzheimer’s Disease." Digital Commons @ East Tennessee State University, 2009. https://dc.etsu.edu/etsu-works/6482.

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33

Vasseur, Janis S. "The geographical implications of Alzheimer's disease : an examination of the impact that Alzheimer's disease hs on family caregivers in Connecticut /." Abstract Full Text (PDF), 2008. http://eprints.ccsu.edu/archive/00000509/02/1965FT.pdf.

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Thesis (M.S.) -- Central Connecticut State University, 2008.<br>Thesis advisor: Cynthia Pope. "... in partial fulfillment of the requirements for the degree of Master of Science in Geography." Includes bibliographical references (leaves 85-90). Also available via the World Wide Web.
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34

Ridha, Basil Hassan. "MRI in Alzheimer's disease: beyond exclusion." Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486616.

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Brain imaging has been mainly used to exclude other secondary causes of dementia, the past decade has highlighted a wider potential role of magnetic resonance imaging in the diagnosis and monitoring progression of Alzheimer's disease. Using a cohort of subjects with autosomal dominant Alzheimer's disease, I found that atrophy rate of the hippocampus, a medial temporal lobe structure crucially involved in memory processing, to be increased at least 5.5 years prior to the onset of the clinical diagnosis of Alzheimer's disease. Rates of whole brain atrophy lagged behind by 2 years. I compared foc
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35

Zhang, Xiaojie. "Roles of TMP21 in Alzheimer's disease." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50490.

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Deposition of amyloid β protein (Aβ) to form neuritic plaques in the brain is the unique pathological feature of Alzheimer’s disease (AD). Aβ is derived from the cleavages of amyloid β precursor protein (APP) by β-secretase at Asp-1 site and by γ-secretase. Beta-site APP cleaving enzyme 1 (BACE1) is the β-secretase. It mainly cleaves APP within the Aβ region at the Glu-11 site to generate truncated Aβ species. Twenty-one kilodalton transmembrane trafficking protein, TMP21 (also named TMED10, p23) is a vesicular trafficking protein and a member of p24 family proteins. TMP21 mediates protein en
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36

Scott, Louise A. "Analysis of apraxia in Alzheimer's disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ53514.pdf.

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MacQuarrie, Colleen. "Experiences in early stage Alzheimer's disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ61663.pdf.

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38

Vestling, Monika. "Alzheimer's disease mutations and cellular signalling /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4993-X.

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39

Tepper, Sherri. "A biopsychosocial model of Alzheimer's disease /." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=59861.

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Research on the etiological characteristics of Alzheimer's disease has yielded inconsistent results. It is suggested that this may be due to the unidirectional focus on biomedical attributes, and the failure to consider psychosocial factors in combination with the biomedical characteristics. A biopsychosocial model of Alzheimer's disease, which integrates the biomedical dimension with psychosocial stressors and social support is proposed and tested in a sample of 172 geriatric patients using polychotomous logistic regression. Results find support for the implication of stress in the disease pr
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40

Beyer, N. B. "Metal ion transport and alzheimer's disease." Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.517106.

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41

van, Helmond Zoe Kerrstin. "Oligomeric A(beta) in Alzheimer's disease." Thesis, University of Bristol, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.521086.

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42

Barker, Rachel Mary. "The plasminogen system in alzheimer's disease." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.529891.

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43

Brooks, W. M. "Profiling gene expression in Alzheimer's disease." Thesis, University of Cambridge, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596943.

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Alzheimer’s disease is a debilitating neurodegenerative disease expected to increase in prevalence during the next few decades. Familial Alzheimer’s disease cases have revealed some molecules that appear to be involved in the disease pathogenesis. However, factors fully explaining the vast majority of case of Alzheimer’s disease which are sporadic, wait to be determined. The present study conducted a broad survey of gene expression in Alzheimer’s disease post mortem tissue with the aim of identifying gene expression products involved in this disease. Initially, a study was carried out to deter
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Hardy, Rachel Margaret. "Coping and awareness in Alzheimer's disease." Thesis, University of Birmingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.420420.

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45

Golden, H. L. "Auditory scene analysis in Alzheimer's disease." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1474234/.

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This thesis explores the behavioural and neuroanatomical picture of Auditory Scene Analysis (ASA) in Alzheimer’s disease (AD). Central auditory dysfunction is an understudied symptom of AD and there has been little connection between the neuropathological profile of the disease, its relationship to generic ASA functions, and real-world listening situations. Utilising novel neuropsychological batteries alongside structural and functional imaging techniques, this thesis aims to bridge this gap through investigations of auditory spatial, speech in noise, and (as a specialised auditory scene) musi
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46

Patel, Tulsi. "Investigating genetic variation in Alzheimer's disease." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/52447/.

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Alzheimer's disease (AD) is the most common form of dementia, now the leading cause of death in the UK, which affects more than 35 million people worldwide. Genome-wide association studies identified 20 genetic loci associated with disease susceptibility, however these only exerted small effects on risk. Next-generation sequencing is now being employed to identify more of the missing heritability. This project utilised whole-exome sequencing to explore genetic variation using the Brains for Dementia Research (BDR) resource, a well-characterised cohort of neuropathologically confirmed samples.
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47

Rowan, Mark Stephen. "Information-selectivity of Alzheimer's disease progression." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/4328/.

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Homeostatic synaptic scaling mechanisms, which normally balance potentiation during learning, may direct the progression of the disease throughout the brain as cells scale up their sensitivity to compensate for lost activation. Such a mechanism would be likely to target those cells with the lowest contribution of information to the network in early stages of the disease, resulting in delayed onset of cognitive symptoms and making timely intervention and treatment of the disease more difficult. These predictions were investigated in a Hopfield-type neural network. Lesioning according to the sca
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48

Jarrett, Joseph Timothy. "Amyloid fibril formation in Alzheimer's disease." Thesis, Massachusetts Institute of Technology, 1993. http://hdl.handle.net/1721.1/70666.

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Orr, Miranda, and Salvatore Oddo. "Autophagic/lysosomal dysfunction in Alzheimer's disease." BioMed Central, 2013. http://hdl.handle.net/10150/610220.

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Autophagy serves as the sole catabolic mechanism for degrading organelles and protein aggregates. Increasing evidence implicates autophagic dysfunction in Alzheimer's disease (AD) and other neurodegenerative diseases associated with protein misprocessing and accumulation. Under physiologic conditions, the autophagic/lysosomal system efficiently recycles organelles and substrate proteins. However, reduced autophagy function leads to the accumulation of proteins and autophagic and lysosomal vesicles. These vesicles contain toxic lysosomal hydrolases as well as the proper cellular machinery to ge
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50

Patel, Yogen. "DNA methylation analysis of Alzheimer's disease." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/dna-methylation-analysis-of-alzheimers-disease(f66ad885-3fdd-4c12-a73a-921cc31ccac2).html.

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There is evidence for a role for epigenetic mechanisms in Alzheimer's disease (AD), the most common age-dependent neurodegenerative disorder. The most studied epigenetic mark DNA methylation -the addition of a methyl group to cytosines located in CpG dinucleotides (5mC) - is known to change with aging and may reflect subtle changes in gene expression. Recently a second type of modified cytosine - a hydroxylated and methylated form (5hmC) - has been detected in the brain and maybe linked to the regulation of gene expression. Case-control differences in post-mortem brain DNA methylation were sou
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