The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Do We Have a Cure for Tuberous Sclerosis Complex?
Open accessAbstract
The recent development of several mouse models for tuberous sclerosis complex (TSC) provides in vivo systems to test new therapies for the neurological manifestations of TSC. Rapamycin is known to antagonize the effects of loss of TSC protein function in vitro and in mouse TSC models, rapamycin can prevent seizures and improve learning task performance. These findings provide new hope for TSC patients suffering from intractable seizures and possibly, for those with autism and cognitive disabilities.
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Epilepsy, which is common in AD and ASD, has enhanced mTORC1 activity.
“Furthermore, epilepsy, which is common in AD and ASD, has enhanced mTORC1 activity (28 -32).”
From Analysis of proteins that rapidly change upon mechanistic/mammalian target of rapamycin complex 1 (mTORC1) repression identifies parkinson protein 7 (PARK7) as a novel protein aberrantly expressed in tuberous sclerosis complex (TSC) (2016) · cites this paper as [32]
The Abstract reports hyperactive mTOR signaling in resected tubers from patients with tuberous sclerosis complex (TSC) and epilepsy, and suggests a possible link to seizures. It does not establish enhanced mTORC1 activity in epilepsy generally or say that epilepsy is common in AD and ASD; its discussion of mTORC1 and mTORC2 does not make that broader claim. (LLM, conf=0.84)
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Cites
The TSC1–TSC2 complex: a molecular switchboard controlling cell growth
Huang, J., & Manning, B. D. (2008) · Biochemical Journal · doi:10.1042/bj20080281 · Cited by 1,237 · cited 1×
“Investigators discovered that loss of TSC1 or TSC2 protein function led to constitutive activation of the mammalian target of rapamycin (mTOR) cascade, a well-recognized and highly evolutionarily conserved signaling pathway known to govern regulation of cell growth (4).”
BackgroundReversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis
Ehninger, D., Han, S., Shilyansky, C., Zhou, Y., Li, W., Kwiatkowski, D. J., Ramesh, V., & Silva, A. J. (2008) · Nature Medicine · doi:10.1038/nm1788 · Cited by 882
Meikle, L., Talos, D. M., Onda, H., Pollizzi, K., Rotenberg, A., Sahin, M., Jensen, F. E., & Kwiatkowski, D. J. (2007) · The Journal of Neuroscience · doi:10.1523/jneurosci.5540-06.2007 · Cited by 462
Activity- and mTOR-dependent suppression of Kv1.1 channel mRNA translation in dendrites
Raab-Graham, K. F., Haddick, P. C. G., Jan, Y. N., & Jan, L. Y. (2006) · Science · doi:10.1126/science.1131693 · Cited by 267
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- 10.1016/j.mrrev.2008.01.001 · DOI
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Niere, F., Namjoshi, S., Song, E., Dilly, G. A., Schoenhard, G., Zemelman, B. V., Mechref, Y., & Raab-Graham, K. F. (2016) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m115.055079 · Cited by 38
Metadata
- Authors
- Crino, P. B.
- Affiliations
- University of Pennsylvania (US)
- Corresponding author
- Crino, Peter B.
- ORCID
- Crino, Peter B.
- Venue
- Epilepsy Currents
- Publisher
- SAGE Publications
- Published
- 2008-10-06
- Volume
- 8
- Issue
- 6
- Pages
- 159-162
- ISSN
- 1535-7511 (ISSN-L)
- 1535-7597
- PMC
- PMC2610234
- OpenAlex
- W1990136008
- Cited by
- 10
- References
- 4
- Citations by year
- 2020: 1 · 2017: 1 · 2016: 1 · 2015: 1
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Epiliepsy currents/Epilepsy currents (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Genetics (clinical) › Tuberous Sclerosis Complex Research
- Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Keywords
- tuberous sclerosis complex, rapamycin, mTOR inhibition, mouse model, seizures, epilepsy, autism spectrum disorder, cognitive disability, learning performance, refractory seizures
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