Sökning: "Frida Ekholm Pettersson"

Visar resultat 1 - 5 av 6 avhandlingar innehållade orden Frida Ekholm Pettersson.

1. 1. T-cell Differentiation and Immunological Homeostasis in Lymphopenic and Kappa Light Chain Deficient Mice

   Författare :Frida Ekholm Pettersson; Fredrik Ivars; Uppsala universitet; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Biochemistry; T cells; differentiation; homeostasis; cytokines; mice; SCID; κ-deficient; Biokemi; Biochemistry; Biokemi; immunologi; Immunology;

   Sammanfattning : 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. LÄS MER

3. 2. Soluble amyloid-β aggregates in Alzheimer’s disease

   Författare :Hillevi Englund; Frida Ekholm Pettersson; Lars NG Nilsson; Lars Lannfelt; Dominic M Walsh; Uppsala universitet; []
   Nyckelord :MEDICIN OCH HÄLSOVETENSKAP; MEDICAL AND HEALTH SCIENCES; Geriatrics and medical gerontology; Geriatrik och medicinsk gerontologi; Geriatrics; geriatrik;

   Sammanfattning : 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. LÄS MER

4. 3. Amyloid-β Protofibril Formation and Neurotoxicity : Implications for Alzheimer’s Disease

   Författare :Ann-Sofi Johansson; Lars Lannfelt; Frida Ekholm Pettersson; Pär Gellerfors; Tobias Hartmann; Uppsala universitet; []
   Nyckelord :Neurosciences; Amyloid-β; Neurotoxicity; Aggregation; Protofibrils; Alzheimer s disease; Neurovetenskap;

   Sammanfattning : 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). LÄS MER

5. 4. Targeting Early Stages of Alzheimer’s Disease in a Transgenic Model

   Författare :Anna Lord; Lars Nilsson; Lars Lannfelt; Frida Ekholm Pettersson; Thomas Bayer; Uppsala universitet; []
   Nyckelord :Geriatrics; geriatrik;

   Sammanfattning : 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. LÄS MER

7. 5. Aβ Conformation Dependent Antibodies and Alzheimer's Disease

   Författare :Dag Sehlin; Lars Lannfelt; Frida Ekholm Pettersson; David Teplow; Uppsala universitet; []
   Nyckelord :Alzheimer s disease; amyloid-beta; protofibrils; conformation; monoclonal antibody; ELISA; MEDICINE; MEDICIN; Geriatrics; Geriatrik;

   Sammanfattning : 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. LÄS MER