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Max-Planck-Institut für Experimentelle Medizin
Research Overview

Research Overview

The myelin sheath is one of the most abundant membrane structures in the vertebrate nervous system. It is produced by two types of specialized glial cells, oligodendrocytes in the central nervous system, and Schwann-cells in the peripheral nervous system. The myelin sheath is formed by the spiral wrapping of glial plasma membrane extensions around the axons, followed by the extrusion of cytoplasm and the compaction of the stacked membrane bilayers.
These tightly packed membrane stacks provide electrical insulation around the axons and maximize their conduction velocity. Axonal insulation by myelin not only facilitates rapid nerve conduction but also regulates axonal transport and protects against axonal degeneration.
Damage to the myelin sheath, as it for example occurs in multiple sclerosis (MS) results therefore in severe neurological disability also as a result of neurodegeneration.
One of our main goals is to come up with new approaches of how to prevent damage and to promote repair in demyelinating diseases such as MS. To realize this goal we need to understand how myelin is formed during normal development.
How oligodendrocytes wrap their plasma membrane around an axon to form myelin with its many layers of a tightly stacked membrane is a so far unresolved question. Our aim is to elucidate the cellular machinery that is required for the formation of myelin. Myelin membrane biogenesis is under extensive control by signal transduction cascades. We are therefore also interested to identify the influence of cell-cell communication on myelin biogenesis. These studies aim to understand the complex interplay between neurons and glia in order to gain insights into mechanisms of myelin formation during the development of the central nervous system.
Myelination has been thought to occur relatively stereotypically according to a predefined genetic program strictly as a developmental process. However, it now appears that myelin biogenesis contributes to brain plasticity being modifiable by experience and various environmental factors. Furthermore, myelin is not limited to early development, but occurs throughout adulthood. In order to integrate the concept of myelin plasticity into the fine tuning of neuronal networks, we have to understand how oligodendrocytes form myelin, how they select axons for myelination and how they regulate myelin growth.
How do oligodendrocytes recognize the axons that need to be myelinated? Which molecules are involved?
Despite of its exceptional stability, myelin disorders are among the most prevalent and disabling diseases in young adults, the most important one being MS. A common structural feature of myelin in demyelinating diseases is the fragmentation of the membrane stacks.
Another important aim is to understand how myelin looses its stability in diseases.
Why is myelin the most common target of autoimmune diseases in the nervous system? We are studying the question how myelin becomes prone to autoimmune attacks.
Once damaged, myelin is recognized and phagocytosed by resident microglia or infiltrating macrophages. Another line of research is to understand the role of microglia/marcophages in myelin membrane clearance. 
In summary, our approach and questions are interdisciplinary aiming at integrating cell biology into neuroscience of normal brain development and demyelinating diseases. Our hope is not only to shed light on the mechanisms of myelin biogenesis, disassembly and clearance, also to open the door to new therapeutic avenues in white matter tissue repair.

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