Our Labs

We are interested in decoding the genomic regulatory code and understanding how genomic regulatory programs drive dynamic changes in cellular states, both in normal and disease processes.

Our laboratory is focused on understanding the molecular biology of membrane transport in a disease-related context covering Alzheimer’s and Lewy Body diseases.

We want to generate a quantitative understanding of the molecular mechanisms underlying Alzheimer’s disease pathogenicity, more specifically the biochemical function of the molecules involved in familial Alzheimer’s disease.

We study the role of local axonal translation in ALS and FTD, as well as the spreading of RNA-binding proteins, including FUS and TDP-43, in ALS. We also focus on muscle innervation and the development of new therapeutic targets to treat neuromuscular disorders.

We investigate the basic mechanisms causing Alzheimer’s disease and Parkinson’s disease starting from the genetic forms of these disorders. We study the complex cellular phase of Alzheimer’s disease using single-cell, genome-wide transcription profiling with spatial and temporal resolution.

Our lab aims to unravel the molecular mechanisms that control neuronal connectivity in developing circuits, and determine how perturbations in this process affect cognitive function.

The regulation of emotional states and their associated response to fear and stress are critical for organisms to survive, interact with their environment and reproduce. We study how emotions emerges during development, what controls the diversity of emotional circuits, and to which extent it relies on intrinsic factors (genes) and/or on our past experiences.

Information processing in the brain depends on specialized circuits that are formed by distinct types of neurons. We study the metabolic and transcriptomic programmes that shape neuronal diversity and circuit assembly in the developing mammalian cortex.

Sleep is a fundamental and evolutionarily conserved behavior, and the only major behavior for which the function remains unknown. The goal of our lab is to understand the synaptic and circuit mechanisms underlying sleep and its function in the brain.

We study the mechanisms gearing protein folding and misfolding and their relation to human disease. In particular, we investigate how protein aggregation affects the interactome by suppressing native interactions but also by introducing novel aggregation-specific interactions.

Our research focuses on the mechanisms of acute and chronic axonal and neuronal degeneration and regeneration, aiming to contribute to the development of new therapeutic strategies for neurodegenerative disorders, such as motor neuron diseases, FTD and stroke.

The major research goal in our laboratory is to understand the molecular and cellular mechanisms underlying the development and evolution of the cerebral cortex, from stem cells to neuronal circuits, from mouse to man, in health and disease.

Dementia and neurodegeneration are an enormous burden on society. Patients require life-long care and there is no cure. At early phases, tau-induced dementia and Parkinson's disease are closely associated with synaptic degeneration. We study the mechanisms of the loss of synaptic communication in disease, but also in the context of hibernating brains where synaptic de-and regeneration occur under physiological conditions. In the lab we make use of human induced neuronal models, rodent models (including those that hibernate) and the incredible power of fruit fly genetics.

We focus on a superfamily of cation channels, the transient receptor potential (TRP) channels, which includes 27 human members. There is a striking diversity in the stimuli that can regulate the gating of the TRP channels, which include physical stimuli such as temperature and voltage, as well as various endogenous and exogenous chemical ligands.