2019
DOI: 10.1016/j.neuron.2019.11.026
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Therapeutic Targeting of mTORC2 in mTORopathies

Abstract: Dysregulated mTOR contributes to neurodevelopmental dysfunction. A new study (Chen et al., 2019) demonstrates that suppression of mTORC2, not mTORC1, ameliorates survival, seizures, and abnormal behaviors in a Pten mutant model, highlighting mTORC2 as a potential therapeutic target in mTORopathies.

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Cited by 8 publications
(3 citation statements)
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“…TSC malformations in the brain, which arise due to uncontrolled tissue growth, result from hyperactivity of mammalian target of rapamycin C1 (mTORC1) complex in neurons, glial cells, and ventricular ependyma [1]. Currently, TSC is classified within mTOR-related disorders, or so-called "mTORopathies," caused by mutations in regulatory genes in the mTOR pathway, e.g., TSC1, TSC2, AKT3, DEPDC5, and STRADA [2][3][4]. The condition was originally described in humans as a multisystem pathology by Bourneville in the 1880s.…”
Section: Introductionmentioning
confidence: 99%
“…TSC malformations in the brain, which arise due to uncontrolled tissue growth, result from hyperactivity of mammalian target of rapamycin C1 (mTORC1) complex in neurons, glial cells, and ventricular ependyma [1]. Currently, TSC is classified within mTOR-related disorders, or so-called "mTORopathies," caused by mutations in regulatory genes in the mTOR pathway, e.g., TSC1, TSC2, AKT3, DEPDC5, and STRADA [2][3][4]. The condition was originally described in humans as a multisystem pathology by Bourneville in the 1880s.…”
Section: Introductionmentioning
confidence: 99%
“…Targeting rictor with the miR-342-3p is also a key mechanism of action of glucocorticoids (dexamethasone) on regulatory T cells (Treg) to control inflammation [ 88 ]. Targeting mTORC2 is also promising for the treatment of several mTORopathies, which are neurological disorders characterized by aberrant mTOR signaling [ 385 ].…”
Section: Targeting the Mtorc2 Pathwaymentioning
confidence: 99%
“…A subset of mTORopathies however, (e.g. those caused by variants in PTEN , PIK3CA , and AKT ), hyperactivate both mTORC1 and mTORC2 [7,8], and mTORC2 hyperactivity has also been reported in human TLE [9]. It is unclear whether mTORC2 hyperactivity contributes to, or can cause, disease phenotypes such as epilepsy.…”
Section: Introductionmentioning
confidence: 99%