7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2-3-dihydro-1h-indol-5-yl)-7h-pyrrolo(2-3-d)pyrimidin-4-amine and Cognitive-Dysfunction

7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2-3-dihydro-1h-indol-5-yl)-7h-pyrrolo(2-3-d)pyrimidin-4-amine has been researched along with Cognitive-Dysfunction* in 2 studies

Other Studies

2 other study(ies) available for 7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2-3-dihydro-1h-indol-5-yl)-7h-pyrrolo(2-3-d)pyrimidin-4-amine and Cognitive-Dysfunction

Article	Year
Suppression of CHOP Reduces Neuronal Apoptosis and Rescues Cognitive Impairment Induced by Intermittent Hypoxia by Inhibiting Bax and Bak Activation. Neural plasticity, 2021, Volume: 2021 Our previous study showed that growth arrest- and DNA damage-inducible gene 153 (GAD153/CHOP) plays an important role in intermittent hypoxia- (IH-) induced apoptosis and impaired synaptic plasticity. This study is aimed at determining which signaling pathway is activated to induce CHOP and the role of this protein in mitochondria-dependent apoptosis induced by IH. In the in vivo study, mice were placed in IH chambers for 8 h daily over a period of 2 weeks; the IH chambers had oxygen (O Topics: Adenine; Animals; Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; Cognitive Dysfunction; Hypoxia; Indoles; Male; Mice; Mice, Inbred C57BL; Neurons; PC12 Cells; Rats; Transcription Factor CHOP	2021
Local Inhibition of PERK Enhances Memory and Reverses Age-Related Deterioration of Cognitive and Neuronal Properties. The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018, 01-17, Volume: 38, Issue:3 Protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) is one of four known kinases that respond to cellular stress by deactivating the eukaryotic initiation factor 2 α (eIF2α) or other signal transduction cascades. Recently, both eIF2α and its kinases were found to play a role in normal and pathological brain function. Here, we show that reduction of either the amount or the activity of PERK, specifically in the CA1 region of the hippocampus in young adult male mice, enhances neuronal excitability and improves cognitive function. In addition, this manipulation rescues the age-dependent cellular phenotype of reduced excitability and memory decline. Specifically, the reduction of PERK expression in the CA1 region of the hippocampus of middle-aged male mice using a viral vector rejuvenates hippocampal function and improves hippocampal-dependent learning. These results delineate a mechanism for behavior and neuronal aging and position PERK as a promising therapeutic target for age-dependent brain malfunction. Topics: Adenine; Aging; Animals; Cognition; Cognitive Dysfunction; eIF-2 Kinase; Enzyme Inhibitors; Hippocampus; Indoles; Learning; Male; Memory; Mice; Pyramidal Cells	2018

Article

Year

Suppression of CHOP Reduces Neuronal Apoptosis and Rescues Cognitive Impairment Induced by Intermittent Hypoxia by Inhibiting Bax and Bak Activation.

Neural plasticity, 2021, Volume: 2021

Our previous study showed that growth arrest- and DNA damage-inducible gene 153 (GAD153/CHOP) plays an important role in intermittent hypoxia- (IH-) induced apoptosis and impaired synaptic plasticity. This study is aimed at determining which signaling pathway is activated to induce CHOP and the role of this protein in mitochondria-dependent apoptosis induced by IH. In the in vivo study, mice were placed in IH chambers for 8 h daily over a period of 2 weeks; the IH chambers had oxygen (O

Topics: Adenine; Animals; Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; Cognitive Dysfunction; Hypoxia; Indoles; Male; Mice; Mice, Inbred C57BL; Neurons; PC12 Cells; Rats; Transcription Factor CHOP

2021

Local Inhibition of PERK Enhances Memory and Reverses Age-Related Deterioration of Cognitive and Neuronal Properties.

The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018, 01-17, Volume: 38, Issue:3

Protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK) is one of four known kinases that respond to cellular stress by deactivating the eukaryotic initiation factor 2 α (eIF2α) or other signal transduction cascades. Recently, both eIF2α and its kinases were found to play a role in normal and pathological brain function. Here, we show that reduction of either the amount or the activity of PERK, specifically in the CA1 region of the hippocampus in young adult male mice, enhances neuronal excitability and improves cognitive function. In addition, this manipulation rescues the age-dependent cellular phenotype of reduced excitability and memory decline. Specifically, the reduction of PERK expression in the CA1 region of the hippocampus of middle-aged male mice using a viral vector rejuvenates hippocampal function and improves hippocampal-dependent learning. These results delineate a mechanism for behavior and neuronal aging and position PERK as a promising therapeutic target for age-dependent brain malfunction.

Topics: Adenine; Aging; Animals; Cognition; Cognitive Dysfunction; eIF-2 Kinase; Enzyme Inhibitors; Hippocampus; Indoles; Learning; Male; Memory; Mice; Pyramidal Cells

2018