The CNS consists of neurons and glial cells: microglia, astrocytes and oligodendrocytes. Neurons form a highly connected network and glial cells are required for its proper functioning, and the maintenance of a healthy CNS. Perturbed neuron-glia interactions and pathologically changed cellular functions are observed in CNS diseases and offer important potential therapeutic targets which are urgently needed.
  • Our main research goal is to understand the molecular basis of CNS cell functions to the benefit of human health.
  • We aim at unraveling the regulation and molecular mechanism of CNS cell identity and function. cell-cell communication and interactions, and we use state of the art -omics approaches and human CNS tissues for these studies. Key findings are validated in various model systems (hiPSCs, organoids, organotypic cultures, primary cells, mice).
  • We delineate the relation and interaction between CNS pathology and altered cellular identity and functions, in order to understand the etiology and progression of CNS diseases. The ultimate aim is to identify possible drug targets to fight CNS diseases. CNS pathologies we currently focus on are neuroinflammation (multiple sclerosis, neuromyelitis optica, sepsis), neurodegeneration (Alzheimer, frontotemporal dementia) and neurodevelopmental disorders (schizophrenia, adverse early life events).

How our research benefits to society

Understanding the functions and interactions of CNS cells and how perturbations therein lead to CNS disease.

To be able to modulate or restore CNS functions to the benefit of human health is of primary relevance. The number of people suffering from CNS disease is rapidly increasing and the underlying pathophysiology often poorly understood. To elucidate the mechanisms involved in these neuropathological processes, and the identification of cellular processes that are perturbed is of great importance as these are the potential points of intervention, for urgently needed therapeutic interventions.

  • Fundamental understanding of the molecular neurobiological systems of the CNS
  • Genetic, molecular and cellular causes underlying the pathophysiology of human CNS diseases (neuroinflammation and neurodegeneration)
  • Identification of therapeutic targets for human CNS diseases
  • omics approaches to delineate CNS disease aetiology and progression
  • state-of-the-art technologies to drive innovation in life sciences and medicine
  • We are characterizing microglia subtypes in relation to Alzheimer pathology. For these studies, we employ omics technologies on human CNS tissues and hiPSCs.

  • We are characterizing how cellular interactions change in relation to Alzheimer’s pathology. Here, we employ omics technologies on human CNS tissues, like large scale single cell gene expression profiling.

  • In this line of research, we want to understand how and where MS lesion emerge, and how they progress. Profiling approaches of human CNS tissues and hiPSC models are used.

  • Frontotemporal dementia is the second most common dementia. The underlying neurobiological pathophysiology is not well understood and the focus of this research line. Approaches used are omics-characterization of human CNS tissues.


Trix van der Sluis-Rozema Secretary of Section Molecular Neurobiology

Department of Biomedical Sciences of Cells and Systems
University Medical Center Groningen
The Section Molecular Neurobiology, Internal Zipcode FB43
Antonius Deusinglaan, 1
9700 AD Groningen, The Netherlands

Visiting address
Department of Biomedical Sciences of Cells and Systems
University Medical Center Groningen
The Section Molecular Neurobiology, Building 3215, 8th floor
Antonius Deusinglaan, 1
9713 AV Groningen, The Netherlands