Myelination and mTOR
Open accessAbstract
Myelinating cells surround axons to accelerate the propagation of action potentials, to support axonal health, and to refine neural circuits. Myelination is metabolically demanding and, consistent with this notion, mTORC1—a signaling hub coordinating cell metabolism—has been implicated as a key signal for myelination. Here, we will discuss metabolic aspects of myelination, illustrate the main metabolic processes regulated by mTORC1, and review advances on the role of mTORC1 in myelination of the central nervous system and the peripheral nervous system. Recent progress has revealed a complex role of mTORC1 in myelinating cells that includes, besides positive regulation of myelin growth, additional critical functions in the stages preceding active myelination. Based on the available evidence, we will also highlight potential nonoverlapping roles between mTORC1 and its known main upstream pathways PI3K‐Akt, Mek‐Erk1/2, and AMPK in myelinating cells. Finally, we will discuss signals that are already known or hypothesized to be responsible for the regulation of mTORC1 activity in myelinating cells.
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The PI3K/AKT/mTOR signaling pathway broadly promotes brain growth and development of the myelin sheath.
“The PI3K/ AKT/mTOR signaling pathway broadly promotes brain growth and development of the myelin sheath [32–35].”
From Neandertal Introgression Sheds Light on Modern Human Endocranial Globularity (2019) · cites this paper as [35]
The Abstract and “Not all roads may lead to mTORC1” section describe positive roles for this signaling in myelin growth, including increased myelination with Akt activation. The paper does not establish that the pathway broadly promotes brain growth, and “Navigating upstream” reports that neuronal mTORC1 hyperactivation can instead cause hypomyelination. Page numbers are unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredOligodendrocyte autophagy, OPC differentiation, and myelination during development are all regulated by MTOR.
“In addition, oligodendrocyte autophagy, OPC differentiation, and myelination during development are all regulated by MTOR [445–447].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [446]
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- Authors
- Figlia, G., Gerber, D., & Suter, U.
- Affiliations
- ETH Zurich (CH)
- Corresponding author
- Suter, Ueli
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2017-12-06
- Volume
- 66
- Issue
- 4
- Pages
- 693-707
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- PMC
- PMC5836902
- OpenAlex
- W2772611711
- Cited by
- 165
- References
- 155
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 15 · 2023: 23 · 2022: 18 · 2021: 21 · 2020: 26 · 2019: 15 · 2018: 13
- FWCI
- 2.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Glia (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Repository for Publications and Research Data (ETH Zurich) (submittedVersion, cc-by)
- ETH Zürich Research Collection (cc-by)
- Funders
- Swiss National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- myelination, mTORC1, myelinating cells, glial metabolism, cellular metabolism, central nervous system myelination, peripheral nervous system myelination, PI3K/Akt signaling, MEK/ERK signaling, AMPK signaling
- MeSH terms
- Animals, Humans, Myelin Sheath, TOR Serine-Threonine Kinases
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