Abstract
Recent work has demonstrated that axonal regeneration in the central nervous system is limited by myelin-derived Nogo binding to an axonal Nogo Receptor. The Nogo system appears to have a physiologic role in regulating structural plasticity. The possibility that the Nogo system contributes to pathologic and compensatory plasticity in Alzheimer's Disease is considered.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Alzheimer Disease / metabolism
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Alzheimer Disease / pathology
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Animals
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Axons / metabolism
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Axons / pathology*
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GPI-Linked Proteins
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Growth Inhibitors / metabolism*
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Myelin Proteins / metabolism*
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Myelin Sheath / pathology
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Nerve Regeneration*
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Neurodegenerative Diseases / metabolism*
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Neurodegenerative Diseases / pathology*
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Neuronal Plasticity
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Nogo Proteins
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Nogo Receptor 1
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Receptors, Cell Surface / metabolism
Substances
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GPI-Linked Proteins
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Growth Inhibitors
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Myelin Proteins
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Nogo Proteins
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Nogo Receptor 1
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Receptors, Cell Surface
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Rtn4 protein, mouse
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Rtn4r protein, mouse