Publications by authors named "Helen Kylefjord"
Article Synopsis
- Recent research on immunotherapy for Alzheimer's disease highlights the need to understand how different antibodies bind to amyloid-beta (Aβ), as this affects their effectiveness and potential side effects.
- Lecanemab, a specific IgG1 antibody, was studied using brain samples from Alzheimer's patients and non-demented controls to explore its interactions with various Aβ forms, revealing high levels of insoluble Aβ, especially Aβ42, in Alzheimer's subjects.
- Findings indicate that lecanemab binds primarily to soluble aggregated Aβ protofibrils rather than insoluble Aβ plaques, suggesting a targeted approach in treating Alzheimer's through the modulation of these specific proteins.
Article Synopsis
- The study investigated the effects of mAb158, an antibody that targets soluble amyloid beta protofibrils, on aged mice with Alzheimer's-related Aβ pathology.
- Mice treated with mAb158 showed significant reductions in Aβ protofibril levels after 4 weeks and amyloid plaque load after 18 weeks, with effects persisting for 12 weeks post-treatment.
- Upon ending the treatment, levels of Aβ protofibrils and plaques increased again, highlighting the need for ongoing treatment to sustain the benefits on Aβ pathology.
Although hepatitis C virus (HCV) is a pathogen of global significance, experimental therapies in current clinical development include highly efficacious all-oral combinations of HCV direct-acting antivirals (DAAs). If approved for use, these new treatment regimens will impact dramatically upon our capacity to eradicate HCV in the majority of virus-infected patients. However, recent data from late-stage clinical evaluations demonstrated that individuals infected with HCV genotype (GT) 3 responded less well to all-oral DAA combinations than patients infected with other HCV GTs.
View Article and Find Full Text PDFSystemic administration of adenoviral vectors leads to a widespread distribution of vector. Therefore, targeting of adenoviral vectors to specific tissues or cell types will require methods to ablate the normal tropism of the vector simultaneously with the introduction of new receptor specificities. To inhibit native receptor binding, we mutated residues in the AB loop of the adenovirus type 5 (Ad5) fiber.
View Article and Find Full Text PDFAdenovirus binds to mammalian cells via interaction of fiber with the coxsackie-adenovirus receptor (CAR). Redirecting adenoviral vectors to enter target cells via new receptors has the advantage of increasing the efficiency of gene delivery and reducing nonspecific transduction of untargeted tissues. In an attempt to reach this goal, we have produced bifunctional molecules with soluble CAR (sCAR), which is the extracellular domain of CAR fused to peptide-targeting ligands.
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