The Axon-Myelin Unit in Development and Degenerative Disease

Stassart, Ruth M.; Möbius, Wiebke; Nave, Klaus‐Armin; Edgar, Julia M.

doi:10.3389/fnins.2018.00467

Cited by 178 publications

(162 citation statements)

References 236 publications

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“…The nature of these observed vesicles and the structures where they occur still needs further investigation. It is clear though, that the morphology of axon‐myelin interactions changes in demyelinating diseases .…”

Section: Discussionmentioning

confidence: 99%

Structural adaption of axons during de‐ and remyelination in the Cuprizone mouse model

2019

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Multiple Sclerosis is an autoimmune disorder causing neurodegeneration mostly in young adults. Thereby, myelin is lost in the inflammatory lesions leaving unmyelinated axons at a high risk to degenerate. Oligodendrocyte precursor cells maintain their regenerative capacity into adulthood and are able to remyelinate axons if they are properly activated and differentiate. Neuronal activity influences the success of myelination indicating a close interplay between neurons and oligodendroglia. The myelination profile determines the distribution of voltage-gated ion channels along the axon. Here, we analyze the distribution of the sodium channel subunit Nav1.6 and the ultrastructure of axons after cuprizone-induced demyelination in transgenic mice expressing GFP in oligodendroglial cells. Using this mouse model, we found an increased number of GFP-expressing oligodendroglial cells compared to untreated mice. Analyzing the axons, we found an increase in the number of nodes of Ranvier in mice that had received cuprizone. Furthermore, we found an enhanced portion of unmyelinated axons showing vesicles in the cytoplasm. These vesicles were labeled with VGlut1, indicating that they are involved in axonal signaling. Our results highlight the flexibility of axons towards changes in the glial compartment and depict the structural changes they undergo upon myelin removal. These findings might be considered if searching for new neuroprotective therapies that aim at blocking neuronal activity in order to avoid interfering with the process of remyelination. Pfeiffer et al Axonal Changes Induced by Myelin Remodeling Brain Pathology 29 (2019) 675-692

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Section: Discussionmentioning

confidence: 99%

Structural adaption of axons during de‐ and remyelination in the Cuprizone mouse model

2019

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“…In the PNS, peripheral neuropathies affect Schwann cell compact myelin. These include Charcot-Marie-Tooth disease (CMT) and its more severe, rapidly progressive form known as Dejerine-Sottas syndrome (DSS), which cause incurable chronic disability (Hartline 2008; Stassart et al 2018). CMT and DSS manifest through both dominant and recessive inheritance, and they harbour a strong genetic component, typically caused by mutations in proteins relevant for the formation and stability of PNS myelin, while axonal forms also exist.…”

Section: Introductionmentioning

confidence: 99%

Neuropathy-related mutations alter the membrane binding properties of the human myelin protein P0 cytoplasmic tail

Raasakka

Ruskamo

Barker

et al. 2019

Preprint

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“…The axon and the surrounding myelin sheath have a very close relationship, morphologically and functionally [11,24]. This is e.g.…”

Section: Introductionmentioning

confidence: 99%

Axonal mitochondria across species adjust in diameter depending on thickness of surrounding myelin

Ineichen

Zhu

Carlström

2019

Preprint

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In the central nervous system (CNS), axons and its surrounding myelin sheaths, generated by oligodendrocytes, greatly depend on each other, where oligodendrocytes provide axons with both trophic and metabolic support. Across spices, assessment of the axon-myelin ultrastructure is the key-approach to visualize de-and re-myelination of axons. However, this assessment omits to provide information on axonal homeostasis or how axon-myelin influence one another. Since mitochondria may adjust in size thus mirroring the intracellular physiological and metabolic status we applied this to myelinated axons in the CNS. We herein show that a large axonal mitochondria diameter correlates with thinner surrounding myelin sheaths across different CNS tracts and species, including human. We also show that the relation between axonal mitochondria diameter and surrounding myelin thickness is a valuable measurement to verify advanced remyelination in two commonly used experimental demyelinating models, namely the cuprizone and the lysolecithin (LPC) model. Lastly, we show that axonal mitochondria adjust in diameter in response to the thickness of the axonal surrounding myelin whereas the opposite adaption was absent. In summary, the link between axonal mitochondria diameter and surrounding myelin thickness provide insight on the axon-myelin relation both during homeostasis and pathological conditions. This link is also translational applicable and can thus contribute to a better understanding on how to study remyelination using experimental models.

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The Axon-Myelin Unit in Development and Degenerative Disease

Cited by 178 publications

References 236 publications

Structural adaption of axons during de‐ and remyelination in the Cuprizone mouse model

Structural adaption of axons during de‐ and remyelination in the Cuprizone mouse model

Neuropathy-related mutations alter the membrane binding properties of the human myelin protein P0 cytoplasmic tail

Axonal mitochondria across species adjust in diameter depending on thickness of surrounding myelin

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