ReviewNeuromolecular medicine2006
The neurobiology of the tuberous sclerosis complex.
Review in Neuromolecular medicine, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 61 citations in OpenAlex.
- Trial
- Tsc1 deletion in Purkinje neurons disrupts the axon initial segment, impairing excitability and cerebellar function.Neurobiology of disease · 2025Article
- Article
- Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025Article
- The role of TSC1 and TSC2 proteins in neuronal axons.Molecular psychiatry · 2024Review
- Enhancing the Impact of Genomics Research in Autism through Integration of Research Results into Routine Care Pathways-A Case Series.Journal of personalized medicine · 2021Article
- Article
- miR-301a Suppression within Fibroblasts Limits the Progression of Fibrosis through the TSC1/mTOR Pathway.Molecular therapy. Nucleic acids · 2020Article
- Epigenetic Therapeutic Intervention for a Rare Epilepsy Disorder.Epilepsy currents · 2020Article
- Multiple Critical Periods for Rapamycin Treatment to Correct Structural Defects inFrontiers in molecular neuroscience · 2018Article
- PAK2 is an effector of TSC1/2 signaling independent of mTOR and a potential therapeutic target for Tuberous Sclerosis Complex.Scientific reports · 2015Article
- Epileptogenic but MRI-normal perituberal tissue in Tuberous Sclerosis Complex contains tuber-specific abnormalities.Acta neuropathologica communications · 2015Article
- Rates and predictors of seizure freedom in resective epilepsy surgery: an update.Neurosurgical review · 2014Review
- Fetal brain mTOR signaling activation in tuberous sclerosis complex.Cerebral cortex (New York, N.Y. : 1991) · 2014Article
- mTOR signaling in neural stem cells: from basic biology to disease.Cellular and molecular life sciences : CMLS · 2013Review
- Tsc1 mutant neural stem/progenitor cells exhibit migration deficits and give rise to subependymal lesions in the lateral ventricle.Genes & development · 2011Article
- Loss of the tuberous sclerosis complex protein tuberin causes Purkinje cell degeneration.Neurobiology of disease · 2011Article
- Analysis of TSC cortical tubers by deep sequencing of TSC1, TSC2 and KRAS demonstrates that small second-hit mutations in these genes are rare events.Brain pathology (Zurich, Switzerland) · 2010Article
- The neuropathology of autism: defects of neurogenesis and neuronal migration, and dysplastic changes.Acta neuropathologica · 2010Article
- Phosphatidylinositol 3-kinase: the oncoprotein.Current topics in microbiology and immunology · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Tuberous sclerosis complex (TSC) is a multisystem disorder that affects numerous organ systems. Brain lesions that form during development, known as tubers, are highly associated with epilepsy, cognitive disability, and autism. Following the identification of two genes and their encoded proteins, TSC1 (hamartin) and TSC2 (tuberin), responsible for TSC, identification of several downstream protein cascades that might be affected in TSC have been discovered. Of primary importance is the mammalian target of rapamycin pathway that controls cell growth and protein synthesis. The mechanisms governing brain lesion growth have not been fully identified but likely altered regulation of the mammalian target of rapamycin cascade by hamartin and tuberin during development leads to aberrant cell growth. Secondary effects of TSC gene mutations might disrupt normal neuronal migration and cerebral cortical lamination. Numerous studies have identified changes in gene and protein expression in animal models of TSC and in human TSC brain specimens that contribute to altered brain cytoarchitecture. This review will provide an overview of the neurobiological aspects of TSC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.