Failures to reconsolidate memory in a mouse model of Alzheimer's disease. - Wikidata - awgldk - TriplyDB

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q37410917

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Mechanisms underlying insulin deficiency-induced acceleration of β-amyloidosis in a mouse model of Alzheimer's disease Phospho-eIF2α level is important for determining abilities of BACE1 reduction to rescue cholinergic neurodegeneration and memory defects in 5XFAD mice PERK mediates eIF2α phosphorylation responsible for BACE1 elevation, CREB dysfunction and neurodegeneration in a mouse model of Alzheimer's disease.Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice.Molecular Differences and Similarities Between Alzheimer's Disease and the 5XFAD Transgenic Mouse Model of Amyloidosis.Differential involvement of brain-derived neurotrophic factor in reconsolidation and consolidation of conditioned taste aversion memory.Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.Evidence for Alzheimer's disease-linked synapse loss and compensation in mouse and human hippocampal CA1 pyramidal neurons.Area-specific alterations of synaptic plasticity in the 5XFAD mouse model of Alzheimer's disease: dissociation between somatosensory cortex and hippocampus.Deletion of the eIF2α Kinase GCN2 fails to rescue the memory decline associated with Alzheimer's disease.Increased fragmentation of sleep-wake cycles in the 5XFAD mouse model of Alzheimer's disease A combination Alzheimer's therapy targeting BACE1 and neprilysin in 5XFAD transgenic mice.Beneficial effects of the β-secretase inhibitor GRL-8234 in 5XFAD Alzheimer's transgenic mice lessen during disease progression.TrkB reduction exacerbates Alzheimer's disease-like signaling aberrations and memory deficits without affecting β-amyloidosis in 5XFAD mice.Fructus mume extracts alleviate cognitive impairments in 5XFAD transgenic mice Cerebral microvascular rather than parenchymal amyloid-β protein pathology promotes early cognitive impairment in transgenic mice Effects of BACE1 haploinsufficiency on APP processing and Aβ concentrations in male and female 5XFAD Alzheimer mice at different disease stages Diosgenin is an exogenous activator of 1,25D₃-MARRS/Pdia3/ERp57 and improves Alzheimer's disease pathologies in 5XFAD mice Postsynaptic degeneration as revealed by PSD-95 reduction occurs after advanced Aβ and tau pathology in transgenic mouse models of Alzheimer's disease Mechanisms that lessen benefits of β-secretase reduction in a mouse model of Alzheimer's disease.Neuronally-directed effects of RXR activation in a mouse model of Alzheimer's disease.Deciphering the molecular profile of plaques, memory decline and neuron loss in two mouse models for Alzheimer's disease by deep sequencing.Mouse models of Alzheimer's disease.Translational Assays for Assessment of Cognition in Rodent Models of Alzheimer's Disease and Dementia.Modulation of neuroinflammation and pathology in the 5XFAD mouse model of Alzheimer's disease using a biased and selective beta-1 adrenergic receptor partial agonist.Neural stem cell transplantation improves spatial learning and memory via neuronal regeneration in amyloid-β precursor protein/presenilin 1/tau triple transgenic mice.Kamikihi-to (KKT) rescues axonal and synaptic degeneration associated with memory impairment in a mouse model of Alzheimer's disease, 5XFAD.Seed-induced Aβ deposition is modulated by microglia under environmental enrichment in a mouse model of Alzheimer's disease.Tripchlorolide improves cognitive deficits by reducing amyloid β and upregulating synapse-related proteins in a transgenic model of Alzheimer's Disease.Cognitive recovery and restoration of cell proliferation in the dentate gyrus in the 5XFAD transgenic mice model of Alzheimer's disease following 2-hydroxy-DHA treatment.Onset of hippocampus-dependent memory impairments in 5XFAD transgenic mouse model of Alzheimer's disease.Sominone improves memory impairments and increases axonal density in Alzheimer's disease model mice, 5XFAD.Geniposide Attenuates the Phosphorylation of Tau Protein in Cellular and Insulin-deficient APP/PS1 Transgenic Mouse Model of Alzheimer's Disease.MK-0677, a Ghrelin Agonist, Alleviates Amyloid Beta-Related Pathology in 5XFAD Mice, an Animal Model of Alzheimer's Disease.

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Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

http://www.wikidata.org/entity/Q37410917

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 10 May 2009

@en

vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

@en

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

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type

label

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

@en

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

@nl

prefLabel

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

@en

Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

@nl

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J.NLM.2009.05.001

P1433

Neurobiology of Learning and Memory

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Failures to reconsolidate memory in a mouse model of Alzheimer's disease.

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P2093

Masuo Ohno

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P2860

Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval

Regulation of NMDA receptor trafficking by amyloid-beta

Why there are complementary learning systems in the hippocampus and neocortex: insights from the successes and failures of connectionist models of learning and memory

The organization of recent and remote memories

Autophosphorylation of alphaCaMKII is differentially involved in new learning and unlearning mechanisms of memory extinction.

Contextual fear, gestalt memories, and the hippocampus.

Inducible, pharmacogenetic approaches to the study of learning and memory.

CREB required for the stability of new and reactivated fear memories.

The neurobiology of consolidations, or, how stable is the engram?

Memory reconsolidation and extinction have distinct temporal and biochemical signatures.

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455-459

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scholarly article

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10.1016/J.NLM.2009.05.001

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3

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92

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2009-05-10T00:00:00Z

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24421053

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19435612

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Alzheimer's disease

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2772829

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