Univ.-Prof. Dr. Claus Lamm
The SCAN-Unit (Claus Lamm) advances our knowledge on (predominantly human) social cognition and behavior and their ultimate and proximate neuro-cognitive mechanisms. We use a wide range of research methods and levels of observation, from genetics to large scale human social behavior, but mainly neuroimaging and psychopharmacology in predominantly neurotypical and healthy populations. A recent focus is the (neuro)computational modeling of trust behavior, its modulation by aging and in lesion as well as in clinical models (with a focus on schizophrenia and ASD), as well as its neural and neurochemical underpinnings (focus so far on dopamine, the amygdala, and prefrontal areas). The associated Cognitive Neuroscience group of Isabella Wagner-Anderson conducts research on the neural underpinnings of learning, memory and navigation, with a particular focus on hippocampal function, risk for neurodegeneration (apolipoprotein e4), and the role of GABA in modulating neural plasticity.
Focal points of interest
One focus within the project will be on learning and in particular trust learning, in healthy neurotypical and in neurodiverse populations. We have previously studied fear and trust in the amygdala and want to understand how GABA-signaling affects these functions to extend our knowledge on connectivity, serotoninergic, and dopaminergic neuromodulation during learning whom to trust. Increased GABA content in the human VMPFC has been found to correlate with increased trait anxiety (using 3 Tesla MR spectroscopy, MRS), while in rats, decreasing GABA transmission in VMPFC or BLA decreased sociability, which could partly explain social withdrawal observed in conditions such as ASD or SCZ. We want to extend our previous human fMRI studies on the amygdala's function [1], including in social anxiety and trust learning to the domain of GABA-ergic neuromodulation. To this end, we use a. MRS of the human amygdala and VMPFC and relate it to psychometric data in a diverse sample, and b. relate MRS-determined GABA to performance in a repeated trust game, brain activation (fMRI) during that game [2], and computational modeling (Active Inference, HGF), extending on our current work on dopaminergic neuromodulation [2] and ASD.
Another focus is on memory, which critically relies on the hippocampus and GABAergic neurotransmission. In humans, hippocampal GABA is linked to neural plasticity and decreases upon aging and neurodegeneration. In rodents, GABAergic interneurons coordinate hippocampal-neocortical coupling during navigation and consolidation. A clear link between hippocampal GABA and aspects of memory in humans is missing. To address this gap, we propose to a. investigate hippocampal pattern separation, spatial navigation (entorhinal grid-like codes, [3]), and memory consolidation, using MRS, fMRI, and intracranial EEG (iEEG); b. link hippocampal GABA in hippocampus-dependent neurocognition to the risk for neurodegeneration in young, healthy risk carriers (APOE4), and in older individuals.
Technical proficiency and instrumentation
Our lab is equipped with a human 3T MRI scanner (Siemens Skyra), EEG, TMS, and focused ultrasound stimulation. We have a strong background in fMRI data analysis methods, computational modeling, pharmacological manipulations, and behavioral setups - including in non-human animals (predominantly dogs, but also ravens and marmosets, behaviorally). We also have extensive knowledge in the use of (neuro)computational modeling in healthy and disease, and the development of novel experimental and gamified task designs for more precise and robust assessments of neuro-cognitive processes.
Aspirations for the next 5 years
We aim to understand the mechanisms of trust learning, of regaining lost trust, and how stress affects these mechanisms. Prefrontal and subcortical regulation processes, including ones mediated by GABA, are supposedly of key importance, but not well-understood. In the domain of memory research, alterations in GABA signaling can cause much of the symptomatology seen in dementia and cognitive decline. A clear picture of how GABA can be modulated and its impact on neurocognition (hippocampal-neocortical circuits that are altered across the lifespan and in dementia) is key. To this end, we seek translational (rodent to human; human clinical) and methods-based collaborations (7T MRS, iEEG).
References
- Sladky, R., Kargl, D., Haubensak, W., Lamm, C., 2024. An active inference perspective for the amygdala complex. Trends in Cognitive Sciences 28, 223--236.
- Mikus, N., Lamm, C., & Mathys, C. (2024). Computational Phenotyping of Aberrant Belief Updating in Individuals With Schizotypal Traits and Schizophrenia. Biological psychiatry, S0006-3223(24)01554-3. Advance online publication. https://doi.org/10.1016/j.biopsych.2024.08.021
- Wagner, I. C., Graichen, L. P., Todorova, B., Lüttig, A., Omer, D. B., Stangl, M., & Lamm, C. (2023). Entorhinal grid-like codes and time-locked network dynamics track others navigating through space. Nature communications, 14(1), 231. https://doi.org/10.1038/s41467-023-35819-3
