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Additive effects of amyloid β fragment and interleukin-1β on IL-6 secretion in rat primary glial cultures.
Stockholm University, Faculty of Science, Department of Neurochemistry.
2002 In: International Journal of Molecular Medicine, ISSN 1107-3756, Vol. 10, 245-250 p.Article in journal (Refereed) Published
Place, publisher, year, edition, pages
2002. Vol. 10, 245-250 p.
URN: urn:nbn:se:su:diva-25920OAI: diva2:200801
Part of urn:nbn:se:su:diva-990Available from: 2006-05-18 Created: 2006-05-18Bibliographically approved
In thesis
1. Inflammatory cytokines and NFκB in Alzheimer’s disease
Open this publication in new window or tab >>Inflammatory cytokines and NFκB in Alzheimer’s disease
2006 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Alzheimer’s disease is the most common form of dementia. It is a neurodegenerative disorder characterized by extracellular senile plaques and intracellular neurofibrillary tangles. The main constituent of the senile plaques is the neurotoxic β-amyloid peptide. Surrounding the senile plaques are activated astrocytes and microglia, believed to contribute to neurotoxicity through secretion of proinflammatory cytokines, like interleukin-1β and interleukin-6. For many inflammatory actions, including the cytokine induction in glial cells, the transcription factor NFκB plays a key role. This suggests that therapeutical strategies aimed to control the development of Alzheimer’s disease could include administration of drugs that hinder NFκB activation.

The major aim of this thesis was to examine the effects of β-amyloid together with interleukin-1β on cytokine expression as well as NFκB activation in glial cells. The possibility to block NFκB activation, and downstream effects like interleukin-6 expression, by using an NFκB decoy was investigated. The possibility to improve the cellular uptake of the decoy by linking it to a cell-penetrating peptide was also investigated.

The results obtained provide supportive evidence that inflammatory cytokines are induced by β-amyloid, and that they can indeed potentiate its effects. The results further demonstrate that by blocking NFκB activation, the induction of interleukin-6 expression can be inhibited. By using an improved cellular delivery system, the uptake of the NFκB decoy and hence the downstream cytokine inhibition could be increased. In conclusion, these results demonstrate the possibility to decrease the inflammatory reactions taken place in Alzheimer’s disease brains, which may ultimately lead to a possible way of controlling this disorder.

Place, publisher, year, edition, pages
Stockholm: Institutionen för neurokemi, 2006. 130 p.
β-amyloid, interleukin-1, interleukin-6, cell-penetrating peptide, PNA
National Category
urn:nbn:se:su:diva-990 (URN)91-7155-265-0 (ISBN)
Public defence
2006-06-09, Magnélisalen, Kemiska övningslaboratoriet, Svante Arrhenius väg 12 A, Stockholm, 13:00
Available from: 2006-05-18 Created: 2006-05-18Bibliographically approved

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