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People living with dementia (PD) are mainly taken care by informal caregivers (IC) who themselves might also be facing health issues during the onset of caregiving role. Being carer for PD creates stressful situations with the risk of social exclusion. The aim of the scoping review is to find out in what way providing care for a person with dementia (PD) might have impact on health and exclusion from social relations experienced by ICs during the onset of the caregiving role. The review should provide investigation-based knowledge on the experiences of IC of PD in the initial stage of caregiving including the experience of stress and exclusion from social relationships, as well as identify factors which might be associated with negative outcomes of being IC of PD.

The symposium aims to take a closer look at what it means to involve older participants in ageing research - beyond the role of research subjects. By discussing projects that deploy different participatory approaches we investigate the manifold ways in which older adults can become co-creators of the research process. We do so comparing such approaches in different domains, with different outcomes and in different stages of the research process. Consequently, this symposium (1) looks at the research process through the lens of benefits and challenges resulting from involving older adults as co-creators; (2) showcases projects across different domains and different jurisdictions that applied participatory approach in ageing research to discuss benefits and challenges, and (3) advances scientific insights into participatory approaches involving older adults. After an introductory contribution outlining theories, concepts and developments of participatory approaches in ageing research, we present insights from three empirical studies in different cultural and thematic settings. In our first presentation, Anna Wanka and Anna Urbaniak open the symposium by presenting an overview of participatory approaches that involve older adults. In the first empirical presentation, Julia Nolte and Hamid Turker discuss the process of involving older adults in data analysis and therefor present data from the US. In the third presentation, Lillian Hunn highlights how the recent COVID-19 pandemic impacted patient involvement in research in Canada. Finally, Anna Urbaniak discusses the process of planning participatory research with hard to reach population among older adults in Austria, namely those who are socially excluded.

Inappropriate and un-regulated inflammation is the hallmark of a variety of inflammatory diseases including Rheumatoid Arthritis (RA). Central to the pathogenesis of this disease is the cytokine Tumour Necrosis Factor α (TNF), a product of activated macrophages. Macrophages are activated by numerous exogenous and endogenous ligands through Toll like receptors (TLR) leading to the activation of numerous protein tyrosine kinases (PTK). These studies have mainly described the LPS pathway and have not focused on endosomal TLRs, which are being increasingly implicated in the pathology of RA. The work presented in this thesis describes the role of Bruton's Tyrosine Kinase (Btk) in TLR8 signalling in human primary macrophages. Using an adenovirus overexpression system and RNAi technology, Btk has been shown to control the production of TNF in R848-stimulated cells. This regulation occurred on a transcriptional level as Btk downregulation decreased the level of the primary TNF transcript at 2h as well as the recruitment of RNA Polymerase II to the promoter of the TNF gene at 1h. This rapid effect of Btk depletion on gene transcription resulted in significantly less TNF protein production at 2h following R848 stimulation. Subsequent analysis of transcription factors potentially involved in the Btk-dependent regulation of TNF transcription revealed that Btk affects both NFkB and AP-1 in TLR8 signalling. In particular, Btk downregulation decreased the binding of NFkB to its consensus site as shown by EMSA as well as the recruitment of p65 to the TNF promoter or 3' enhancer region as shown by ChIP. The regulation of p65 by Btk occurred at the level of p65 phosphorylation on Serine 536 and did not affect the degradation of IkBα. AP-1 activity in EMSA was also decreased under the Btk knockdown conditions, with cJun and ATF-2 but not cFos being involved in Btk signalling. At the same time, Btk did not alter p38, ERK and JNK MAPK activity ruling out their involvement in the Btk-dependent control of AP-1 in R848-challenged macrophages. These data extend current knowledge regarding the involvement of Tec kinases in the regulation of cytokine production under inflammatory conditions by providing a potential mechanism of transcriptional control.