Increased PKA signaling disrupts recognition memory and spatial memory: role in Huntington's disease. - Wikidata - wikimedia - TriplyDB

Increased PKA signaling disrupts recognition memory and spatial memory: role in Huntington's disease.

Increased PKA signaling disrupts recognition memory and spatial memory: role in Huntington's disease.

http://www.wikidata.org/entity/Q45303900

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The PDE1/5 Inhibitor SCH-51866 Does Not Modify Disease Progression in the R6/2 Mouse Model of Huntington's Disease Global and local missions of cAMP signaling in neural plasticity, learning, and memory PDE4 as a target for cognition enhancement Role of protein kinase A in regulating mitochondrial function and neuronal development: implications to neurodegenerative diseases Phosphodiesterases in neurodegenerative disorders Identification of hepta-histidine as a candidate drug for Huntington's disease by in silico-in vitro- in vivo-integrated screens of chemical libraries Synaptic mutant huntingtin inhibits synapsin-1 phosphorylation and causes neurological symptoms.A two years longitudinal study of a transgenic Huntington disease monkey.Phosphodiesterase Inhibitors as a Therapeutic Approach to Neuroprotection and Repair.Disruption of striatal-enriched protein tyrosine phosphatase (STEP) function in neuropsychiatric disorders Regulation of hippocampal cGMP levels as a candidate to treat cognitive deficits in Huntington's disease.Striatal pre-enkephalin overexpression improves Huntington's disease symptoms in the R6/2 mouse model of Huntington's disease A role for Kalirin-7 in corticostriatal synaptic dysfunction in Huntington's disease Early-onset sleep defects in Drosophila models of Huntington's disease reflect alterations of PKA/CREB signaling.NAAG peptidase inhibitors and deletion of NAAG peptidase gene enhance memory in novel object recognition test.Regulation of feedback between protein kinase A and the proteasome system worsens Huntington's disease Phosphodiesterase inhibition rescues chronic cognitive deficits induced by traumatic brain injury Investigational drugs for the management of Huntington's disease: are we there yet?Targeting CAG repeat RNAs reduces Huntington's disease phenotype independently of huntingtin levels.Hyperkinetic disorders and loss of synaptic downscaling.How does adenosine control neuronal dysfunction and neurodegeneration?Cognitive dysfunction in Huntington's disease: mechanisms and therapeutic strategies beyond BDNF.Translational Assays for Assessment of Cognition in Rodent Models of Alzheimer's Disease and Dementia.Dysregulation of Corticostriatal Connectivity in Huntington's Disease: A Role for Dopamine Modulation Suppression of inhibitory GABAergic transmission by cAMP signaling pathway: alterations in learning and memory mutants.Adenosine A2A receptor inactivation alleviates early-onset cognitive dysfunction after traumatic brain injury involving an inhibition of tau hyperphosphorylation Neurotrophin receptor p75(NTR) mediates Huntington's disease-associated synaptic and memory dysfunction.Early down-regulation of PKCδ as a pro-survival mechanism in Huntington's disease.Increased 5-methylcytosine and decreased 5-hydroxymethylcytosine levels are associated with reduced striatal A2AR levels in Huntington's disease.Fingolimod (FTY720) enhances hippocampal synaptic plasticity and memory in Huntington's disease by preventing p75NTR up-regulation and astrocyte-mediated inflammation.PDE10 inhibition increases GluA1 and CREB phosphorylation and improves spatial and recognition memories in a Huntington's disease mouse model.Prostaglandin E2 EP1 receptor antagonist improves motor deficits and rescues memory decline in R6/1 mouse model of Huntington's disease.Cyclic nucleotide signaling changes associated with normal aging and age-related diseases of the brain.A negative allosteric modulator of PDE4D enhances learning after traumatic brain injury.The PDE4 cAMP-Specific Phosphodiesterases: Targets for Drugs with Antidepressant and Memory-Enhancing Action.Restoring GABAergic inhibition rescues memory deficits in a Huntington's disease mouse model.RTP801 Is Involved in Mutant Huntingtin-Induced Cell Death.Rescuing prefrontal cAMP-CREB pathway reverses working memory deficits during withdrawal from prolonged alcohol exposure.PDE inhibition and cognition enhancement.Transcriptional profiling and biomarker identification reveal tissue specific effects of expanded ataxin-3 in a spinocerebellar ataxia type 3 mouse model.

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P2860

Increased PKA signaling disrupts recognition memory and spatial memory: role in Huntington's disease.

http://www.wikidata.org/entity/Q45303900

description

2011 nî lūn-bûn

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2011年の論文

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年学术文章

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2011年學術文章

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2011年學術文章

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2011年學術文章

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name

Increased PKA signaling disrup ...... role in Huntington's disease.

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Increased PKA signaling disrup ...... role in Huntington's disease.

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type

label

Increased PKA signaling disrup ...... role in Huntington's disease.

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Increased PKA signaling disrup ...... role in Huntington's disease.

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prefLabel

Increased PKA signaling disrup ...... role in Huntington's disease.

@en

Increased PKA signaling disrup ...... role in Huntington's disease.

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Human Molecular Genetics

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Increased PKA signaling disrup ...... role in Huntington's disease.

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Ana Saavedra

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Olga Carretón

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P2860

A protein factor essential for microtubule assembly

A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington's disease chromosomes.

Striatal-enriched protein tyrosine phosphatase expression and activity in Huntington's disease: a STEP in the resistance to excitotoxicity

Cyclic nucleotide phosphodiesterases: molecular regulation to clinical use

Morris water maze: procedures for assessing spatial and related forms of learning and memory

The operant serial implicit learning task reveals early onset motor learning deficits in the Hdh knock-in mouse model of Huntington's disease

Phosphorylation of the Ras-GRF1 exchange factor at Ser916/898 reveals activation of Ras signaling in the cerebral cortex

Brain-derived neurotrophic factor restores synaptic plasticity in a knock-in mouse model of Huntington's disease

Impaired spatial working memory but spared spatial reference memory following functional loss of NMDA receptors in the dentate gyrus

Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice

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4232-4247

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scholarly article

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10.1093/HMG/DDR351

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21

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20

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Esther Perez-Navarro

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2011-08-11T00:00:00Z

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51565944

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21835884

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Huntington disease