Reversal of learning deficits in a Tsc2+/− mouse model of tuberous sclerosis
By D. Ehninger, Sangyeul Han, Carrie Shilyansky, Weidong Li, D. Kwiatkowski, V. Ramesh, Alcino J. Silva. Nature Medicine, 2008
854 citations recorded by the source corpus.
Subfields: Oncology, Physiology
View Paper: https://www.semanticscholar.org/paper/8487891707f5249572ba1fdfd8fb503e66f57832
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Citations in the corpus
- Disentangling the heterogeneity of autism spectrum disorder through genetic findings (2014, positive): “30,31 Moreover, mice with heterozygous and homozygous loss of TSC1 localized to the cerebellum show abnormal social interaction, as well as repetitive behaviours and vocalizations.”
- The Neurology of mTOR (2014, positive): “which are reversible by a short course of rapamycin administration even in adulthood (Ehninger et al., 2008).”
- Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits (2011, positive): “Recent studies in mouse models are very encouraging in this regard, including Rett syndrome (Guy et al., 2007), fragile X syndrome (Dölen et al., 2007), neurofibromatosis type 1 (Costa et al., 2002), Down’s syndrome (Fernandez et al., 2007), and tuberous sclerosis (Ehninger et al., 2008).”
- The autistic neuron: troubled translation? (2008, background): “Taken together, the association of mutations in FMRP, TSC1/2, and PTEN with autism suggests that defects in translational repression may represent one possible mechanism leading to autistic phenotypes.”
- Mutations causing syndromic autism define an axis of synaptic pathophysiology (2011, background): “Like FXS, (1) TSC is a singlegene disorder with core symptoms of ASD and ID, (2) the affected gene(s) lie in a signaling pathway that couples cell surface receptors to mRNA translation, (3) there are well validated mouse models of the disease, and (4) some mutant phenotypes in these mouse models hav”
- Synaptic dysfunction in neurodevelopmental disorders associated with autism and intellectual disabilities. (2012, background): “One particularly interesting phenotype reported in the Tsc2 +/ − mouse is an enhancement of late-phase LTP (Ehninger et al. 2008a).”
- Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits (2014, neutral): “Tsc2+/ mice however exhibit normal social preference in a three-chamber test (Ehninger et al., 2008; Ehninger et al., 2012) but deficient social interaction in a dyadic reciprocal social test (Sato et al., 2012).”
- Advancing the understanding of autism disease mechanisms through genetics (2016, positive): “Translational inhibition by eukaryotic translation initiation factor (eIF) 4E and eIF4G interaction inhibitor (4EGI-1) and rapamycin have been effective in alleviating behavioral and neuronal phenotypes in models with perturbations in the mTOR pathway 144,183–186 , 240– 242 .”