Elderly poverty is a prominent problem, and financial well-being in elderly is often considered low. A common cause for elderly poverty is a lack of sufficient pension awareness and engagement, especially at a young age. Independent of the pension scheme in a particular country, pension funds and policymakers around the world struggle to increase the engagement of pension plan consumers that would affect a consumer's future financial well-being positively. An often-proposed intervention to overcome the present bias that leads to not engaging with pension communications is to stimulate the imagery of the future self in pension plan consumers. Yet, current pension communications fall behind expectations in stimulating imagery of the future self and thus fail to improve pension awareness and engagement. In light of recent evidence on a new technology coined Augmented Reality (AR), this project proposes an experimental approach to investigate the impact of AR on the imagery of the future self and the downstream effects on pension awareness and engagement. Building on a series of laboratory, online, and field experiments, I apply findings from recent AR research in consumer behavior to find evidence and theoretically explain the effects AR can have on pension awareness and engagement. Combining findings from laboratory studies with field-evidence from the world’s third largest pension provider (APG) will shine light on how to improve pension communication with AR to improve future financial well-being. The proposed results are societally relevant as they can help to promote pension engagement that results in future financial well-being. My strong background in experimental consumer behavior research with a focus on AR technology and consumer engagement, combined with my supervisor’s expertise in pension and financial well-being research, and the strong research and training environment at Maastricht University (UM) will guarantee a successful project completion.

Cardiac hypertrophy is the principal risk factor for the development of heart failure and lethal arrhythmias. A complex web of interconnected signalling pathways has been implicated in hypertrophy and species of non-coding RNA molecules, microRNAs, have been shown to regulate these pathways. The recognition of microRNAs as potential therapeutic targets marks the principal step towards new therapeutic concepts. The SIRENE project represents the advancement of the therapeutic strength of miRNA silencing in clinically relevant heart failure models towards a valuable proposition for counteracting pathological hypertrophic signalling and heart failure development. In specific, during the related ERC CALMIRS project, it was found that sustained knockdown of endogenous miR-199b in the adult mouse heart in vivo leads to profound protective effects against symptoms of heart failure. Therefore, a new class of RNA antagonists, targeting miRNAs is powerful and holds great promise to become the next generation therapeutics. At this stage the newly developed antagonists are unique in their affinity and specificity for miR-199b and current data demonstrates a profound rescue by miR-199b antagonists on heart failure symptoms such as pressure overload induced cardiac morphological, histological, functional and molecular abnormalities in mice. The challenge of the SIRENE project is to identify immediate and longer term opportunities for commercialisation with high clinical and commercial feasibility. Therefore different business models will be studied in terms of market research, IP strategy and business development to eventually consolidate a commercial strategy and business case for presenting our business proposition to strategic partners or venture capitalists. Simultaneously, dose-range finding and efficacy studies will be conducted in rats, a clinically relevant and larger animal model of heart failure, for further preclinical development.

Recovery from injury, illness, and/or disease is associated with skeletal muscle disuse. Muscle disuse leads to a loss of muscle mass, strength, and functional independence, and represents a “catabolic crisis” for the elderly who are already at a greater risk for low muscle mass and strength due to age-related sarcopenia. Muscle mass is determined by the balance between muscle protein synthesis (MPS) and muscle protein breakdown (MPB). When MPB exceeds MPS, the result is a negative net protein balance and muscle loss. Decreased MPS rates occur following the onset of immobilization-induced disuse, but there is no information on the response of MPB. mRNA and protein expression data indicate that the early stages of disuse (0-5 days) result in activation of the ubiquitin proteasome system, and presumably MPB suggesting that the initial stages of disuse represent a critical period to intervene with appropriate countermeasures to attenuate the loss of muscle mass and strength. Leucine is a key amino acid in the regulation of muscle protein metabolism that has been shown to inhibit MPB. The current proposal REALISM will 1) identify whether MPB is elevated during the early stages (72 hours) of immobilization-induced disuse, 2) determine whether leucine can reduce MPB and the loss of muscle mass during the early stages of immobilization, and 3) determine whether leucine can preserve muscle mass and strength in the elderly during more prolonged periods of immobilization. REALISM will identify the mechanisms underlying disuse atrophy in response to immobilization and examine potential therapeutic strategies to offset the loss of muscle mass and strength. The M3 laboratory of Dr. van Loon at Maastricht University (UM) offers the most ideal environment for me to conduct REALISM, and take a major step towards the achievement of my career goal of setting up my own research program and establishing myself as an independent scientist.