Scientific Mission

The Institute of Translational Neuroscience is an independent research institution at the Medical Faculty of the Westfälische Wilhelms-University Münster embedded in the Department of Mental Health at the Münster University Medical Center (UKM, Director: Prof. Dr. med. Bernhard Baune). It is dedicated to provide new options for diagnostic and/or therapeutic strategies for human diseases of the nervous system. This “bench to bedside” approach builds on molecular research pursued during the last 30 years which paved the avenue for novel therapeutic strategies to be assessed in man. It follows the idea that neuroscience is a discipline providing understanding of human disease and eventually its cure, rather than to explain man itself. Translation defines the goal of basic research, the patient. While experimental studies are pursued in close collaboration with the Institute of Anatomy, University of Cologne (Director: Prof. Dr. med. Johannes Vogt), clinical studies are performed in close collaboration with the Institute of Translational Psychiatry, WWU Münster (Director: Prof. Dr. med. Dr. phil. Udo Dannlowski).

In addition to translational research, philosophical aspects of the mind-body debate are addressed and a focus of the Institute’s teaching activities. The ever-recurring attempts of the neurosciences to explain all mental phenomena in physical terms alone are revised by critical reappraisal of classical concepts, e.g. Wilder Penfield’s “storehouse of memories”. Our analyzes question the idea of a realization of memory in solely naturalistic terms. These studies are performed in part at the Montreal Neurological Institute (Prof. Dr. Richard Leblanc, Prof. Dr. Jack Antel), Quebec, Canada, and in close collaboration with Prof. Dr. med. Frank Stahnisch at the Hotchkiss Brain Institute, University of Calgary, Alberta, Canada.

Latest publications

Chalas N, Daube C, Kluger DS, Abbasi O, Nitsch R, Gross J (in press). Speech onsets and sustained speech contribute differentially to delta and theta speech tracking in auditory cortex. Cereb Cortex 
doi: 10.1093/cercor/bhac502.


When we attentively listen to an individual's speech, our brain activity dynamically aligns to the incoming acoustic input at multiple timescales. Although this systematic alignment between ongoing brain activity and speech in auditory brain areas is well established, the acoustic events that drive this phase-locking are not fully understood. Here, we use magnetoencephalographic recordings of 24 human participants (12 females) while they were listening to a 1 h story. We show that whereas speech-brain coupling is associated with sustained acoustic fluctuations in the speech envelope in the theta-frequency range (4-7 Hz), speech tracking in the low-frequency delta (below 1 Hz) was strongest around onsets of speech, like the beginning of a sentence. Crucially, delta tracking in bilateral auditory areas was not sustained after onsets, proposing a delta tracking during continuous speech perception that is driven by speech onsets. We conclude that both onsets and sustained components of speech contribute differentially to speech tracking in delta- and theta-frequency bands, orchestrating sampling of continuous speech. Thus, our results suggest a temporal dissociation of acoustically driven oscillatory activity in auditory areas during speech tracking, providing valuable implications for orchestration of speech tracking at multiple time scales.

Endle H, Horta G, Stutz B, Muthuraman M, Tegeder I, Schreiber Y, Snodgrass IF, Gurke R, Liu ZW, Sestan-Pesa M, Radyushkin K, Streu N, Fan W, Baumgart J, Li Y, Kloss F, Groppa S, Opel N, Dannlowski U, Grabe HJ, Zipp F, Rácz B, Horvath TL, Nitsch R, Vogt J (2022). AgRP neurons control feeding behavior at cortical synapses via peripherally-derived lysophospholipids. Nature Metabolism 4(6):683-692.


Phospholipid levels are influenced by peripheral metabolism. Within the central nervous system, synaptic phospholipids regulate glutamatergic transmission and cortical excitability. Whether changes in peripheral metabolism affect brain lipid levels and cortical excitability remains unknown. Here, we show that levels of lysophosphatidic acid (LPA) species in the blood and cerebrospinal fluid are elevated after overnight fasting and lead to higher cortical excitability. LPA-related cortical excitability increases fasting-induced hyperphagia, and is decreased following inhibition of LPA synthesis. Mice expressing a human mutation (Prg-1R346T) leading to higher synaptic lipid-mediated cortical excitability display increased fasting-induced hyperphagia.Accordingly, human subjects with this mutation have higher body mass index and prevalence of type 2 diabetes. We further show that the effects of LPA following fasting are under the control of hypothalamic agouti-related peptide (AgRP) neurons. Depletion of AgRP-expressing cells in adult mice decreases fasting-induced elevation of circulating LPAs, as well as cortical excitability, while blunting hyperphagia. These findings reveal a direct influence of circulating LPAs under the control of hypothalamic AgRP neurons on cortical excitability, unmasking an alternative non-neuronal route by which the hypothalamus can exert a robust impact on the cortex and thereby affect food intake.

(full article)