The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome
Open accessAbstract
The functional relevance of brain-derived neurotrophic factor (BDNF) is beginning to be well appreciated not only in mice, but also in humans. Because reduced levels typically correlate with impaired neuronal function, increasing BDNF levels with well-tolerated drugs diffusing into the central nervous system may help in ameliorating functional deficits. With this objective in mind, we used the sphingosine-1 phosphate receptor agonist fingolimod, a drug that crosses the blood–brain barrier. In addition, fingolimod has recently been introduced as the first oral treatment for multiple sclerosis. In cultured neurons, fingolimod increases BDNF levels and counteracts NMDA-induced neuronal death in a BDNF-dependent manner. Ongoing synaptic activity and MAPK signaling is required for fingolimod-induced BDNF increase, a pathway that can also be activated in vivo by systemic fingolimod administration. Mice lacking Mecp2, a gene frequently mutated in Rett syndrome, show decreased levels of BDNF, and fingolimod administration was found to partially rescue these levels as well as the size of the striatum, a volumetric sensor of BDNF signaling in rodents. These changes correlate with increased locomotor activity of the Mecp2 -deficient animals, suggesting that fingolimod may improve the functional output of the nervous system, in addition to its well-documented effects on lymphocyte egress from lymph nodes.
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Cites
Rett syndrome is caused by mutations in X-linked MECP2, encoding methyl-CpG-binding protein 2
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Dysfunction in GABA signalling mediates autism-like stereotypies and Rett syndrome phenotypes
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“In the absence of lesion, the Bdnf gene is primarily expressed in neurons, and its transcription is activated by excitatory input in a cAMP- and calcium-response element-binding protein (CREB)dependent fashion (8, 9).”
BackgroundThe disease progression of Mecp2 mutant mice is affected by the level of BDNF expression
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Differentiation of mouse embryonic stem cells into a defined neuronal lineage
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Cited by
Advancing the understanding of autism disease mechanisms through genetics
de la Torre-Ubieta, L., Won, H., Stein, J. L., & Geschwind, D. H. (2016) · Nature Medicine · doi:10.1038/nm.4071 · Cited by 827
An update on the biology of sphingosine 1-phosphate receptors
Blaho, V. A., & Hla, T. (2014) · Journal of Lipid Research · doi:10.1194/jlr.r046300 · Cited by 516
Neuronal plasticity and neurotrophic factors in drug responses
Castrén, E., & Antila, H. (2017) · Molecular Psychiatry · doi:10.1038/mp.2017.61 · Cited by 284
Progress toward treatments for synaptic defects in autism
Delorme, R., Ey, E., Toro, R., Leboyer, M., Gillberg, C., & Bourgeron, T. (2013) · Nature Medicine · doi:10.1038/nm.3193 · Cited by 218
MECP2 disorders: from the clinic to mice and back
Lombardi, L. M., Baker, S. A., & Zoghbi, H. Y. (2015) · Journal of Clinical Investigation · doi:10.1172/jci78167 · Cited by 221
Metadata
- Authors
- Deogracias, R., Yazdani, M., Dekkers, M. P. J., Guy, J., Ionescu, M. C. S., Vogt, K. E., & Barde, Y.-A.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2012-08-13
- Volume
- 109
- Issue
- 35
- Pages
- 14230-14235
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2076073786
- Cited by
- 256
- References
- 10
- FWCI
- 14.53
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome. https://app.cochat.ai/papers/10.1073/pnas.1206093109
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- Deogracias, R., Yazdani, M., Dekkers, M. P. J., Guy, J., Ionescu, M. C. S., Vogt, K. E., & Barde, Y.-A. (2012). Fingolimod, a sphingosine-1 phosphate receptor modulator, increases BDNF levels and improves symptoms of a mouse model of Rett syndrome. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1206093109
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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