Protein may offer
key to remyelination
key to remyelination
Kick-starting a process
that might repair the damage done in multiple sclerosis could start with
disabling a process that blocks myelin regeneration, according to Baylor
College of Medicine researchers.
that might repair the damage done in multiple sclerosis could start with
disabling a process that blocks myelin regeneration, according to Baylor
College of Medicine researchers.
Daam2 and another protein,
PIP5K, comprise a pathway regulating Wnt signaling and myelination. Wnt
signaling plays an essential role in developmental and regenerative myelination
of the central nervous system. Wnt signaling pathways are present at high
levels in precursors of myelin-making oligodendrocyte, and Wnt blocks the
ability of cells to differentiate. Cells that differentiate are mature and can
carry out their prescribed function.
PIP5K, comprise a pathway regulating Wnt signaling and myelination. Wnt
signaling plays an essential role in developmental and regenerative myelination
of the central nervous system. Wnt signaling pathways are present at high
levels in precursors of myelin-making oligodendrocyte, and Wnt blocks the
ability of cells to differentiate. Cells that differentiate are mature and can
carry out their prescribed function.
Daam2 promotes Wnt
signaling and receptor complex formation through PIP5K-PIP2. Analysis of Daam2
function in oligodendrocytes revealed that it suppresses oligodendrocyte
differentiation during development, after white matter injury, and is expressed
in human white matter lesions.
signaling and receptor complex formation through PIP5K-PIP2. Analysis of Daam2
function in oligodendrocytes revealed that it suppresses oligodendrocyte
differentiation during development, after white matter injury, and is expressed
in human white matter lesions.
Results of mouse model
studies sometimes do not translate to humans and may be years away from being a
marketable treatment. The authors note that the results suggest drugs that
inhibit Daam2-PIP5K function may stimulate remyelination after white matter
injury.
studies sometimes do not translate to humans and may be years away from being a
marketable treatment. The authors note that the results suggest drugs that
inhibit Daam2-PIP5K function may stimulate remyelination after white matter
injury.
The report appears in the
journal Neuron.
journal Neuron.
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