Demyelinating polyneuropathies are characterized by a primary defect of Schwann cells which leads to a slowly progressive demyelination and a secondary axonal loss that underlies clinical impairment. Unfortunately, no causal therapy is available for the vast majority of demyelinating neuropathies, as the pathological mechanisms remain poorly understood.
In previous studies we observed that individual Schwann cells display very different morphological and molecular characteristics in mouse models for demyelinating polyneuropathies. Indeed, in demyelinating polyneuropathies, myelin disassembly is not a concerted process of all Schwann cells, but occurs rather focally in individual cells. This fascinating observation has been described more than 60 years ago and is referred to as segmental demyelination that explains the slowly progressive nature of the disease. Why do individual Schwann cells disintegrate whereas others aligned with the very same nerve fiber remain intact?
To answer this question we chose to combine new molecular and imaging techniques to (1) isolate and characterize specific Schwann cell populations that are prone to degeneration in mouse models for demyelinating polyneuropathies. The goal is to unravel the initial mechanisms of disease manifestation that are responsible for the subsequent process of demyelination. Vice versa, we are aiming at a better understanding of the repair mechanisms in peripheral nerves, given the fact that Schwann cells are in principle able to remyelinate demyelinated segments. However, Schwann cells lose their ability to reconstitute the original myelin sheath length during remyelination and consequently nerve function is only partially restored. By applying surgical and genetic techniques, we are (2) investigating the mechanisms of longitudinal myelin growth and the reassembly of myelin sheath segments in chronic nerve disorders. Here, both, longitudinal and radial myelin growth require an enormous metabolic effort, especially with regard to lipids, which constitute about 70% of the myelin sheath. Next to the Schwann cell intrinsic biosynthesis of lipids, circulating lipids appear to play an important role for Schwann cell function and systemic dyslipidemia has been suggested to play a central role in the pathomechanism of diabetic polyneuropathy. How do Schwann cells integrate lipid-associated signals? To address this question we (3) characterize mouse models for peripheral neuropathies with altered systemic lipid homeostasis. In addition, we are genetically manipulating regulatory pathways in Schwann cells that are linked to lipid metabolism.
With the intended approaches it is not only our goal to gain insight into the profound disease- and repair mechanisms of demyelinating neuropathies, but also to substantially contribute to the development of new therapeutic strategies for this life-burdening diseases.
Hinter Mind steht eine Gruppe Yoga-Begeisterter, die ihr Hobby zunächst professionell gelernt und dann zum Beruf gemacht hat. Hier stellen wir uns dir vor.
Karin Meyer
Gründerin
Ich habe Yoga während meines Studiums kennengelernt. Für mich ist Yoga seit dem ein echter Glücklichmacher, der mein Leben wunderbar ergänzt und bereichert. So kam irgendwann der Wunsch, anderen dieses tolle Hobby weiterzugeben und davon profitieren zu lassen.
Steve Jans
Gründer
Dass Yoga etwas für Esoteriker ist, ist ein reines Klischee. Für mich ist es vielmehr ein Alltagsbegleiter. Mit Mind habe ich mir einen Traum erfüllt, der schon sehr lange in mir gewachsen ist. Ich freue mich, meine Begeisterung für Yoga nun mit anderen zu teilen!
Miriam Lose
Gründerin
Im Einklang mit sich zu leben bedeutet für mich eine bewusste Ernährung, genügend Erholung – und Ausgeglichenheit durch meine tägliche Portion Yoga. Diese Erfahrung kann ich bei Mind weitergeben und mache dies mit echter Leidenschaft. Ich freue mich auf deinen Besuch bei uns.