Abstract
Cognitive decline remains an unaddressed problem for the elderly. We show that myelination is highly active in young mice and greatly inhibited in aged mice, coinciding with spatial memory deficits. Inhibiting myelination by deletion of Olig2 in oligodendrocyte precursor cells impairs spatial memory in young mice, while enhancing myelination by deleting the muscarinic acetylcholine receptor 1 in oligodendrocyte precursor cells, or promoting oligodendroglial differentiation and myelination via clemastine treatment, rescues spatial memory decline during aging.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / genetics
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Aging / pathology*
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Animals
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Demyelinating Diseases / complications
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Demyelinating Diseases / genetics
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Demyelinating Diseases / metabolism
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Demyelinating Diseases / pathology*
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Memory Disorders / etiology
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Memory Disorders / genetics
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Memory Disorders / metabolism
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Memory Disorders / pathology*
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Mice
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Mice, Transgenic
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Myelin Basic Protein / genetics
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Myelin Basic Protein / metabolism
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Myelin Sheath / metabolism
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Myelin Sheath / pathology*
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Oligodendrocyte Precursor Cells / metabolism
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Oligodendrocyte Precursor Cells / pathology
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Oligodendrocyte Transcription Factor 2 / genetics
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Oligodendrocyte Transcription Factor 2 / metabolism
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Oligodendroglia / metabolism
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Oligodendroglia / pathology
Substances
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Myelin Basic Protein
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Oligodendrocyte Transcription Factor 2