Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice. - Wikidata - thesis-toulmin - TriplyDB

Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice.

Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice.

http://www.wikidata.org/entity/Q30486668

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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 Performance enhancement at the cost of potential brain plasticity: neural ramifications of nootropic drugs in the healthy developing brain Mood disorders in Huntington's disease: from behavior to cellular and molecular mechanisms Ampakines cause sustained increases in brain-derived neurotrophic factor signaling at excitatory synapses without changes in AMPA receptor subunit expression Developing stem cell therapies for juvenile and adult-onset Huntington's disease Fragile X syndrome and targeted treatment trials.Mouse models of polyglutamine diseases in therapeutic approaches: review and data table. Part II.Lessons learned from the transgenic Huntington's disease rats Glutamate receptor ion channels: structure, regulation, and function AMPAKINE enhancement of social interaction in the BTBR mouse model of autism The Huntington's disease mutation impairs Huntingtin's role in the transport of NF-κB from the synapse to the nucleus.Protective effects of low-intensity pulsed ultrasound on aluminum-induced cerebral damage in Alzheimer's disease rat model.Improvement of neuropathology and transcriptional deficits in CAG 140 knock-in mice supports a beneficial effect of dietary curcumin in Huntington's disease.Activation of signaling pathways following localized delivery of systemically administered neurotrophic factors across the blood-brain barrier using focused ultrasound and microbubbles.Chronic intermittent hypoxia-induced deficits in synaptic plasticity and neurocognitive functions: a role for brain-derived neurotrophic factor.Long-term memory deficits are associated with elevated synaptic ERK1/2 activation and reversed by mGluR5 antagonism in an animal model of autism.Imbalanced pattern completion vs. separation in cognitive disease: network simulations of synaptic pathologies predict a personalized therapeutics strategy.Pharmacological enhancement of memory or cognition in normal subjects Repetitive self-grooming behavior in the BTBR mouse model of autism is blocked by the mGluR5 antagonist MPEP.Rescuing the Corticostriatal Synaptic Disconnection in the R6/2 Mouse Model of Huntington's Disease: Exercise, Adenosine Receptors and Ampakines Estrogen's Place in the Family of Synaptic Modulators.Challenges for and current status of research into positive modulators of AMPA receptors.BDNF signaling and survival of striatal neurons.Brain-derived neurotrophic factor is associated with age-related decline in hippocampal volume.7,8-dihydroxyflavone rescues spatial memory and synaptic plasticity in cognitively impaired aged rats.BDNF upregulation rescues synaptic plasticity in middle-aged ovariectomized rats.BDNF overexpression in the forebrain rescues Huntington's disease phenotypes in YAC128 mice AMPAkines have novel analgesic properties in rat models of persistent neuropathic and inflammatory pain.Therapeutic approaches to preventing cell death in Huntington disease Brief ampakine treatments slow the progression of Huntington's disease phenotypes in R6/2 mice Electroconvulsive shock ameliorates disease processes and extends survival in huntingtin mutant mice.Neurogenic and neurotrophic effects of BDNF peptides in mouse hippocampal primary neuronal cell cultures The biochemistry of memory: The 26year journey of a 'new and specific hypothesis'.Striatal neurons expressing full-length mutant huntingtin exhibit decreased N-cadherin and altered neuritogenesis.The likelihood of cognitive enhancement Long-term potentiation and long-term depression: a clinical perspective.Striatal synaptic dysfunction and hippocampal plasticity deficits in the Hu97/18 mouse model of Huntington disease Impaired alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking and function by mutant huntingtin.Conditional BDNF release under pathological conditions improves Huntington's disease pathology by delaying neuronal dysfunction.Cellular therapy and induced neuronal replacement for Huntington's disease.

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Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice.

http://www.wikidata.org/entity/Q30486668

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2009 nî lūn-bûn

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2009 թուականի Մարտին հրատարակուած գիտական յօդուած

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2009 թվականի մարտին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Proceedings of the National Academy of Sciences of the United States of America

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Up-regulating BDNF with an amp ...... ington's disease knockin mice.

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Christine M Gall

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Christopher S Rex

http://www.w3.org/2001/XMLSchema#string

Danielle A Simmons

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Gary Lynch

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Linda Palmer

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Vadim Fedulov

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Vijay Pandyarajan

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P2860

Facilitation of task performance and removal of the effects of sleep deprivation by an ampakine (CX717) in nonhuman primates.

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

Chronic elevation of brain-derived neurotrophic factor by ampakines

Glutamate-based therapeutic approaches: ampakines

Impaired synaptic plasticity in mice carrying the Huntington's disease mutation

Time course of early motor and neuropathological anomalies in a knock-in mouse model of Huntington's disease with 140 CAG repeats

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

BDNF function in adult synaptic plasticity: the synaptic consolidation hypothesis.

LTP consolidation: substrates, explanatory power, and functional significance.

Integrin-driven actin polymerization consolidates long-term potentiation

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10.1073/PNAS.0811228106

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12

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106

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24180803

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19264961

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Huntington disease

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2660722

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