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Showing result 1 - 5 of 18 swedish dissertations matching the above criteria.
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1. Cellular responses to amyloid-beta protofibrils : Focus on astrocytes, extracellular vesicles and antibody treatment
Abstract : Knowledge about the cellular mechanisms behind the initiation and propagation of Alzheimer’s disease (AD) is limited. Decades of research have focused on neuronal abnormalities in AD, but recently more attention has been given to the glial cells. READ MORE
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2. 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
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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. Aβ Conformation Dependent Antibodies and Alzheimer's Disease
Abstract : Soluble intermediates of the amyloid-β (Aβ) aggregation process are suggested to play a central role in the pathogenesis of Alzheimer’s disease (AD) by causing synaptic dysfunction and neuronal loss. In this thesis, soluble Aβ aggregates have been studied with a particular focus on the Aβ protofibril, which has served as the antigen for developing conformation dependent monoclonal antibodies. READ MORE
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5. 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