Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models. - Wikidata - awgldk - TriplyDB

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.

Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.

http://www.wikidata.org/entity/Q46380915

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The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease mice Mild chronic cerebral hypoperfusion induces neurovascular dysfunction, triggering peripheral beta-amyloid brain entry and aggregation Inhibitory interneuron deficit links altered network activity and cognitive dysfunction in Alzheimer model.Altered longevity-assurance activity of p53:p44 in the mouse causes memory loss, neurodegeneration and premature death Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer's disease model.Knockdown of BACE1-AS Nonprotein-Coding Transcript Modulates Beta-Amyloid-Related Hippocampal Neurogenesis Amyloid beta-protein monomer folding: free-energy surfaces reveal alloform-specific differences Effects of grape seed-derived polyphenols on amyloid beta-protein self-assembly and cytotoxicity Tau Oligomers: The Toxic Player at Synapses in Alzheimer's Disease Disaggregases, molecular chaperones that resolubilize protein aggregates Targeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer's disease immunotherapeutics Alzheimer's disease-like APP processing in wild-type mice identifies synaptic defects as initial steps of disease progression.Interactions between Aβ oligomers and presynaptic cholinergic signaling: age-dependent effects on attentional capacities IVIg protects the 3xTg-AD mouse model of Alzheimer’s disease from memory deficit and Aβ pathology Structural Correlates of Antibodies Associated with Acute Reversal of Amyloid -related Behavioral Deficits in a Mouse Model of Alzheimer Disease Phospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's disease Chronic Anatabine Treatment Reduces Alzheimer's Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of AD Novel insights into protein misfolding diseases revealed by ion mobility-mass spectrometry.Blocking early GABA depolarization with bumetanide results in permanent alterations in cortical circuits and sensorimotor gating deficits Intracellular amyloid formation in muscle cells of Abeta-transgenic Caenorhabditis elegans: determinants and physiological role in copper detoxification.Cystatin C-cathepsin B axis regulates amyloid beta levels and associated neuronal deficits in an animal model of Alzheimer's disease.Neprilysin overexpression inhibits plaque formation but fails to reduce pathogenic Abeta oligomers and associated cognitive deficits in human amyloid precursor protein transgenic mice.COL25A1 triggers and promotes Alzheimer's disease-like pathology in vivo.Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer's Disease.Allele-specific RNAi mitigates phenotypic progression in a transgenic model of Alzheimer's disease.Reduced IGF-1 signaling delays age-associated proteotoxicity in mice Transsynaptic progression of amyloid-β-induced neuronal dysfunction within the entorhinal-hippocampal network.Many neuronal and behavioral impairments in transgenic mouse models of Alzheimer's disease are independent of caspase cleavage of the amyloid precursor protein Alzheimer disease models and human neuropathology: similarities and differences Optical trapping with high forces reveals unexpected behaviors of prion fibrils.Enkephalin elevations contribute to neuronal and behavioral impairments in a transgenic mouse model of Alzheimer's disease.Brain amyloid-β oligomers in ageing and Alzheimer's disease.Physiologic brain activity causes DNA double-strand breaks in neurons, with exacerbation by amyloid-β The multi-functional drug tropisetron binds APP and normalizes cognition in a murine Alzheimer's model.FcγRIIb mediates amyloid-β neurotoxicity and memory impairment in Alzheimer's disease.Antroquinonol Lowers Brain Amyloid-β Levels and Improves Spatial Learning and Memory in a Transgenic Mouse Model of Alzheimer's Disease.Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer's disease model.Biochemical and immunohistochemical analysis of an Alzheimer's disease mouse model reveals the presence of multiple cerebral Abeta assembly forms throughout life.Candidate anti-A beta fluorene compounds selected from analogs of amyloid imaging agents

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Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.

http://www.wikidata.org/entity/Q46380915

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name

Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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type

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Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.

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Journal of Biological Chemistry

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Accelerating amyloid-beta fibr ...... Alzheimer disease mouse models

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Hilary Gerstein

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

Irene H Cheng

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Jorge J Palop

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Jukka Puoliväli

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Justin Legleiter

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Karen H Ashe

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Kimberly Scearce-Levie

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Lennart Mucke

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Nga Bien-Ly

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Paul J Muchowski

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Alzheimer Disease in the US Population

Global prevalence of dementia: a Delphi consensus study

Dysfunction of amyloid precursor protein signaling in neurons leads to DNA synthesis and apoptosis

The amyloid precursor protein: beyond amyloid

Globular amyloid beta-peptide oligomer - a homogenous and stable neuropathological protein in Alzheimer's disease

Cytoplasmic domain of the beta-amyloid protein precursor of Alzheimer's disease: function, regulation of proteolysis, and implications for drug development

A specific amyloid-beta protein assembly in the brain impairs memory

Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound-B

Diffusible, nonfibrillar ligands derived from Abeta1-42 are potent central nervous system neurotoxins

Twenty years of the Alzheimer's disease amyloid hypothesis: a genetic perspective

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23818-23828

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scholarly article

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10.1074/JBC.M701078200

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P433

33

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282

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Sylvain E Lesné

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2007-06-04T00:00:00Z

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6288944

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17548355

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Alzheimer's disease