Synapses rely on fundamental resources that fuel their partial autonomy in transmitting and encoding information. These resources encompass local energy supply through mitochondria, local protein synthesis through synapse-associated ribosome, and inter-cellular communication at the synaptic interface. Under conditions of either excessive energy consumption, starvation, or neuronal adjustments, synaptic resources are challenged and finally depleted. Consequently, stress responses occur, which initially aim at compensating challenging conditions but ultimately leading to synaptic and neuronal dysfunction. A variety of stress-inducing factors – associated to neuroinflammation – has been described in the past, such as metabolic changes, reactive oxygen species, and infection. As a fundamental pathophysiological principle in many neuropsychiatric diseases, our mission is to unravel the mechanisms of inflammation-associated synaptic stress.

Our experiments focus on the molecular control of synaptic autonomy under stress, encompassing cutting-edge epigenetic techniques, mRNA biology investigations, and advanced tissue culture models. Beyond local processes at synaptic sites, we are investigating mechanisms how synaptic sensing controls nuclear gene expression along synapse-to-nucleus communication axes.

Experimental methods:

• Brain organoids and assembloids
• Organotypic brain tissue cultures
• ChIPSeq-analyses
• mRNA biology
• Single-nuclei sequencing
• Crispr/Cas genetic engineering

Collaborating Partners:

Prof. Dr. Lars Dölken (Institute of Virology, MHH)

For collaboration requests, please contact Dr. Fabian Gather (Group Leader, Gather.Fabian@mh-hannover.de) and Prof. Dr. Maximilian Lenz (neuroanatomie@mh-hannover.de).