Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.
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The neurotrophic compound J147 reverses cognitive impairment in aged Alzheimer's disease miceMild chronic cerebral hypoperfusion induces neurovascular dysfunction, triggering peripheral beta-amyloid brain entry and aggregationInhibitory 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 deathAmyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networksLevetiracetam 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 NeurogenesisAmyloid beta-protein monomer folding: free-energy surfaces reveal alloform-specific differencesEffects of grape seed-derived polyphenols on amyloid beta-protein self-assembly and cytotoxicityTau Oligomers: The Toxic Player at Synapses in Alzheimer's DiseaseDisaggregases, molecular chaperones that resolubilize protein aggregatesTargeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer's disease immunotherapeuticsAlzheimer'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 capacitiesIVIg protects the 3xTg-AD mouse model of Alzheimer’s disease from memory deficit and Aβ pathologyStructural Correlates of Antibodies Associated with Acute Reversal of Amyloid -related Behavioral Deficits in a Mouse Model of Alzheimer DiseasePhospholipase A2 reduction ameliorates cognitive deficits in a mouse model of Alzheimer's diseaseChronic Anatabine Treatment Reduces Alzheimer's Disease (AD)-Like Pathology and Improves Socio-Behavioral Deficits in a Transgenic Mouse Model of ADNovel 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 deficitsIntracellular 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 miceTranssynaptic 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 proteinAlzheimer disease models and human neuropathology: similarities and differencesOptical 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-βThe 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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P2860
Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh
2007年學術文章
@zh-hant
name
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@en
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@nl
type
label
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@en
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@nl
prefLabel
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@en
Accelerating amyloid-beta fibr ...... lzheimer disease mouse models.
@nl
P2093
P2860
P356
P1476
Accelerating amyloid-beta fibr ...... Alzheimer disease mouse models
@en
P2093
Hilary Gerstein
Irene H Cheng
Jorge J Palop
Jukka Puoliväli
Justin Legleiter
Karen H Ashe
Kimberly Scearce-Levie
Lennart Mucke
Nga Bien-Ly
Paul J Muchowski
P2860
P304
23818-23828
P356
10.1074/JBC.M701078200
P407
P577
2007-06-04T00:00:00Z