Search for dissertations about: "Frida Ekholm-Pettersson"
Found 5 swedish dissertations containing the words Frida Ekholm-Pettersson.
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1. T-cell Differentiation and Immunological Homeostasis in Lymphopenic and Kappa Light Chain Deficient Mice
Abstract : T lymphocytes are primarily involved in adaptive, cell-mediated, immune reactions. In this thesis T cells were studied regarding central and peripheral differentiation and homeostatic mechanisms for maintanance of the immune repertoire.The influence by mature T cells on thymic development was studied in C. READ MORE
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2. Soluble amyloid-β aggregates in Alzheimer’s disease
Abstract : Soluble oligomeric aggregates of the amyloid-β (Aβ) peptide are suggested to initiate Alzheimer's disease (AD), leading to impaired synapse signalling, widespread neuronal death and loss of cognitive functions. These aggregates seem tightly linked to disease progression, and have therefore gained much attention as potential novel disease markers. READ MORE
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3. Amyloid-β Protofibril Formation and Neurotoxicity : Implications for Alzheimer’s Disease
Abstract : Alzheimer’s disease (AD) is the most common cause of dementia. A characteristic feature of AD is the presence of amyloid plaques in the cortex and hippocampus of the brain. The principal component of these plaques is the amyloid-β (Aβ) peptide, a cleavage product from proteolytic processing of amyloid precursor protein (APP). READ MORE
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4. Targeting Early Stages of Alzheimer’s Disease in a Transgenic Model
Abstract : The Arctic mutation causes early-onset Alzheimer’s disease (AD), and makes amyloid-β (Aβ) peptides more prone to form Aβ protofibrils. The aims of this thesis were to investigate the mechanisms of the Arctic mutation in vivo, and to use transgenic models to determine the role of early intermediates of Aβ aggregation, like protofibrils, in the pathogenesis. READ MORE
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5. Amyloid-β Protofibrils in Alzheimer´s Disease : Focus on Antibodies, Inflammation and Astrocytes
Abstract : Soluble amyloid-beta (Aβ) aggregates, including Aβ protofibrils, play a central role in Alzheimer’s disease (AD) and constitute a potential diagnostic biomarker and a therapeutic target. Aβ protofibrils promote synapse dysfunction and neurodegeneration, but the mechanisms behind these effects remain unclear. READ MORE