COGEMS Study: Neural mechanisms of cognitive and emotional processes in MS and their relevance for disease severity
Multiple Sclerosis (MS) is an autoimmune disease of the central nervous system leading to demyelination, axonal damage and neurodegeneration and thus to impairment of motor and sensory skills. In addition to these key somatic symptoms, MS is also linked to dysregulated functioning of cognitive and emotional processes and these factors interact with key somatic symptoms. For example, MS is associated with depression on a phenomenological level, MS patients are characterized by reduced levels of the depression-related neurotransmitters, and several studies have shown that psychotherapy for depression treatment can improve immunological factors and clinical disability in addition to depression in MS patients.
Despite this interaction, however, biological emotional mechanisms in MS have not yet been investigated sufficiently in terms of neural responses to emotional stimuli although this would be important for several reasons.
First, the impact of emotional stimuli might critically rely on the cognitive coping with these stimuli which are closely reflected by immediate brain responses to such stimuli. Second, dysregulated neural responses to depression-related affective stimuli are key mechanisms of depression in patients not suffering from MS that reflect increased emotional reactivity and deficits in engaging regulatory processes and are closely related to severity of depression.
Consequently, we conduct the research project COGEMS that aims to investigate the neural processes related to emotional and cognitive processes in MS and the link of these factors to clinical disability. For this purpose, we will examine depressed and non-depressed relapsing-remitting MS patients and healthy controls in two functional MRI experiments.
Using this approach, we hope to improve our understanding of the neural mechanisms of emotional and cognitive factors in MS, their role for disease severity, and thus finally to reveal novel neurobiological targets for MS treatment.
Prof. Dr. Friedemann Paul (AG Klinische Neuroimmunologie, NCRC),
Dr. habil. rer. nat. Martin Weygandt (AG Klinische Neuroimmunologie, NCRC),
Prof. Dr. rer. nat. John-Dylan Haynes (Bernstein Center for Computational Neuroscience Berlin/ Klinik für Neurologie),
Prof. Dr. phil. Stefan M. Gold (Klinik für Psychiatrie und Psychotherapie CBF - Forschung Klinische Psychiatrie)
Weygandt, M., L. Meyer-Arndt, J. R. Behrens, K. Wakonig, J. Bellmann-Strobl, K. Ritter, M. Scheel, A. U. Brandt, C. Labadie, S. Hetzer, S. M. Gold, F. Paul, and J. D. Haynes. "Stress-Induced Brain Activity, Brain Atrophy, and Clinical Disability in Multiple Sclerosis." Proc Natl Acad Sci U S A 113, no. 47 (Nov 22 2016): 13444-49. https://dx.doi.org/10.1073/pnas.1605829113.