We aim to understand the biological link between aging and age-related neurodegenerative diseases. By identifying early causal mechanisms, we hope to target pathological changes before they cause disease.

Loss of protein homeostasis accelerates ageing and contributes to age-related diseases, which include neurodegenerative diseases such as Parkinson’s disease and Amyotrophic Lateral Sclerosis (ALS). Consequently, disease-specific aggregation-prone proteins can accumulate and form condensates and aggregates. How aggregation-prone proteins cause disease is still incompletely understood. Our group aims to identify and understand biological mechanisms that drive the age-related toxicity of aggregation-prone proteins and their link with condensation and aggregation. Using genetic and phenomics screens in C. elegans we have identified several cellular and organismal mechanisms involved, which include cellular factors that drive toxic structural changes in aggregation-prone proteins and metabolic factors that likely modify toxicity likely at an organismal scale. Using an experimental pipeline to monitor protein condensation and aggregation as well as consequences for cellular function and behaviour, we can link molecular changes to organismal consequences in living and aging animals. Together with academic and industrial collaborators, we use our results and tools for the development of candidate therapeutic interventions to prevent or delay protein toxicity in aging and age-related diseases.

Our main field or research interests in aging biology include:

  • Cellular mechanisms regulating protein homeostasis
  • Cellular mechanisms driving protein condensation and aggregation
  • Organismal mechanisms driving protein toxicity
  • Microbiome and metabolic regulation of protein toxicity
  • Disease-protein driven neuronal circuit imbalances and consequences for behaviour
  • Interventions to boost resilience and mitigate toxicity of aggregation-prone proteins
  • Parkinson’s disease, Amyotrophic Lateral Sclerosis (ALS), Alzheimer’s disease, Proteinopathies, Synucleinopathies, TDP-43 proteinopathies

Our research and benefits to society

With our research we aim to uncover biological mechanisms of aging and age-related diseases and deliver mechanistic targets for interventions to prevent or delay the onset of disease. Using genetic and phenomics screens in the genetically tractable model organism C. elegans, we have identified several cellular and metabolic mechanisms that protect against the toxicity of neurodegenerative disease-related proteins and provided evidence of their relevance in human or mammalian models. 
By developing C. elegans models for disease and establishing automated tools and pipelines to monitor disease-relevant pathological and behavioral phenotypes, we have accelerated mechanistic- and drug discovery, by us, other researchers, and companies in the field.  In addition, we collaborate with clinicians and pharmaceutical companies to maximize opportunities of forwarding our discoveries and tools to clinical application.

We train bachelor, master, and PhD students in the areas of biology, biomedical sciences, medical sciences, biochemistry, neurosciences and related fields to expand our expertise and knowledge for future research. 
Our research has been highlighted in local and national news media. We provide lectures for the public and reach a broad audience through our social media channels. Within the UMCG we collaborate with the department of neurology, medicinal chemistry, and microbiology with whom we have received grants to study how microbiome and metabolic changes drive age-related protein toxicity. We collaborate and publish regularly with multiple international experts worldwide, ranging from structural biologists to human geneticists, with the shared aim to find therapeutic solutions for age-related neurodegenerative diseases. These collaborations involve exchange of trainees with foreign labs, exchange of reagents, expertise, and execution of specialized experiments. We participate, in addition, in EU-based collaborative networks such as HealthAge.


European Research Institute for the Biology of Ageing (ERIBA)
University Medical Center Groningen (UMCG)
Building 3226, Room 03.34
PO Box 196, Internal Zip Code FA50
9700 AD Groningen
The Netherlands

Visiting Address

European Research Institute for the Biology of Ageing (ERIBA)
University Medical Center Groningen (UMCG)
Antonius Deusinglaan, 1
Building 3226
9713 AV Groningen
The Netherlands