The Open Competition Domain Science – XS grants of a maximum of € 50,000 are intended to support promising ideas and to facilitate innovative and more speculative initiatives within the seven Domain Science disciplines. The proposed research is ground-breaking and high-risk. What counts is that all results, be they positive or negative, must contribute to the advancement of science.
TicklishSkin - Towards novel sensory-based detection of autism through tickle response analysis
Konstantina Kilteni (Donders Institute for Brain, Cognition and Behaviour)
Autism Spectrum Disorder (ASD) affects over 190,000 people in the Netherlands; yet, no reliable biological markers exist to support early diagnosis despite strong evidence that early intervention improves outcomes. This project explores an unconventional but promising idea: that heightened sensitivity to tickling may serve as a sensory biomarker for autism. Using a specialized device and state-of-the-art brain and physiological recordings, we will compare responses to ticklish stimuli in autistic and neurotypical adults in terms of self-reports, physiology, and brain activation. If a clear link is found, this could pave the way for simple, accessible, and early screening tools for autism.
Harnessing Uncharted Pathways for Antibiotic Discovery
Willem Velema (Institute for Molecules and Materials, FNWI)
We propose a new, label-free test to map how antibodies recognize their targets, using interferometric scattering (iSCAT) microscopy. Instead of adding fluorescent tags, iSCAT watches single antibodies label-free bind in real time. This provides not only qualitative information about bindings, but also binding speeds—key for improving antibodies and training AI to predict epitopes. Today, iSCAT sees only a small areas. We will engineer a more sensitive setup that views many spots at once, so we can track multiple peptide interactions. That will cut experiment time and improve data quality, enabling faster vaccine, drug design and pandemic readiness.
Chemotactic predator powered by degradation for potential pathogenic bacterial elimination
Daniela Wilson (Institute for Molecules and Materials, FNWI)
Directional migration is a fundamental survival strategy, allowing cells or bacteria to move towards nutrients and away from toxins1,2. Inspired by this principle, we propose the development of a degradation-powered chemotactic predator capable of actively homing to and selectively eliminating pathogenic bacteria. This high-risk and high-gain strategy provides both a minimal model for studying chemotaxis and a transformative approach to targeted antimicrobial therapy. By harnessing recent advances in nanotechnology and biomedicine, the project aims to pioneer a new class of biodegradable, precision medicine tool with the potential to revolutionize bacterial treatment and shape the future of nanomedicine.
Building Resilient Ecosystems from the Ground Up
Dina in 't Zandt (Radboud Institute for Biological and Environmental Sciences)
Ecosystem degradation due to extreme disturbances from humans and climate change risk their collapse. Ecosystem collapse means the loss of vital ecosystem services such as carbon and water cycling. As extreme disturbances become more frequent, we urgently need innovative ways to build resilience into ecosystems. We propose that resilience could be enhanced through a paradigm shift from aboveground ecosystem components to the soil microbiota that we know are crucial in stabilising ecosystems. By examining microbial community connectedness across a unique forest disturbance gradient in Tasmania, we will test whether microbes could be harnessed to enhance resilience in disturbed systems.
Molecular drivers of selective vulnerability in neurodegenerative diseases: a focus on Charcot-Marie-Tooth disease
Maria Landinez Macias (Donders Institute for Brain, Cognition and Behaviour)
Neurodegenerative diseases are characterized by degeneration of specific neuronal types. In Charcot-Marie-Tooth (CMT) disease, peripheral motor and sensory neurons are selectively affected. For all neurodegenerative diseases, it remains unclear how mutations in widely expressed genes lead to such cell-type-specific degeneration. We hypothesize that CMT-vulnerable cells are closer to a threshold that triggers neurodegeneration via stress signaling pathways. This threshold may depend on protein synthesis rate, tRNA and tRNA synthetase levels, and expression of key proteins activating the integrated stress response. We will quantify these factors in affected versus unaffected cells in mouse models to understand their role in CMT vulnerability.