Why does remyelination fail in multiple sclerosis?

By Robin J. M. Franklin. Nature Reviews Neuroscience, 2002

871 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/8333ace23fdec4aa4a87e5261bbad7d4e0ae1355

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Developmental Neuroscience

In Molecular Biology

In Pathology and Forensic Medicine

Citations in the corpus

Remyelination is extensive in a subset of multiple sclerosis patients. (2006, background): “It is unresolved as to why in some patients remyelination is widespread whilst in others it is sparse (Franklin, 2002).”
Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation (2005, background): “Although multiple factors probably cooperate to cause remyelination failur”
Myelin Impairs CNS Remyelination by Inhibiting Oligodendrocyte Precursor Cell Differentiation (2006, background): “The adult CNS contains a precursor cell population that responds to demyelination by undergoing rapid proliferation, migration, and differentiation into new oligodendrocytes (Horner et al., 2000; Franklin, 2002).”
Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion (2004, result): “The same time course has been observed in experimental demyelination and is in keeping with other evidence that macrophages provide trophic factors that drive remyelination.(36,37) Within a week or two, numerous differentiated oligodendrocytes (somewhat smaller cells strongly reactive for CNP) appea”
Injection of adult neurospheres induces recovery in a chronic model of multiple sclerosis (2003, background): “The problems posed by the chronic and inflammatory nature of the disease—through the formation of glia scars and by the depletion of the local pool(s) of oligodendrocyte progenitors that should re-ensheath demyelinated axon”
Translocator protein (18 kDa) (TSPO) as a therapeutic target for neurological and psychiatric disorders (2010, background): “and contribute to an environment that supports neuronal viability and regeneration, and myelin sheath formatio”
Remyelination in the CNS: from biology to therapy (2008, background): “The subsequent population of demyelinated areas by OPCs is referred to as the recruitment phase of remyelination; it involves OPC migration in addition to the ongoing proliferatio”
Polydendrocytes (NG2 cells): multifunctional cells with lineage plasticity (2009, background): “Many studies have attempted to identify the signals that promote or inhibit polydendrocyte differentiation in vitro and in vivo”
BRAIN REGENERATION IN PHYSIOLOGY AND PATHOLOGY: THE IMMUNE SIGNATURE DRIVING THERAPEUTIC PLASTICITY OF NEURAL STEM CELLS (2011, background): “, oligodendrocytes), and the complete reconstruction of the original anatomical organization is not necessarily required to obtain functional recovery (76, 77).”