ArticleNeurobiology of disease2014
Rapamycin improves peripheral nerve myelination while it fails to benefit neuromuscular performance in neuropathic mice.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Peripheral Myelin Protein-22 and Its Prominence in Charcot-Marie-Tooth Disease.Chemical reviews · 2026Review
- Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Quantitative proteomics unveils known and previously unrecognized alterations in neuropathic nerves.Journal of neurochemistry · 2024Article
- A translatable RNAi-driven gene therapy silences PMP22/Pmp22 genes and improves neuropathy in CMT1A mice.The Journal of clinical investigation · 2022Article
- Evaluating the beneficial effects of dietary restrictions: A framework for precision nutrigeroscience.Cell metabolism · 2021Review
- Article
- Wrestling and Wrapping: A Perspective on SUMO Proteins in Schwann Cells.Biomolecules · 2021Review
- Emerging Therapies for Charcot-Marie-Tooth Inherited Neuropathies.International journal of molecular sciences · 2021Review
- Phagocytosis by Peripheral Glia: Importance for Nervous System Functions and Implications in Injury and Disease.Frontiers in cell and developmental biology · 2021Review
- Held Up in Traffic-Defects in the Trafficking Machinery in Charcot-Marie-Tooth Disease.Frontiers in molecular neuroscience · 2021Review
- Direct relationship between increased expression and mistrafficking of the Charcot-Marie-Tooth-associated protein PMP22.The Journal of biological chemistry · 2020Article
- HSP90 Inhibitor, NVP-AUY922, Improves Myelination in Vitro and Supports the Maintenance of Myelinated Axons in Neuropathic Mice.ACS chemical neuroscience · 2019Article
- siRNA Blocking of Mammalian Target of Rapamycin (mTOR) Attenuates Pathology in Annonacin-Induced Tauopathy in Mice.Neurotoxicity research · 2019Article
- mTORC1 Is Transiently Reactivated in Injured Nerves to Promote c-Jun Elevation and Schwann Cell Dedifferentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Myelination and mTOR.Glia · 2018Review
- Dual mTORC1/mTORC2 blocker as a possible therapy for tauopathy in cellular model.Metabolic brain disease · 2018Article
- mTORC1 Activation by Loss ofFrontiers in cellular neuroscience · 2018Article
- Dual function of the PI3K-Akt-mTORC1 axis in myelination of the peripheral nervous system.eLife · 2017Article
- Promoting peripheral myelin repair.Experimental neurology · 2016Review
- AUTEN-67, an autophagy-enhancing drug candidate with potent antiaging and neuroprotective effects.Autophagy · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Charcot--Marie-Tooth disease type 1A (CMT1A) is a hereditary peripheral neuropathy characterized by progressive demyelination and distal muscle weakness. Abnormal expression of peripheral myelin protein 22 (PMP22) has been linked to CMT1A and is modeled by Trembler J (TrJ) mice, which carry the same leucine to proline substitution in PMP22 as affected pedigrees. Pharmacologic modulation of autophagy by rapamycin in neuron-Schwann cell explant cultures from neuropathic mice reduced PMP22 aggregate formation and improved myelination. Here we asked whether rapamycin administration by food supplementation, or intraperitoneal injection, could alleviate the neuropathic phenotype of affected mice and improve neuromuscular performance. Cohorts of male and female wild type (Wt) and TrJ mice were assigned to placebo or rapamycin treatment starting at 2 or 4months of age and tested monthly on the rotarod. While neither long-term feeding (8 or 10months) on rapamycin-enriched diet, or short-term injection (2months) of rapamycin improved locomotor performance of the neuropathic mice, both regimen benefited peripheral nerve myelination. Together, these results indicate that while treatment with rapamycin benefits the myelination capacity of neuropathic Schwann cells, this intervention does not improve neuromuscular function. The observed outcome might be the result of the differential response of nerve and skeletal muscle tissue to rapamycin.
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Registered trials
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