ro-4956371 and Cognitive-Dysfunction

ro-4956371 has been researched along with Cognitive-Dysfunction* in 2 studies

Other Studies

2 other study(ies) available for ro-4956371 and Cognitive-Dysfunction

Article	Year
mGluR5 antagonism increases autophagy and prevents disease progression in the Science signaling, 2017, Dec-19, Volume: 10, Issue:510 Huntington's disease (HD) is a neurodegenerative disease caused by an expansion in the huntingtin protein (also called Htt) that induces neuronal cell death with age. We found that the treatment of 12-month-old symptomatic heterozygous and homozygous Topics: Animals; Apoptosis; Autophagy; Caspase 3; Cognitive Dysfunction; Disease Models, Animal; Disease Progression; Gene Knock-In Techniques; Humans; Huntingtin Protein; Huntington Disease; Imidazoles; Male; Mice; Motor Activity; Neurons; Pyridines; Receptor, Metabotropic Glutamate 5	2017
Chronic Pharmacological mGluR5 Inhibition Prevents Cognitive Impairment and Reduces Pathogenesis in an Alzheimer Disease Mouse Model. Cell reports, 2016, 05-31, Volume: 15, Issue:9 Beta-amyloid (Aβ) oligomers contribute to the pathophysiology of Alzheimer disease (AD), and metabotropic glutamate receptor 5 (mGluR5) has been shown to act as a receptor for both Aβ oligomers and cellular prion proteins. Furthermore, the genetic deletion of mGluR5 in an APPswe/PS1ΔE9 mouse model of AD improves cognitive function and reduces Aβ plaques and Aβ oligomer concentrations. Here, we show that chronic administration of the orally bioavailable mGluR5-selective negative allosteric modulator CTEP, which is similar in structure, potency, and selectivity to Basimglurant (RO4917523), which is currently in phase II clinical development for major depressive disorder and fragile X syndrome, reverses cognitive decline in APPswe/PS1ΔE9 mice and reduces Aβ plaque deposition and soluble Aβ oligomer concentrations in both APPswe/PS1ΔE9 and 3xTg-AD male mice. These findings suggest that CTEP or its analogue Basimglutant might potentially be an effective therapeutic for the treatment of AD patients. Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Cognitive Dysfunction; Disease Models, Animal; Imidazoles; Memory; Mice, Inbred C57BL; Mice, Transgenic; Plaque, Amyloid; Pyridines; Receptor, Metabotropic Glutamate 5	2016

Article

Year

mGluR5 antagonism increases autophagy and prevents disease progression in the

Science signaling, 2017, Dec-19, Volume: 10, Issue:510

Huntington's disease (HD) is a neurodegenerative disease caused by an expansion in the huntingtin protein (also called Htt) that induces neuronal cell death with age. We found that the treatment of 12-month-old symptomatic heterozygous and homozygous

Topics: Animals; Apoptosis; Autophagy; Caspase 3; Cognitive Dysfunction; Disease Models, Animal; Disease Progression; Gene Knock-In Techniques; Humans; Huntingtin Protein; Huntington Disease; Imidazoles; Male; Mice; Motor Activity; Neurons; Pyridines; Receptor, Metabotropic Glutamate 5

2017

Chronic Pharmacological mGluR5 Inhibition Prevents Cognitive Impairment and Reduces Pathogenesis in an Alzheimer Disease Mouse Model.

Cell reports, 2016, 05-31, Volume: 15, Issue:9

Beta-amyloid (Aβ) oligomers contribute to the pathophysiology of Alzheimer disease (AD), and metabotropic glutamate receptor 5 (mGluR5) has been shown to act as a receptor for both Aβ oligomers and cellular prion proteins. Furthermore, the genetic deletion of mGluR5 in an APPswe/PS1ΔE9 mouse model of AD improves cognitive function and reduces Aβ plaques and Aβ oligomer concentrations. Here, we show that chronic administration of the orally bioavailable mGluR5-selective negative allosteric modulator CTEP, which is similar in structure, potency, and selectivity to Basimglurant (RO4917523), which is currently in phase II clinical development for major depressive disorder and fragile X syndrome, reverses cognitive decline in APPswe/PS1ΔE9 mice and reduces Aβ plaque deposition and soluble Aβ oligomer concentrations in both APPswe/PS1ΔE9 and 3xTg-AD male mice. These findings suggest that CTEP or its analogue Basimglutant might potentially be an effective therapeutic for the treatment of AD patients.

Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Cognitive Dysfunction; Disease Models, Animal; Imidazoles; Memory; Mice, Inbred C57BL; Mice, Transgenic; Plaque, Amyloid; Pyridines; Receptor, Metabotropic Glutamate 5

2016