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Nat Neurosci. 2016 Aug;19(8):995-8. doi: 10.1038/nn.4325. Epub 2016 Jun 13.

Age-related myelin degradation burdens the clearance function of microglia during aging.

Author information

1
Max Planck Institute of Experimental Medicine, Göttingen, Germany.
2
Department of Psychiatry, Ludwig-Maximillian University, Munich, Germany.
3
Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.
4
Department of Psychiatry and Psychotherapy, Freiburg, Germany.
5
Department of Neuroscience, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
6
Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
7
Department of Developmental and Cell Biology, University of California, Irvine, Irvine, California, USA.
8
German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
9
Munich Cluster of Systems Neurology (SyNergy), Munich, Germany.

Abstract

Myelin is synthesized as a multilamellar membrane, but the mechanisms of membrane turnover are unknown. We found that myelin pieces were gradually released from aging myelin sheaths and were subsequently cleared by microglia. Myelin fragmentation increased with age and led to the formation of insoluble, lipofuscin-like lysosomal inclusions in microglia. Thus, age-related myelin fragmentation is substantial, leading to lysosomal storage and contributing to microglial senescence and immune dysfunction in aging.

PMID:
27294511
DOI:
10.1038/nn.4325
[Indexed for MEDLINE]

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