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Charles A. Hoeffer

Researcher at University of Colorado Boulder

Publications -  60
Citations -  5258

Charles A. Hoeffer is an academic researcher from University of Colorado Boulder. The author has contributed to research in topics: Synaptic plasticity & Long-term potentiation. The author has an hindex of 27, co-authored 54 publications receiving 4351 citations. Previous affiliations of Charles A. Hoeffer include Baylor College of Medicine & Howard Hughes Medical Institute.

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mTOR signaling: at the crossroads of plasticity, memory and disease.

TL;DR: Although the majority of evidence linking mTOR function to synaptic plasticity comes from studies utilizing rapamycin, studies in genetically modified mice also suggest that mTOR couples receptors to the translation machinery for establishing long-lasting synaptic changes that are the basis for higher order brain function, including long-term memory.
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The maternal interleukin-17a pathway in mice promotes autism-like phenotypes in offspring

TL;DR: In this paper, the authors used both genetic mutants and blocking antibodies in mice to find that retinoic acid receptor-related orphan nuclear receptor gamma t (RORγt)-dependent effector T lymphocytes [for example, T helper 17 (TH17) cells] and the effector cytokine interleukin 17a (IL-17a) are required in mothers for MIA-induced behavioral abnormalities in offspring.
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Dysregulation of mTOR Signaling in Fragile X Syndrome

TL;DR: Elevated mTOR signaling may provide a functional link between overactivation of group I mGluRs and aberrant synaptic plasticity in the fragile X mouse, mechanisms relevant to impaired cognition in fragile X syndrome.
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Dysregulation of the mTOR Pathway Mediates Impairment of Synaptic Plasticity in a Mouse Model of Alzheimer's Disease

TL;DR: Evidence is provided that inhibition of mTOR signaling correlates with impairment in synaptic plasticity in hippocampal slices from an AD mouse model and in wild-type slices exposed to exogenous Aβ1-42, which supports the notion that the mTOR pathway modulates Aβ-related synaptic dysfunction in AD.
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Removal of FKBP12 enhances mTOR-Raptor interactions, LTP, memory, and perseverative/repetitive behavior.

TL;DR: The results indicate that FKBP12 plays a critical role in the regulation of mTOR-Raptor interactions, LTP, memory, and perseverative behaviors.