Myelin plasticity in adulthood and aging

Chapman, Timothy W.; Hill, Robert A.

doi:10.1016/j.neulet.2019.134645

Cited by 50 publications

(34 citation statements)

References 116 publications

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“…Functional deficits due to myelin damage are dependent on the degree of myelin loss and the extent to which repair occurs, with late stages of disease often coinciding with failed myelin repair. The cellular mechanisms that allow for the continued refinement and dynamic myelin plasticity, observed in adulthood [6][7][8] , are thought to be co-opted for myelin repair in these degenerative conditions. Yet, it is not fully known how these cycles of degeneration and repair occur at the cellular level in vivo.…”

Section: Introductionmentioning

confidence: 99%

Age and axon-specific forms of cortical remyelination by divergent populations of NG2-glia

Chapman

Olveda

Pereira

et al. 2020

Preprint

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Myelin is critical for neural circuit function and its destruction is widespread in neurodegenerative disease and aging. In these conditions, homeostatic repair mechanisms initiate oligodendrocyte replacement by resident progenitor cells called NG2-glia. To investigate the cellular dynamics of this repair we developed a novel demyelination model by combining intravital myelin imaging with a targeted single-cell ablation technique called 2Phatal. Oligodendrocyte 2Phatal activated a stereotyped degeneration cascade which triggered remyelination by local NG2-glia. Remyelination efficiency was dependent on initial myelin patterning and dynamic imaging revealed rapid repair mechanisms resulting in near-seamless transitions between myelin loss and repair. A subset of morphologically complex NG2-glia executed this remyelination, pointing towards unrecognized functional diversity within this population. Age-related demyelination mirrored the degenerative cascade observed with 2Phatal, while remyelination in aging was defective due to failed oligodendrogenesis. Thus, oligodendrocyte 2Phatal revealed cellular diversity within the oligodendrocyte lineage and uncovered novel forms of rapid remyelination.

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Section: Introductionmentioning

confidence: 99%

Age and axon-specific forms of cortical remyelination by divergent populations of NG2-glia

Chapman

Olveda

Pereira

et al. 2020

Preprint

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“…In white matter, on axon size and myelination have been proposed to cause restriction in this diffu-sion [15]. Myelination and oligodendrogenesis play well understood roles in sensory-motor learning, and oligodendrogenesis (and therefore myelination) was recently revealed to be an important contributor to spatial memory consolidation [28,[60][61][62][63] (for more in-depth reviews, please see [64,65]). Some studies indicating that learning elevates hippocampal FA also noted effects on MBP, a main component of the myelin sheath, and GAP-43, a marker for axon remodeling [19,46].…”

Section: Discussionmentioning

confidence: 99%

Diffusion tensor-MRI detects exercise-induced neuroplasticity in the hippocampal microstructure in mice

Islam

Luo

Valaris

et al. 2020

BPL

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Background: Despite considerable research on exercise-induced neuroplasticity in the brain, a major ongoing challenge in translating findings from animal studies to humans is that clinical and preclinical settings employ very different techniques. Objective: Here we aim to bridge this divide by using diffusion tensor imaging MRI (DTI), an advanced imaging technique commonly applied in human studies, in a longitudinal exercise study with mice. Methods: Wild-type mice were exercised using voluntary free-wheel running, and MRI scans were at baseline and after four weeks and nine weeks of running. Results: Both hippocampal volume and fractional anisotropy, a surrogate for microstructural directionality, significantly increased with exercise. In addition, exercise levels correlated with effect size. Histological analysis showed more PDGFRα+ oligodendrocyte precursor cells in the corpus callosum of running mice. Conclusions: These results provide compelling in vivo support for the concept that similar adaptive changes occur in the brains of mice and humans in response to exercise.

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“…In fact, ADAMTS-4 is expressed in wild-type animals in oligodendrocytes, which are the cells responsible for myelination in the CNS [121]. Therefore, the participation of ADAMTS-4 in axonal growth either in vivo or in vitro may depend in part on its contribution to myelination processes under normal conditions and thus the regulation of motor capacities in adult mice [122].…”

Section: Adamts Functions In Normal and Pathological Cnsmentioning

confidence: 99%

New Insights into ADAMTS Metalloproteases in the Central Nervous System

et al. 2020

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Components of the extracellular matrix (ECM) are key players in regulating cellular functions throughout the whole organism. In fact, ECM components not only participate in tissue organization but also contribute to processes such as cellular maintenance, proliferation, and migration, as well as to support for various signaling pathways. In the central nervous system (CNS), proteoglycans of the lectican family, such as versican, aggrecan, brevican, and neurocan, are important constituents of the ECM. In recent years, members of this family have been found to be involved in the maintenance of CNS homeostasis and to participate directly in processes such as the organization of perineural nets, the regulation of brain plasticity, CNS development, brain injury repair, axonal guidance, and even the altering of synaptic responses. ADAMTSs are a family of “A disintegrin and metalloproteinase with thrombospondin motifs” proteins that have been found to be involved in a multitude of processes through the degradation of lecticans and other proteoglycans. Recently, alterations in ADAMTS expression and activity have been found to be involved in neuronal disorders such as stroke, neurodegeneration, schizophrenia, and even Alzheimer’s disease, which in turn may suggest their potential use as therapeutic targets. Herein, we summarize the different roles of ADAMTSs in regulating CNS events through interactions and the degradation of ECM components (more specifically, the lectican family of proteoglycans).

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Myelin plasticity in adulthood and aging

Cited by 50 publications

References 116 publications

Age and axon-specific forms of cortical remyelination by divergent populations of NG2-glia

Age and axon-specific forms of cortical remyelination by divergent populations of NG2-glia

Diffusion tensor-MRI detects exercise-induced neuroplasticity in the hippocampal microstructure in mice

New Insights into ADAMTS Metalloproteases in the Central Nervous System

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