Sökning: "slow progression"
Visar resultat 21 - 25 av 84 avhandlingar innehållade orden slow progression.
21. Design and Synthesis of Inhibitors Targeting the Aspartic Proteases HIV-1 PR and BACE-1
Sammanfattning : This thesis describes the synthesis of molecules designed for inhibition of two aspartic proteases, viral HIV-1 PR and human BACE-1. It also reports on the structure activity relationships of the targeted enzyme inhibitors. It is estimated that currently 33 million people are infected with HIV, the causative agent of AIDS. LÄS MER
22. Immune deterioration in HIV-1 and HIV-2 infection with a focus on CD8 T cell exhaustion
Sammanfattning : Thanks to the development of antiretroviral treatment (ART), human immunodeficiency virus (HIV) infection is now considered a chronic infection rather than the death sentence it used to be. Despite constant expansion and improvement of treatment options, even optimal therapy cannot prevent the impact of HIV on the human immune system. LÄS MER
23. Ligand-induced structural changes in HIV-1 envelope glycoprotein
Sammanfattning : The first step in HIV-1 entry is the interaction between viral envelope glycoprotein gp120 and CD4 receptor on permissive host cells. The interaction initiates a series of sequential conformational rearrangements that exposes epitopes involved in interaction with co-receptors. LÄS MER
24. Welander distal myopathy : clinical and genetic studies
Sammanfattning : Distal myopathies are a group of muscular disorders described in many countries with different inheritance patterns and variable progression rates. Welander distal myopathy (WDM) is characterised by autosomal dominant inheritance, late onset and distal distribution of muscular weakness. Most cases originate from the middle parts of Sweden. LÄS MER
25. Neuroinflammation and amyloid-β in early Alzheimer’s disease. Insight into the earliest events using mouse models
Sammanfattning : Alzheimer’s disease (AD) is the leading cause of dementia and most common neurodegenerative disease worldwide, but there currently exists no effective treatment that can stop nor slow the progression of the disease. The current dogma in the field postulates that the appearance of extracellular amyloid-beta (Aβ) plaques, a histopathological hallmark of the disease, is the trigger for downstream, detrimental events, including neuronal loss, extensive neuroinflammation and cognitive decline. LÄS MER